*Cancer is DEAD: Cancer cures from A to Z.

http://massspectrumbotanicals.com/

Out of all of my media projects, I’ve never been more infuriated than by this research thrust. You’d be hard-pressed to find someone that wouldn’t agree that the medical establishment isn’t really trying to cure cancer, and they’re all correct.

The cure for cancer isn’t one single silver bullet if only we could find it (or they’d stop suppressing it). There are scores of cures for cancer, and many of them all well known and out in the open, yet nonpursued by probably the majority of the medical doctors or industries out there. This presentation proves the beyond the shadow of a doubt.

You’d think that the sorts of people in the business of saving lives, especially those who deal in cancer ‘treatments’, would have a hobby of reading the sorts of scholarly papers I dug through to compile this. From there you’d think that from what they learn via this hypothetical hobby they’d be constantly excited to tell their next cancer patient about the latest simple and often natural remedies they can also do themselves to have the best shot at surviving.

But the fact is this isn’t how it works. In the wake of building this presentation I’ve never been more convinced the the overarching totality of the medical establishment are a massive group of psychopaths. When they know about proven effective and safe treatments, or are shown them by their patients, and they consciously dismiss and shrug them off, how can these people not be deranged sociopaths when their patients face horrifying death?

If you’ve ever witnessed the process of death via brain cancer for instance, you’d catch my drift. I had an aunt die this way and it’s amongst the most disturbing ways you could ever contemplate your last days on earth. Now my mom has lung cancer and they’ve pissed of the wrong person. May their monopoly on suffering go crashing into the abyss. Considering that about 550,000 people die annually from cancer, I apologize to those for whom it’s already too late, but I present to you my most important presentation to date…

DISCLAIMER: I’m not suggesting people don’t follow their doctors orders. I explain this better at the end of the presentation. There isn’t likely any sure silver bullet to curing existing cancer, while in the right combination in your diet you shouldn’t ever have to worry about getting it.

Cancer is DEAD: Cancer cures from A to Z
Version 1.0
By Ignorance Isn’t Bliss
ignoranceisfutile.org…

Acai Berries
Source: Fruits from the Açaí Palm.
en.wikipedia.org…
www.youtube.com…

Brazilian berry destroys cancer cells in lab, UF study shows
news.ufl.edu…

Published today in the Journal of Agricultural and Food Chemistry, the study showed extracts from acai (ah-SAH’-ee) berries triggered a self-destruct response in up to 86 percent of leukemia cells tested, said Stephen Talcott, an assistant professor with UF’s Institute of Food and Agricultural Sciences. “Acai berries are already considered one of the richest fruit sources of antioxidants,” Talcott said. “This study was an important step toward learning what people may gain from using beverages, dietary supplements or other products made with the berries.”

Acrylamide (BAD)

www.cancer.gov…

*Acrylamide is a chemical used primarily for industrial purposes.
*Acrylamide has been found in certain foods, with especially high levels in potato chips, French fries, and other food products produced by high-temperature cooking.
*Food and cigarette smoke are the major sources of exposure to acrylamide.
*Acrylamide is considered to be a mutagen and a probable human carcinogen, based mainly on studies in laboratory animals.
*Scientists do not yet know with any certainty whether the levels of acrylamide typically found in some foods pose a health risk for humans.

How does cooking produce acrylamide?
Asparagine is an amino acid (a building block of proteins) that is found in many vegetables, with higher concentrations in some varieties of potatoes. When heated to high temperatures in the presence of certain sugars, asparagine can form acrylamide. High-temperature cooking methods, such as frying, baking, or broiling, have been found to produce acrylamide (3), while boiling and microwaving appear less likely to do so. Longer cooking times can also increase acrylamide production when the cooking temperature is above 120 degrees Celsius (4, 5).

Aloe-emodin
Sources: Aloe Vera Plant, Aloe Vera Juice (inexpensive at Hispanic Markets).

Aloe-Emodin Induces Apoptosis in T24 Human Bladder Cancer Cells
www.ncbi.nlm.nih.gov…

AE inhibited cell viability, and induced G2/M arrest and apoptosis in T24 cells. AE increased the levels of Wee1 and cdc25c, and may have led to inhibition of the levels of cyclin-dependent kinase 1 and cyclin B1, which cause G2/M arrest. AE induced p53 expression and was accompanied by the induction of p21 and caspase-3 activation, which was associated with apoptosis. In addition, AE was associated with a marked increase in Fas/APO1 receptor and Bax expression but it inhibited Bcl-2 expression.

Protein kinase C involvement in aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell
www.ncbi.nlm.nih.gov…

This study demonstrated aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell lines CH27 (human lung squamous carcinoma cell) and H460 (human lung non-small cell carcinoma cell). Aloe-emodin- and emodin-induced apoptosis was characterized by nuclear morphological changes and DNA fragmentation.

The antiproliferative activity of aloe-emodin is through p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines
www.ncbi.nlm.nih.gov…

The aim of this study is to investigate the anticancer effect of aloe-emodin in two human liver cancer cell lines, Hep G2 and Hep 3B. We observed that aloe-emodin inhibited cell proliferation and induced apoptosis in both examined cell lines, but with different the antiproliferative mechanisms.

Aloe-emodin Is a New Type of Anticancer Agent with Selective Activity against Neuroectodermal Tumors
cancerres.aacrjournals.org…

Here we report that aloe-emodin (AE), a hydroxyanthraquinone present in Aloe vera leaves, has a specific in vitro and in vivo antineuroectodermal tumor activity. The growth of human neuroectodermal tumors is inhibited in mice with severe combined immunodeficiency without any appreciable toxic effects on the animals. The compound does not inhibit the proliferation of normal fibroblasts nor that of hemopoietic progenitor cells. The cytotoxicity mechanism consists of the induction of apoptosis, whereas the selectivity against neuroectodermal tumor cells is founded on a specific energy-dependent pathway of drug incorporation. Taking into account its unique cytotoxicity profile and mode of action, AE might represent a conceptually new lead antitumor drug.

Aloe-emodin induced in vitro G2/M arrest of cell cycle in human promyelocytic leukemia HL-60 cells
www.ncbi.nlm.nih.gov…

Aloe-emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with aloe-emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with aloe-emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of aloe-emodin.

Aloe-emodin-induced apoptosis in human gastric carcinoma cells
www.ncbi.nlm.nih.gov…

The purpose of this study was to investigate the anticancer effect of aloe-emodin, an anthraquinone compound present in the leaves of Aloe vera, on two distinct human gastric carcinoma cell lines, AGS and NCI-N87. We demonstrate that aloe-emodin induced cell death in a dose- and time-dependent manner. Noteworthy is that the AGS cells were generally more sensitive than the NCI-N87 cells. Aloe-emodin caused the release of apoptosis-inducing factor and cytochrome c from mitochondria, followed by the activation of caspase-3, leading to nuclear shrinkage and apoptosis.

Aloe-emodin induces in vitro G2/M arrest and alkaline phosphatase activation in human oral cancer KB cells
www.ncbi.nlm.nih.gov…

Aloe-emodin is a natural anthraquinone compound from the root and rhizome of Rheum palmatum. In this study, KB cells were treated with 2.5, 5, 10, 20, and 40 microM aloe-emodin for 1 to 5 days. The results showed that aloe-emodin inhibited cancer cells in a dose-dependent manner. Treatment with aloe-emodin at 10 to 40 microM resulted in cell cycle arrest at G2/M phase. The alkaline phosphatase (ALP) activity in KB cells increased upon treatment with aloe-emodin when compared to controls. This is one of the first studies to focus on the expression of ALP in human oral carcinomas cells treated with aloe-emodin. These results indicate that aloe-emodin has anti-cancer effect on oral cancer, which may lead to its use in chemotherapy and chemopreventment of oral cancer.

Anandamide
Source: Cannabis
www.ncbi.nlm.nih.gov…
The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation
www.ncbi.nlm.nih.gov…

Anandamide was the first brain metabolite shown to act as a ligand of “central” CB1 cannabinoid receptors. Here we report that the endogenous cannabinoid potently and selectively inhibits the proliferation of human breast cancer cells in vitro. Anandamide dose-dependently inhibited the proliferation of MCF-7 and EFM-19 cells with IC50 values between 0.5 and 1.5 μM and 83–92% maximal inhibition at 5–10 μM. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 μM anandamide. The anti-proliferative effect of anandamide was not due to toxicity or to apoptosis of cells but was accompanied by a reduction of cells in the S phase of the cell cycle. …These data suggest that anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor.

Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines
onlinelibrary.wiley.com…

ANA induced a decrease of EGFR levels on LNCaP, DU145, and PC3 prostatic cancer cells by acting through cannabinoid CB1 receptor subtype and this leaded to an inhibition of the EGF-stimulated growth of these cells. Moreover, the G1 arrest of metastatic DU145 and PC3 growth was accompanied by a massive cell death by apoptosis and/or necrosis while LNCaP cells were less sensitive to cytotoxic effects of ANA. The apoptotic/necrotic responses induced by ANA on these prostatic cancer cells were also potentiated by the acidic ceramidase inhibitor, N-oleoylethanolamine and partially inhibited by the specific ceramide synthetase inhibitor, fumonisin B1 indicating that these cytotoxic actions of ANA might be induced via the cellular ceramide production. The potent anti-proliferative and cytotoxic effects of ANA on metastatic prostatic cancer cells might provide basis for the design of new therapeutic agents for effective treatment of recurrent and invasive prostatic cancers.

Anandamide is an endogenous inhibitor for the migration of tumor cells and T lymphocytes
www.springerlink.com…

Cell migration is of paramount importance in physiological processes such as immune surveillance, but also in the pathological processes of tumor cell migration and metastasis development. The factors that regulate this tumor cell migration, most prominently neurotransmitters, have thus been the focus of intense investigation. While the majority of neurotransmitters have a stimulatory effect on cell migration, we herein report the inhibitory effect of the endogenous substance anandamide on both tumor cell and lymphocyte migration. …Using the specific agonist docosatetraenoylethanolamide (DEA), we have observed that the norepinephrine-induced migration of colon carcinoma cells is inhibited by the CB1-R. The SDF-1–induced migration of CD8+ T lymphocytes was, however, inhibited via the CB2-R, as shown by using the specific agonist JWH 133. Therefore, specific inhibition of tumor cell migration via CB1-R engagement might be a selective tool to prevent metastasis formation without depreciatory effects on the immune system of cancer patients.

The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells
gut.bmj.com…

These findings suggest anandamide may be a useful chemopreventive/therapeutic agent for colorectal cancer as it targets cells that are high expressors of COX-2, and may also be used in the eradication of tumour cells that have become resistant to apoptosis.

Apigenin
Foods: Parsley, Celery, Coriander, Licorice, Majoram, Oregano, Rosemary, Tarragon, Citrus, Tea and Wheat.
en.wikipedia.org…

Selective growth-inhibitory, cell-cycle deregulatory and apoptotic response of apigenin in normal versus human prostate carcinoma cells
www.ncbi.nlm.nih.gov…

The growth-inhibitory and apoptotic potential of apigenin was also observed in a variety of prostate carcinoma cells representing different stage and androgen responsiveness. Apigenin may be developed as a promising chemopreventive and/or chemotherapeutic agent against prostate cancer.

Apigenin induces apoptosis…in breast cancer cells
www.ncbi.nlm.nih.gov…

Apigenin is a low toxicity and non-mutagenic phytopolyphenol and protein kinase inhibitor. It exhibits anti-proliferating effects on human breast cancer cells. Here we examined several human breast cancer cell lines having different levels of HER2/neu expression and found that apigenin exhibited potent growth-inhibitory activity in HER2/neu-overexpressing breast cancer cells but was much less effective for those cells expressing basal levels of HER2/neu.

Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells
www.ncbi.nlm.nih.gov…

Recently we demonstrated that several flavonoids can inhibit the proliferation of certain human thyroid cancer cell lines. Among the flavonoids tested, apigenin and luteolin are the most effective inhibitors of these tumor cell lines. In the present study, we investigated the signal transduction mechanism associated with the growth inhibitory effect of apigenin, using a human anaplastic thyroid carcinoma cell line, ARO.

Induction of cell cycle arrest and apoptosis by apigenin in human prostate carcinoma cells
www.ncbi.nlm.nih.gov…

Apigenin, a common dietary flavonoid abundantly present in fruits and vegetables, may have the potential for prevention and therapy for prostate cancer. Here, we report for the first time that apigenin inhibits the growth of androgen-responsive human prostate carcinoma LNCaP cells and provide molecular understanding of this effect.

Induction of apoptosis by apigenin in leukaemia HL-60 cells
www.ejcancer.info…(99)00168-9/abstract

The potency of these flavonoids on these features of apoptosis were in the order of: apigenin>quercetin>myricetin>kaempferol in HL-60 cells treated with 60μM flavonoids. These results suggest that flavonoid-induced apoptosis is stimulated by the release of cytochrome c to the cytosol, by procaspase-9 processing, and through a caspase-3-dependent mechanism. The induction of apoptosis by flavonoids may be attributed to their cancer chemopreventive activity. Furthermore, the potency of flavonoids for inducing apoptosis may be dependent on the numbers of hydroxyl groups in the 2-phenyl group and on the absence of the 3-hydroxyl group. This provides new information on the structure–activity relationship of flavonoids.

5,6-Dichloro-ribifuranosylbenzimidazole- and apigenin-induced sensitization of colon cancer cells to TNF–mediated apoptosis
ajpgi.physiology.org…

Here we report that inhibition of CK2 in HCT-116 and HT-29 cells with the use of two specific CK2 inhibitors, 5,6-dichloro-ribifuranosylbenzimidazole (DRB) and apigenin, effected a synergistic reduction in cell survival when used in conjunction with TNF-. Furthermore, there was a demonstrable synergistic reduction in colony formation in soft agar with the use of the same combinations.

Apoptosis
en.wikipedia.org…

Apoptosis (aka Programmed Cell Death) is the internal mechanism of basically all biological cells to self-destruct when ‘malfunctioning’. With cancer cells mutate and overcome this design, making them in a sense immortal. So for about as long as cancer has been understood the holy grail in cancer research has been in discovering how to reinstitute apoptosis in cancer cells safely.

The thing is this holy grail has been found in numerous forms, yet the understanding of the general public is that it hasn’t and can only be solved with damaging radiation and chemotherapy. You might ask yourself why that is, and why haven’t known safe apoptosis inducers been aggressively pursued? Perhaps preventing terrorist attacks on national monuments are more important than the 550,000 individuals who die every year from cancer?

Arachidonyl Ethanolamide
Source: Cannabis

Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1
www.ncbi.nlm.nih.gov…

The major finding was that AEA induced apoptosis of CxCa cell lines via aberrantly expressed vanilloid receptor-1, whereas AEA binding to the classical CB1 and CB2 cannabinoid receptors mediated a protective effect. Furthermore, unexpectedly, a strong expression of the three forms of AEA receptors was observed in ex vivo CxCa biopsies.

Artemisinin
Source: Wormwood Plant
en.wikipedia.org…

Artemisinin Induces Apoptosis in Human Cancer Cells
ar.iiarjournals.org…

Artemisinin is a chemical compound extracted from the wormwood plant, Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and retard the growth of implanted fibrosarcoma tumors in rats. In the present research, we investigated its mechanism of cytotoxicity to cancer cells. …This rapid induction of apoptosis in cancer cells after treatment with DHA indicates that artemisinin and its analogs may be inexpensive and effective cancer agents.

Effects of artemisinin and its derivatives on growth inhibition and apoptosis of oral cancer cells
onlinelibrary.wiley.com…

Artemisinin is of special biological interest because of its outstanding antimalarial activity. Recently, it was reported that artemisinin has antitumor activity. Its derivatives, artesunate, arteether, and artemeter, also have antitumor activity against melanoma, breast, ovarian, prostate, CNS, and renal cancer cell lines. Recently, monomer, dimer, and trimer derivatives were synthesized from deoxoartemisinin, and the dimers and the trimers were found to have much more potent antitumor activity than the monomers. …The deoxoartemisinin trimer was found to have greater antitumor effect on tumor cells than other commonly used chemotherapeutic drugs, such as 5-FU, cisplatin, and paclitaxel. Furthermore, the ability of artemisinin and its derivatives to induce apoptosis highlights their potential as chemotherapeutic agents, for many anticancer drugs achieve their antitumor effects by inducing apoptosis in tumor cells.

Transferrin receptor-dependent cytotoxicity of artemisinin–transferrin conjugates on prostate cancer cells and induction of apoptosis
www.ncbi.nlm.nih.gov…

Artemisinin, a natural product isolated from Artemisia annua, contains an endoperoxide group that can be activated by intracellular iron to generate toxic radical species. Cancer cells over-express transferrin receptors (TfR) for iron uptake while most normal cells express nearly undetectable levels of TfR. We prepared a series of artemisinin-tagged transferrins (ART-Tf) where different numbers of artemisinin units are attached to the N-glycoside chains of transferrin (Tf). The Tf bearing approximately 16 artemisinins retains the functionality of both Tf and artemisinin. Reduction of TfRs by TfR siRNA transfection significantly impaired the ability of ART-Tf, but not dihydroartemisinin, to kill cells. We also demonstrate that the ART-Tf conjugate kills the prostate carcinoma cell line DU 145 by the mitochondrial pathway of apoptosis.

Transferrin overcomes drug resistance to artemisinin in human small-cell lung carcinoma cells
www.cancerletters.info…(02)00005-8/abstract

Multiple drug resistance is a significant problem in small-cell lung cancer (SCLC). Artemisinin (ART) is a natural product used to treat drug-resistant malaria. The drug is effective because the Fe2+ present in infected erythrocytes acts non-enzymatically to convert ART to toxic products. We tested the effects of ART on drug-sensitive (H69) and multi-drug-resistant (H69VP) SCLC cells, pretreated with transferrin (TF) to increase the intracellular Fe2+ level. …These data indicate the potential use of ART and TF in drug-resistant SCLC.

Dihydroartemisinin induces apoptosis and sensitizes human ovarian cancer cells to carboplatin therapy
www.ncbi.nlm.nih.gov…

The present study was designed to determine the effects of artemisinin (ARS) and its derivatives on human ovarian cancer cells, to evaluate their potential as novel chemotherapeutic agents used alone or in combination with a conventional cancer chemotherapeutic agent, and to investigate their underlying mechanisms of action. Human ovarian cancer cells (A2780 and OVCAR-3), and immortalized non-tumourigenic human ovarian surface epithelial cells (IOSE144), were exposed to four ARS compounds for cytotoxicity testing. The in vitro and in vivo antitumour effects and possible underlying mechanisms of action of dihydroartemisinin (DHA), the most effective compound, were further determined in ovarian cancer cells. …These effects were also observed in in vivo ovarian A2780 and OVCAR-3 xenograft tumour models. In conclusion, ARS derivatives, particularly DHA, exhibit significant anticancer activity against ovarian cancer cells in vitro and in vivo, with minimal toxicity to non-tumourigenic human OSE cells, indicating that they may be promising therapeutic agents for ovarian cancer, either used alone or in combination with conventional chemotherapy.

β-Elemene
Source: Ginger Root
en.wikipedia.org…

Antitumor effect of β-elemene in non-small-cell lung cancer cells is mediated via induction of cell cycle arrest and apoptotic cell death
www.springerlink.com…

Beta-elemene is a novel anticancer drug, which was extracted from the ginger plant. However, the mechanism of action of beta-elemene in non-small-cell lung cancer (NSCLC) remains unknown. Here we show that beta-elemene had differential inhibitory effects on cell growth between NSCLC cell lines and lung fibroblast and bronchial epithelial cell lines. …These data indicate that the effect of beta-elemene on lung cancer cell death may be through a mitochondrial release of the cytochrome c-mediated apoptotic pathway.

Elemene displays anti-cancer ability on laryngeal cancer cells in vitro and in vivo
www.springerlink.com…

Elemene inhibited the growth of HEp-2 cells in vitro in a dose- and time-dependent manner with an IC50 of 346.5 μM (24 h incubation). Increased apoptosis was observed in elemene-administered cells. Elemene is suspected to enhance caspase-3 activity, and thus inhibit protein expression of eIFs (4E, 4G), bFGF, and VEGF. In vivo, the growth of HEp-2 cell-transplanted tumors in nude mice was inhibited by intraperitoneal injection of elemene. Compared with control groups, elemene significantly inhibited the protein expression of eIFs (4E and 4G), bFGF, and VEGF and decreased the MVD. Conclusions: Elemene inhibits the growth of HEp-2 cells in vitro and in vivo. These data provide useful information for further clinical study on the treatment of LSCC by elemene.

Antiproliferative effect of β-elemene in chemoresistant ovarian carcinoma cells
www.springerlink.com…

In this study, we show that beta-elemene inhibited the proliferation of cisplatin-resistant human ovarian cancer cells and their parental cells, but had only a marginal effect in human ovary cells, indicating differential inhibitory effects on cell growth between ovarian cancer cells and normal ovary cells.

Effect of Local Arterial Infusion of β_elemene on Breast Cancer Tissue Inhibition and Cell Apoptosis and Proliferation
en.cnki.com.cn…

The effect of local arterial infusion of β_elemene on breast cancer tissue inhibition and cell apoptosis and proliferation was observed.

N-(beta-Elemene-13-yl)tryptophan methyl ester induces apoptosis in human leukemia cells
www.ncbi.nlm.nih.gov…

Beta-elemene is an active component of herb medicine Curcuma Wenyujin and N-(beta-elemene-13-yl)tryptophan methyl ester (ETME) was synthesized for increasing its antitumor activity. ETME induced apoptosis in human leukemia HL-60 and NB4 cells at concentrations less than 40 microM. The apoptosis induction ability of ETME was associated with the production of hydrogen peroxide (H(2)O(2)), the decrease of mitochondrial membrane potential, and the activation of caspase-3 that was blocked by catalase. ETME in combination with arsenic trioxide (As(2)O(3)), an agent used to treat acute promyelocytic leukemia, synergistically induced apoptosis in both cell lines by enhanced production of H(2)O(2). These data suggest that ETME induces apoptosis and synergizes with As(2)O(3) in leukemia cells through a H(2)O(2)-dependent pathway.

ß-Glucan
Foods: Mushrooms, Grains & Yeast.
Mushrooms: Shiitake (Lentinula edodes), Reishi (Ganoderma lucidum & Ganoderma tsugae), Maitake (Grifola frondosa), Oyster Mushroom (Pleurotus ostreatus), Cauliflower Mushroom (Sparassis).
Grains: Oats, Barley.
Fights cancer and eases the effects of radiation.
NOTE: Literally all of the listed mushrooms above have other important anti-cancer effects not necessarily specified by this presentation.

ß-Glucan…Uses Antibodies to Target Tumors for Cytotoxic Recognition by Leukocyte Complement Receptor Type 3 (CD11b/CD18)
www.jimmunol.org…

ß-Glucans were identified 36 years ago as a biologic response modifier that stimulated tumor rejection. In vitro studies have shown that ß-glucans bind to a lectin domain within complement receptor type 3 (CR3; known also as Mac-1, CD11b/CD18, or Mß2-integrin, that functions as an adhesion molecule and a receptor for factor I-cleaved C3b, i.e., iC3b) resulting in the priming of this iC3b receptor for cytotoxicity of iC3b-opsonized target cells. This investigation explored mechanisms of tumor therapy with soluble ß-glucan in mice. Normal mouse sera were shown to contain low levels of Abs reactive with syngeneic or allogeneic tumor lines that activated complement, depositing C3 onto tumors. Implanted tumors became coated with IgM, IgG, and C3, and the absent C3 deposition on tumors in SCID mice was reconstituted with IgM or IgG isolated from normal sera. Therapy of mice with glucan- or mannan-rich soluble polysaccharides exhibiting high affinity for CR3 caused a 57–90% reduction in tumor weight. In young mice with lower levels of tumor-reactive Abs, the effectiveness of ß-glucan was enhanced by administration of a tumor-specific mAb, and in SCID mice, an absent response to ß-glucan was reconstituted with normal IgM or IgG. The requirement for C3 on tumors and CR3 on leukocytes was highlighted by therapy failures in C3- or CR3-deficient mice. Thus, the tumoricidal function of CR3-binding polysaccharides such as ß-glucan in vivo is defined by natural and elicited Abs that direct iC3b deposition onto neoplastic cells, making them targets for circulating leukocytes bearing polysaccharide-primed CR3. Therapy fails when tumors lack iC3b, but can be restored by tumor-specific Abs that deposit iC3b onto the tumors.

Beta glucan induces proliferation and activation of monocytes in peripheral blood of patients with advanced breast cancer
www.ncbi.nlm.nih.gov…

Glucans are glucose polymers that constitute a structural part of fungal cell wall. They can stimulate the innate immunity by activation of monocytes/macrophages. In human studies it has been shown that beta glucan has an immunomodulatory effect and can increase the efficacy of the biological therapies in cancer patients. In this prospective clinical trial we assessed in vivo effects of short term oral beta glucan administration on peripheral blood monocytes and their expression of activation markers in patients with advanced breast cancer. …Oral beta glucan administration seems to stimulate proliferation and activation of peripheral blood monocytes in vivo in patients with advanced breast cancer.

Yeast ß-Glucan Amplifies Phagocyte Killing of iC3b-Opsonized Tumor Cells
www.jimmunol.org…

Anti-tumor mAbs hold promise for cancer therapy, but are relatively inefficient. Therefore, there is a need for agents that might amplify the effectiveness of these mAbs. One such agent is -glucan, a polysaccharide produced by fungi, yeast, and grains, but not mammalian cells. -Glucans are bound by C receptor 3 (CR3) and, in concert with target-associated complement fragment iC3b, elicit phagocytosis and killing of yeast. -Glucans may also promote killing of iC3b-opsonized tumor cells engendered by administration of anti-tumor mAbs. In this study, we report that tumor-bearing mice treated with a combination of -glucan and an anti-tumor mAb show almost complete cessation of tumor growth.

Chemosensitization of Carmustine with Maitake β-Glucan on Androgen-Independent Prostatic Cancer Cells
www.liebertonline.com…

This study demonstrates a sensitized cytotoxic effect of BCNU with β-glucan in PC-3 cells, which was associated with a drastic (~80%) inactivation of Gly-I. Therefore, the BCNU/β-glucan combination may help to improve current treatment efficacy by targeting Gly-I, which appears to be critically involved in prostate cancer viability.

ß-Hydroxyisovalerylshikonin
Source: Lithospermum (herbs).
www.wikigenes.org…

ß-Hydroxyisovalerylshikonin Inhibits the Cell Growth of Various Cancer Cell Lines and Induces Apoptosis in Leukemia HL–60 Cells
jb.oxfordjournals.org…

ß-Hydroxyisovalerylshikonin (ß-HIVS), which was isolated from the plant, Lithosper-mium radix, inhibited the growth of various lines of cancer cells derived from human solid, tumors at low concentrations between 10-8 and 10-6 M. When HL-60 cells were treated with 10-6 M ß-HIVS for 3 h, characteristic features of apoptosis, such as DNA fragmentation, nuclear fragmentation, and activation of caspase-3–like activity, were observed.

β-Hydroxyisovalerylshikonin and Cisplatin Act Synergistically to Inhibit Growth and to Induce Apoptosis of Human Lung Cancer DMS114 Cells
www.ncbi.nlm.nih.gov…

beta-Hydroxyisovalerylshikonin (beta-HIVS) and cisplatin (CDDP) had a synergistic growth-inhibitory effect on cultured human small-cell lung carcinoma DMS114 cells, as well as on human leukemia U937 and epidermoid carcinoma A431 cells, while beta-HIVS and CDDP alone at the same respective concentrations had little effect.

Betulin
Source: The bark of Red Alder trees & White Birch trees, and the mushroom Chaga that grows on White Birch.
en.wikipedia.org…

Anti-Cancer Effect of Betulin on a Human Lung Cancer Cell Line
www.thieme-connect.com…

Betulin is a representative compound of Betula platyphylla, a tree species belonging to the Betulaceae family. In this investigation, we revealed that betulin showed anticancer activity on human lung cancer A549 cells by inducing apoptosis and changes in protein expression profiles were observed.

Betulinic Acid Inhibits Prostate Cancer Growth
cancerres.aacrjournals.org…

Betulinic acid is a pentacyclic triterpene natural product initially identified as a melanoma-specific cytotoxic agent that exhibits low toxicity in animal models. Subsequent studies show that betulinic acid induces apoptosis and antiangiogenic responses in tumors derived from multiple tissues;

Apoptotic activity of betulinic acid derivatives on murine melanoma B16 cell line
www.ncbi.nlm.nih.gov…

Exposure of B16 cells to betulinic acid, 23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid caused a rapid increase in reactive oxidative species production and a concomitant dissipation of mitochondrial membrane potential in a dose- and time-dependent manner, which resulted in cell apoptosis, as demonstrated by fluorescence microscopy, gel electrophoresis and flow-cytometric analysis. Cell cycle analysis further demonstrated that both 3-oxo-23-hydroxybetulinic acid and 23-hydroxybetulinic acid dramatically increased DNA fragmentation at the expense of G1 cells at doses as low as 12.5 and 25 microg/ml, respectively, thereby showing their potent apoptotic properties. Our results showed that hydroxylation at the C3 position of betulinic acid is likely to enhance the apoptotic activity of betulinic acid derivatives (23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid) on murine melanoma B16 cells.

Betulinic acid induces apoptosis in human neuroblastoma cell lines
www.ncbi.nlm.nih.gov…

Neuroblastoma has long been recognized to show spontaneous regression during fetal development and in the majority of stage 4s infants <1 year of age with disseminated disease. Stage 4s disease regresses with no chemotherapy in 50% of the patients. The mechanism by which this occurs is not understood but may be programmed cell death or apoptosis. Betulinic acid (BA) has been reported to induce apoptosis in human melanoma with in vitro and in vivo model systems.

Betulinic acid induces apoptosis in skin cancer cells
onlinelibrary.wiley.com…

Betulinic acid (BA), a pentacyclic triterpene of plant origin, induces cell death in melanoma cells and other malignant cells of neuroectodermal origin. Little is known about additional biological effects in normal target cells. We show, in this study, that BA induces differentiation as well as cell death in normal human keratinocytes (NHK).

Betulinic acid: A new cytotoxic compound against malignant head and neck cancer cells
onlinelibrary.wiley.com…

In two HNSCC cell lines betulinic acid induced apoptosis, which was characterized by a dose-dependent reduction in cell numbers, emergence of apoptotic cells, and an increase in caspase activity. Western blot analysis of the expression of various Bcl-2 family members in betulinic acid–treated cells showed, surprisingly, a suppression of the expression of the proapoptotic protein Bax but no changes in Mcl-1 or Bcl-2 expression.

In vivo and in vitro anti-inflammatory and anti-nociceptive effects of the methanol extract of Inonotus obliquus
www.ncbi.nlm.nih.gov…

The mushroom Inonotus obliquus (Fr.) Pilát (Hymenochaetaceae), has been traditionally used for the treatment of gastrointestinal cancer, cardiovascular disease and diabetes in Russia, Poland and most of Baltic countries. This study was designed to investigate the anti-inflammatory and anti-nociceptive effects of the methanol extract from Inonotus obliquus (MEIO) in vivo and in vitro. MEIO (100 or 200 mg/(kg day), p.o.) reduced acute paw edema induced by carrageenin in rats, and showed analgesic activity, as determined by an acetic acid-induced abdominal constriction test and a hot plate test in mice.

Blueberries
en.wikipedia.org…

Effect of Anthocyanin Fractions from Selected Cultivars of Georgia-Grown Blueberries on Apoptosis and Phase II Enzymes
pubs.acs.org…

The response correlated positively with dose. The QR activity was lower in all cells treated with an anthocyanin fraction from Tifblue, Powderblue, Brightblue, and Brightwell cultivars than in control cells (P < 0.05). The activity decreased gradually when treated with increased concentrations of anthocyanin fractions (50−150 μg/mL) in the Tifblue and Powderblue cultivars. The GST activity was lower (P < 0.05) in cells treated with anthocyanin fractions from all of the cultivars and at all concentrations. These results indicated that apoptosis was confirmed in HT-29 cells when treated with anthocyanins from blueberry cultivars at 50−150 μg/mL concentrations, but these same concentrations decrease QR and GST activities rather than induce them.

Availability of blueberry phenolics for microbial metabolism in the colon and the potential inflammatory implications
www.ncbi.nlm.nih.gov…

Blueberries are a rich source of phenylpropanoid-derived phytochemicals, widely studied for their potential health benefits. Of particular interest for colonic health are the lower molecular weight phenolic acids and their derivatives, as these are the predominant phenolic compounds detected in the colon. Blueberries contained a wide variety of phenolic acids, the majority of which (3371.14 ± 422.30 mg/kg compared to 205.06 ± 45.34 mg/kg for the free phenolic acids) were attached to other plant cell-wall components and therefore, likely to become available in the colon. Cytokine-induced stimulation of the inflammatory pathways in colon cells was four-fold up-regulated in the presence of the free phenolic acid fraction. Incubation of the bound phenolic acids with human faecal slurries resulted in qualitative and quantitative differences in the phenolic compounds recovered. The metabolites obtained by incubation with faecal slurries from one volunteer significantly decreased (1.67 ± 0.69 ng/cm3) prostanoid production, whereas an increase (10.78 ± 5.54 ng/cm3) was obtained with faecal slurries from another volunteer. These results suggest that any potential protective effect of blueberry phenolics as anti-inflammatory agents in the colon is a likely result of microbial metabolism. Studies addressing a wide-range of well-characterised human volunteers will be required before such health claims can be fully established.

Broccoli
Relatives: Romanesco, Broccoflower, Cauliflower, Kale, Raab, Brussel Sprouts, Cabbage, Collards and Kohl Rabi.
en.wikipedia.org…
Don’t boil!

Natural Compound in Broccoli Slows Breast Cancer Stem Cells
breastcancer.about.com…

In lab studies, when breast cancer cells were exposed to sulforaphane extract from broccoli, the growth of cancer stems cells slowed down and tumors shrank. The researchers speculate about the possible use of sulforaphane extract to prevent as well as treat breast cancer, someday.

Sprouts contain 3X the amount of Sulforaphane Glucosinolate
www.broccosprouts.com…

Johns Hopkins University researchers found that young broccoli sprouts, in particular, contained high concentrations of SGS.
The scientists believe that SGS boosts the body’s own antioxidant defense system, including Phase 2 detoxification enzymes, which promote long-lasting antioxidant activity in the body.

Diindolylmethane (DIM)
www.activamune.com…

At the University of California at Berkeley, the Chairman of the Nutritional Sciences Department and the Director of the National Institutes of Health Cancer Research Program were studying the biological properties of Diindolylmethane (DIM), a naturally occurring compound found in Brassica vegetables (broccoli, cauliflower, cabbage, kale, brussels sprouts), when they made a remarkable discovery: DIM is a potent activator of the immune response system. They patented their discovery and ActivaMune was launched as a first-in-class nutritional supplement to enhance the immune system and support multiple organs throughout the body: breast, prostate, cardiovascular, vision, skin and colon health. ActivaMune’s unique and patented formula combines multiple nutrients for maximum effectiveness: Diindolylmethane (DIM), Sulforaphane, Selenium, Lycopene, Lutein, Zeaxanthin, Calcium and Vitamins C, D3 & E.

Butyric Acid
en.wikipedia.org…
This is formed naturally during the digestion of dietary fibers. Not enough BA and you’re prone to colon cancer. If you get colon cancer you it’s time to go into fiber overdrive.
onlinelibrary.wiley.com…

Caffeic Acid
Sources: Sweetpotato Leaves, Propolis, Apples, White Grapes, White Wine, Olives, Olive Oil, Spinach, Cabbage, Turnips, Radish, Cauliflower, Bok Choy, Arugula, Kale, Asparagus, and Coffee.
en.wikipedia.org…
Caffeic Acid isn’t related to Caffeine.

Growth Suppression of Human Cancer Cells by Polyphenolics from Sweetpotato (Ipomoea batatas L.) Leaves
pubs.acs.org…

Sweetpotato leaves (Ipomoea batatas L.) contain a high content of polyphenolics that consist of caffeic acid, chlorogenic acid, 3,4-di-O-caffeoylquinic acid, 3,5-di-O-caffeoylquinic acid, 4,5-di-O-caffeoylquinic acid, and 3,4,5-tri-O-caffeoylquinic acid. We investigated the suppression of the proliferation of selected human cancer cells by phenolic compounds isolated from sweetpotato leaf. …Growth suppression of HL-60 cells by 3,4,5-tri-O-caffeoylquinic acid was determined to be the result of apoptotic death of the cells. These results indicate that 3,4,5-tri-O-caffeoylquinic acid may have potential for cancer prevention.

Caffeic acid phenethyl ester induces mitochondria-mediated apoptosis in human myeloid leukemia U937 cells
www.springerlink.com…

Caffeic acid phenyl ester (CAPE), a biologically active ingredient of propolis, has several interesting biological properties including antioxidant, anti-inflammatory, antiviral, immunostimulatory, anti-angiogenic, anti-invasive, anti-metastatic and carcinostatic activities. Recently, several groups have reported that CAPE is cytotoxic to tumor cells but not to normal cells. In this study, we investigated the mechanism of CAPE-induced apoptosis in human myeloid leukemia U937 cells. Treatment of U937 cells with CAPE decreased cell viability in a dose-dependent and time-dependent manner.

Caffeic Acid Phenethyl Ester Induces Apoptosis by Inhibition of NFκB and Activation of Fas in Human Breast Cancer MCF-7 Cells
www.jbc.org…

Our findings demonstrate that NFκB inhibition is sufficient to induce apoptosis and that Fas activation plays a role in NFκB inhibition-induced apoptosis in MCF-7 cells.

The antioxidant caffeic acid phenethyl ester induces apoptosis associated with selective scavenging of hydrogen peroxide in human leukemic HL-60 cells
www.ncbi.nlm.nih.gov…

These results suggest that apoptosis induced by CAPE is associated with mitochondrial dysfunction, GSH depletion and selective scavenging of H2O2 in human leukemic HL-60 cells.

Effect of caffeic acid phenethyl ester on proliferation and apoptosis of colorectal cancer cells in vitro
www.ncbi.nlm.nih.gov…

After HCT116 cells were exposed to CAPE (80, 40, 20, 10, 5, and 2.5 mg/L) for 24, 48, 72, 96 h, CAPE displayed a strong growth inhibitory effect in a dose- and time-dependent manner against HCT116 cells. FCM analysis showed that the ratio of G(0)/G(1) phase cells increased, S phase ratio decreased and apoptosis rate increased after HCT116 cells were exposed to CAPE (10, 5, and 2.5 mg/L) for 24 h. CAPE treatment was associated with decreased cytoplasmic beta-catenin, nuclear beta-catenin and a concurrent increase in beta-catenin protein expression at cell-cell junctions.

Capsaicin
Foods: Hot Peppers.
Sources: Pepper Spray (It’s probably a very bad idea to try and breath this stuff).
Capsaicin (what makes peppers “hot”) has been proven to trigger apoptosis in multiple lines of cancer.

Capsaicin Displays Anti-Proliferative Activity against Human Small Cell Lung Cancer in Cell Culture and Nude Mice Models via the E2F Pathway
www.ncbi.nlm.nih.gov…

BrdU assays and PCNA ELISAs showed that capsaicin displays robust anti-proliferative activity in four human SCLC cell lines. Furthermore, capsaicin potently suppressed the growth of H69 human SCLC tumors in vivo as ascertained by CAM assays and nude mice models. The second part of our study attempted to provide insight into molecular mechanisms underlying the anti-proliferative activity of capsaicin. We found that the anti-proliferative activity of capsaicin is correlated with a decrease in the expression of E2F-responsive proliferative genes like cyclin E, thymidylate synthase, cdc25A and cdc6, both at mRNA and protein levels.

Capsaicin-induced cell death in a human gastric adenocarcinoma cell line
www.wjgnet.com…

Capsaicin, a pungent ingredient found in red pepper, has long been used in spices, food additives, and drugs. Cell death induced by the binding of capsaicin was examined in a human gastric adenocarcinoma cell line (AGS cells).
…Recently, a series of studies have demonstrated that capsaicin inhibits mutagenicity and DNA binding of some chemical carcinogens, possibly by suppressing their metabolic activation[16-18]. With cells in culture, capsaicin-inhibited proliferation of HeLa, ovarian carcinoma, and mammary adenocarcinoma by decreasing NADH oxidase activity[19]. Capsaicin can also alter the expression of tumor forming-related genes by mediating the overexpression of p53 and/or c-myc genes in a Korean stomach cancer cell line[20]. Capsaicin was found to induce apoptosis in T cells by increasing the reactive oxygen species and by a subsequent mitochondrial ransmembrane potential[21]. In this report, we examined the underlying mechanism by which capsaicin induces apoptotic cell death in a human gastric adenocarcinoma cell line (AGS).

Capsaicin-induced apoptosis and reduced release of reactive oxygen species in MBT-2 Murine Bladder Tumor cells
www.springerlink.com…

Capsaicin, the major pungent ingredient in genusCapsicum, has recently been tried as an intravesical drug for overactive bladder and it has also been shown to induce apoptotic cell death in many cancer cells. In this study, we investigated the apoptosis-inducing effect and alterations in the cellular redox state of capsaicin in MBT-2 murine bladder tumor cells. Capsaicin induced apoptotic MBT-2 cell death in a time- and dose-dependent manner. The capsaicin-induced apoptosis was blocked by the pretreatment with Z-VAD-fmk, a broad-range caspase inhibitor, or AcDEVD-CHO, a caspase-3 inhibitor.

Capsaicin-induced apoptosis in human breast cancer MCF-7 cells through caspase-independent pathway
www.spandidos-publications.com…

Our results suggest that capsaicin induces cellular apoptosis through a caspase-independent pathway in MCF-7 cells, and that reactive oxygen species and intracellular calcium ion fluctuation has a minimal role in the process.

TRPV6 mediates capsaicin-induced apoptosis in gastric cancer cells
www.ncbi.nlm.nih.gov…

In this study, both gastric cancer and normal epithelial cells were treated with capsaicin and examined for apoptosis by Annexin V binding. Our results showed that capsaicin induces apoptosis in both cells, although cancer cells are more susceptible. This susceptibility is dependent on the availability of TRPV6, a calcium-selective channel protein, as overexpression of TRPV6 in normal cells increased capsaicin-induced apoptosis and knockdown of TRPV6 in cancer cells suppressed this action. Our results further demonstrated that capsaicin increases mitochondrial permeability through activation of Bax and p53 in a JNK-dependent manner.

Capsaicin Shows Promise In Inhibiting Growth Of Pancreatic Cancer
www.medicalnewstoday.com…

“In our study, we discovered that capsaicin fed orally to mice with human pancreatic tumors was an extremely effective inhibitor of the cancer process, inducing apoptosis in cancer cells,” said Sanjay K. Srivastava, Ph.D., lead investigator and assistant professor, department of pharmacology, University of Pittsburgh School of Medicine. “Capsaicin triggered the cancerous cells to die off and significantly reduced the size of the tumors.”

Capsaicin Mediates Cell Death in Bladder Cancer T24 Cells Through Reactive Oxygen Species Production and Mitochondrial Depolarization
www.ncbi.nlm.nih.gov…

RESULTS: CAP decreased the viability of T24 cells in a dose-dependent manner without marked apoptosis. CAP induced ROS production and mitochondrial membrane depolarization, thereby inducing cell death, not apoptosis, in T24 cells at a concentration of 100 microM or higher. Furthermore, these effects of CAP could be reversed by capsazepine, the antagonist of transient receptor potential vanilloid type 1 channel. In vivo experiment showed that CAP significantly slowed the growth of T24 bladder cancer xenografts as measured by size (661.80 +/- 62.03 vs 567.02 +/- 43.94 mm(3); P <.01).
CONCLUSIONS: CAP mediates cell death in T24 cells through calcium entry-dependent ROS production and mitochondrial depolarization, and it may have a role in the management of bladder cancer.

Carotenoids
Foods: Carrots, Sweet Potato, Kale, Apricots, Mangos, Squash, Spinach, Kale, Collard Greens, Salmon, Shellfish, Egg Yolks, Hot Peppers, Brown Algae.

Carotenoids Affect Proliferation of Human Prostate Cancer Cells
jn.nutrition.org…

We investigated whether various carotenoids present in foodstuffs were potentially involved in cancer-preventing action on human prostate cancer. The effects of 15 kinds of carotenoids on the viability of three lines of human prostate cancer cells, PC-3, DU 145 and LNCaP, were evaluated. When the prostate cancer cells were cultured in a carotenoid-supplemented medium for 72 h at 20 µmol/L, 5,6-monoepoxy carotenoids, namely, neoxanthin from spinach and fucoxanthin from brown algae, significantly reduced cell viability to 10.9 and 14.9% for PC-3, 15.0 and 5.0% for DU 145, and nearly zero and 9.8% for LNCaP, respectively.

Serum carotenoids and mortality from lung cancer
onlinelibrary.wiley.com…

Higher serum levels of carotenoids such as – and β-carotenes may play a role in preventing death from lung cancer

Human Breast Cancer Cells Treated with Carotenoids or Retinoids
jn.nutrition.org…

These results demonstrate that ER status is an important, although not essential factor for breast cancer cell response to carotenoid and retinoid treatments, and the mode of action of all-t-RA in MCF-7 and Hs578T cells is not through the induction of RAR. Other mechanistic pathways that are either followed by or concomitant with growth inhibition are possible.

Carotenoids, antioxidants and ovarian cancer risk in pre- and postmenopausal women
onlinelibrary.wiley.com…

From a population-based study of 549 cases of ovarian cancer and 516 controls, we estimated the consumption of the antioxidant vitamins A, C, D and E and various carotenoids, including alpha- and beta-carotene and lycopene, using a validated dietary questionnaire. Multivariate logistic regression was used to calculate the exposure odds ratios adjusted for established ovarian cancer risk factors. Intakes of carotene, especially alpha-carotene, from food and supplements were significantly and inversely associated with risk for ovarian cancer, predominantly in postmenopausal women. Intake of lycopene was significantly and inversely associated with risk for ovarian cancer, predominantly in premenopausal women. Food items most strongly related to decreased risk for ovarian cancer were raw carrots and tomato sauce. Consumption of fruits, vegetables and food items high in carotene and lycopene may reduce the risk of ovarian cancer.

Ceramide
Source: Chemical supply houses.
www.scbt.com…
This one is interesting as it is synthesized in the body in response to ‘traditional’ treatments. It seems obvious to go straight to it.

Ceramide mediates cancer therapy-induced apoptosis
www.ncbi.nlm.nih.gov…

Ceramide, which accumulates in response to different types of cellular stress such as chemo- and radiotherapy, strongly induced expression of CD95-L, cleavage of caspases and apoptosis. Antisense CD95-L as well as dominant-negative FADD inhibited ceramide- and cellular stress-induced apoptosis.

Induction of Apoptotic Cell Death and Prevention of Tumor Growth by Ceramide
cancerres.aacrjournals.org…

We measured the levels of ceramide, a candidate lipid mediator of apoptosis, in human metastatic colorectal cancer and tested in vitro and in vivo effects of various ceramide analogues in inducing apoptosis in metastatic colon cancer. Human colon cancer showed a >50% decrease in the cellular content of ceramide when compared with normal colon mucosa.

Multidrug resistance modulators and doxorubicin synergize to elevate ceramide levels and elicit apoptosis in drug-resistant cancer cells
www.ncbi.nlm.nih.gov…

These results demonstrate that MDR modulators can be used separately, in combination, or in conjunction with chemotherapy at clinically relevant concentrations to manipulate cellular ceramide levels and restore sensitivity in the drug resistant setting. As such, this represents a new direction in the treatment of cancer.

Ionizing radiation acts on cellular membranes to generate ceramide and initiate apoptosis
www.ncbi.nlm.nih.gov…

The present studies show that ionizing radiation, like TNF, induces rapid sphingomyelin hydrolysis to ceramide and apoptosis in bovine aortic endothelial cells. Elevation of ceramide with exogenous ceramide analogues was sufficient for induction of apoptosis. Protein kinase C activation blocked both radiation-induced sphingomyelin hydrolysis and apoptosis, and apoptosis was restored by ceramide analogues added exogenously. Ionizing radiation acted directly on membrane preparations devoid of nuclei, stimulating sphingomyelin hydrolysis enzymatically through a neutral sphingomyelinase. These studies provide the first conclusive evidence that apoptotic signaling can be generated by interaction of ionizing radiation with cellular membranes and suggest an alternative to the hypothesis that direct DNA damage mediates radiation-induced cell kill.

Cinnamaldehyde
Food: Cinnamon
en.wikipedia.org…

Cinnamaldehyde induces apoptosis by ROS-mediated mitochondrial permeability transition in human promyelocytic leukemia HL-60 cells
www.ncbi.nlm.nih.gov…

Cinnamaldehyde is an active compound isolated from the stem bark of Cinnamomum cassia, a traditional oriental medicinal herb, which has been shown to inhibit tumor cell proliferation. In this study, we investigated the effects of cinnamaldehyde on the cytotoxicity, induction of apoptosis and the putative pathways of its actions in human promyelocytic leukemia cells. …Taken together, our data indicate that cinnamaldehyde induces the ROS-mediated mitochondrial permeability transition and resultant cytochrome c release. This is the first report on the mechanism of the anticancer effect of cinnamaldehyde.

Induction of apoptotic cell death by 2′-hydroxycinnamaldehyde is involved with ERK-dependent inactivation of NF-κB in TNF-α-treated SW620 colon cancer cells
www.ncbi.nlm.nih.gov…

These results demonstrate that HCA inhibits cell growth through induction of apoptotic cell death by ERK pathway-dependent NF-kappaB inactivation.

More cinnamon, less cancer
www.torontosun.com…

It has been know for a few years that several types of spices contain large amounts of cancer-fighting compounds that could help in the prevention of the disease. In addition to the well-known health properties of tumeric and ginger, a recent study has suggested that cinnamon could be equally useful in reducing tumour growth by blocking the formation of new vessels using a process called angiogenesis.

Cinnamon extract induces tumor cell death through inhibition of NFκB and AP1
www.biomedcentral.com…

Cinnamon extract strongly inhibited tumor cell proliferation in vitro and induced active cell death of tumor cells by up-regulating pro-apoptotic molecules while inhibiting NFκB and AP1 activity and their target genes such as Bcl-2, BcL-xL and survivin. Oral administration of cinnamon extract in melanoma transplantation model significantly inhibited tumor growth with the same mechanism of action observed in vitro.

Citral
Food: Lemon Grass
Sources: Asian grocery’s (lemon grass), Health food stores (extracts).

An essential oil and its major constituent isointermedeol induce apoptosis in human leukaemia HL-60 cells
www.ncbi.nlm.nih.gov…

An essential oil from a lemon grass variety of Cymbopogon flexuosus (CFO) and its major chemical constituent sesquiterpene isointermedeol (ISO) were investigated for their ability to induce apoptosis in human leukaemia HL-60 cells because dysregulation of apoptosis is the hallmark of cancer cells. …The easy and abundant availability of the oil combined with its suggested mechanism of cytotoxicity make CFO highly useful in the development of anti-cancer therapeutics.

Citral is a New Inducer of Caspase-3 in Tumor Cell Lines
www.thieme-connect.com…

Citral, 3,7-dimethyl-2,6-octadien-1-al, a key component of the lemon-scented essential oils extracted from several herbal plants such as lemon grass (Cymbopogon citratus), melissa (Melissa officinalis), verbena (Verbena officinalis) is used as a food additive and as a fragrance in cosmetics. In this study, we investigated the anti-cancer potential of citral and its mode of action. Concentrations of 44.5 μM, comparable to the concentration of citral in a cup of tea prepared from 1 g of lemon grass, induced apoptosis in several hematopoietic cancer cell lines. Apoptosis was accompanied by DNA fragmentation and caspase-3 catalytic activity induction. Citral activity (22.25 μM) was compared to a reference compound like staurosporine (0.7 μM), in respect to DNA fragmentation and caspase-3 enzymatic activity. The apoptotic effect of citral depended on the α,β-unsaturated aldehyde group.

Citral inhibits cell proliferation and induces apoptosis and cell cycle arrest in MCF-7 cells
www.ncbi.nlm.nih.gov…

In this study, we investigated the effect of citral (3,7-dimethyl-2,6-octadienal), a key component of essential oils extracted from several herbal plants, on the proliferation rate, cell cycle distribution, and apoptosis of the human breast cancer cell line MCF-7. The effects of this compound were also tested on cyclo-oxygenase activity. Citral treatment caused inhibition of MCF-7 cell growth (IC(50)-48 h: 18 x 10(-5)m), with a cycle arrest in G(2)/M phase and apoptosis induction. Moreover, we observed a decrease in prostaglandin E(2) synthesis 48 h after citral treatment. These findings suggest that citral has a potential chemopreventive effect.

Cocklebur
Xanthium Strumarium Plant.
en.wikipedia.org…
There’s more than one compound in it that appears effective. The following is a “Microtubule Interfering Substance”, one of the several different ways to kill a cancer:

Pharmacologically Active Natural Compounds for Lung Cancer
www.anaturalhealingcenter.com…

Regarding lung cancer, a methanolic extract of the leaves of Xanthium strumarium L. (Asteraceae) exhibited a strong inhibition of the proliferation of cultured human tumor cells, including A549 NSCLC cell line. The active constituents have been identified as 8-epi-xanthatin (Figure 1) and its epoxide, two xanthanolide sesquiterpene lactones. Their IC50 values have been calculated as 4.5 and 3.0 microM respectively, where the positive control cisplatin was 4.7 microM. (IC50 is the concentration of a compound
needed to reduce growth of a population of cells by 50 percent in vitro. At higher concentrations (64 and 58 mM, respectively) the two xantholides showed a promising farnesyltransferase (FTase) inhibitory effect. 21 Farnesylation of certain oncoproteins (especially Ras proteins) is required for their oncogenic activity, and thus FTase inhibition could specifically stop Ras-mediated cellular proliferation. Synthetic FTase inhibitors have demonstrated activity against various human cancer cell lines, including NSCLC.22 An earlier study showed X. strumarium extracts are able to effectively inhibit tubuline polymerization in mammalian tissues,23 which could be a plausible explanation of these findings.

Cod Liver Oil
en.wikipedia.org…

Women and Lung Cancer – Could Cod Liver Oil Improve Survival
lungcancer.about.com…

My Scandinavian, cod-liver-oil-serving grandma was right again – based on the results of a new Norwegian study. Women who used cod liver oil daily for a year prior to their diagnosis of lung cancer, had a 44% lower chance of dying. Though my grandmother would have turned 100 last week, support for her advice will be published next month in the International Journal of Cancer. Researchers looked at questionnaires completed by over 68,000 women between 1996 and 1999. They then analyzed 2,242 women who developed cancer following the questionnaire and up to the year 2007. Women who used cod liver oil daily, had a 23% lower chance of dying from solid tumors in general (breast, colorectal, and lung cancers), and a 44% reduced risk of dying from lung cancer.

Coenzyme Q10
Foods: Fish, chicken, peanuts, seasame seeds, pistachios, olive oil, soy beans, grapeseed, parsley, perilla, broccoli (and relatives).
Sources: Health food stores (extracts).
en.wikipedia.org…
Co-Q10 is present in most “eukaryotic” cells (muscle tissues and more). It’s produced naturally in the body, which uses it for cell growth and to protect cells from damage that could lead to cancer. In animals it’s most concentrated in the heart. Co-Q10 both boosts the immune system, and has been shown to induce apoptosis.

www.cancer.gov…

Low blood levels of coenzyme Q10 have been found in patients with myeloma, lymphoma, and cancers of the breast, lung, prostate, pancreas, colon, kidney, and head and neck. Studies suggest that coenzyme Q10 may help the immune system work better. Partly because of this, coenzyme Q10 is used as adjuvant therapy for cancer. Adjuvant therapy is treatment given following the primary treatment to increase the chances of a cure.

www.cancer.gov…

Clinical trials have shown that coenzyme Q10 helps protect the heart from the damaging side effects of doxorubicin, a drug used to treat cancer.

Normalizattion of BCL-2 family members in breast cancer by Coenzyme Q10
www.ishib.org…

Because of their integral role in intrinsic apoptosis any imbalance can lead to a variety of diseases; under expression can lead to degenerative diseases while over expression can lead to cancer and autoimmune disease. Due to their life or death role in the cell, Bcl-2 family members are currently the targets of many therapies in various disease states. Bcl-2 itself is over expressed in most tumors and all anti-apoptotic Bcl-2 family members are considered to have oncogenic potential. Conversely, the pro-apoptotic members are considered to be tumor suppressors
and many mimetics are foci for cancer research. …Both pro- and anti-apoptotic protein levels were measured in the two breast cancer cell lines after Q10 exposure. Protein levels were measured at 4,8,12, and 24 hours respectively in order to capture evidence of Q10’s normalizing influence on disrupted apoptotic function. In the MCF-7 cell line Bcl-2 levels were seen to significantly drop after only 4 hours of Q10 exposure.

Copper (BAD)
Listing of foods that DO and DON’T contain copper:
www.gicare.com…
Substances that reduce copper include: Tetrathiomolybdate, Trientine, Disulfiram, Penicillamine, Zinc and others. Look for entries for these substances. Get a good water filter!

Role of copper in tumour angiogenesis–clinical implications
www.ncbi.nlm.nih.gov…

The formation of new blood vessels is the initial step in progressive tumour development and metastasis. The first stage in tumour angiogenesis is the activation of endothelial cells. Copper ions stimulate proliferation and migration of endothelial cells. It has been shown that serum copper concentration increases as the cancer disease progresses and correlates with tumour incidence and burden. Copper ions also activate several proangiogenic factors, e.g., vascular endothelial growth factor, basic fibroblast growth factor, tumour necrosis factor alpha and interleukin 1. This review concerns a brief introduction into the basics of tumour blood vessel development as well as the regulatory mechanisms of this process. The role of copper ions in tumour angiogenesis is discussed. The new antiangiogenic therapies based on a reduction of copper levels in tumour microenvironment are reviewed.

Increased Expression of the Copper Efflux Transporter ATP7A Mediates Resistance to Cisplatin, Carboplatin, and Oxaliplatin in Ovarian Cancer Cells
clincancerres.aacrjournals.org…

The 1.5-fold higher expression of ATP7A in the 2008/MNK cells was sufficient to alter Cu cellular pharmacokinetics but not confer Cu resistance. In contrast, it was sufficient to render the 2008/MNK cells resistant to cisplatin, carboplatin, and oxaliplatin. Resistance was associated with increased rather than decreased whole-cell Pt drug accumulation and increased sequestration of Pt into the vesicular fraction. Cu triggered relocalization of ATP7A away from the perinuclear region, whereas at equitoxic concentrations the Pt drugs did not.

Cuminum Cyminum
Food: Cumin Seeds.
en.wikipedia.org…
Primary ingredient in Chili Powder.

Cumin: natures potent cancer combatant
findarticles.com…

This herb has been seen to effectively decrease the incidence of chemically induced tumors of the stomach, colon, and cervix. Its significant antioxidant activity and the ability to modulate the metabolism of carcinogens (toxins) explain its cancer-preventive prowess. Cumin seeds are known to induce the activity of glutathione-S-transferase, a protective enzyme that helps eliminate cancer-causing substances. Cumin offers a significant level of caffeic, chlorogenic, ferulic, and other phenolic acids that have anti-inflammatory potential.

Antitumor and Antibacterial Activities of …Cuminum Cyminum Seeds
www.insipub.com…

1-(2-Ethyl, 6-Heptyl) Phenol (EHP), a biologically active compound formerly extracted bybenzene from Cuminum cyminum (cumin) Egyptian seeds and of activity against a number of fungalpathogens, exhibited antitumor activity against six types of tumor cell lines (HEPG2, HELA, HCT116,MCF7, HEP2, CACO2).

Curcumin
Foods: Tumeric roots / powder, curry powder, yellow mustard.
Sources: Health food stores (extracts), large farmers markets (roots), Indian grocery stores (tumeric powder in bulk).
en.wikipedia.org…
Tumeric has been proven to kill throat cancer cells. It seems obvious that the effectiveness in the case of throat cancer is from the curcumin, the active ingredient, passing directly over the cancer cells. Therefore, the I.I.B. idea for lung cancer is to run liquid curcumin extract thru a “nebulizer” apparatus to inhale it. Check back for updates as to whether or not this turns out to be harsh on the lungs.

Turmeric Spice Kills Throat Cancer Cells
www.associatedcontent.com…
news.bbc.co.uk…

On Tuesday, the British Journal of Cancer published a propitious study from Cork Cancer Research Centre (“CCRC”) at the University College Cork in Ireland that found that curcumin—a compound in the curry spice turmeric—begins killing esophageal cancer cells within 24 hours. According to the CCRC study, curcumin ostensibly acts as a free radical scavenger that triggers a lethal cell death signal that causes cancerous cells in the throat to digest and kill themselves.

Induction of apoptosis in human lung cancer cells by curcumin
www.cancerletters.info…(04)00053-9/abstract

This study investigated the cellular and molecular changes induced by curcumin leading to the induction of apoptosis in human lung cancer cell lines—A549 and H1299. A549 is p53 proficient and H1299 is p53 null mutant. The lung cancer cells were treated with curcumin (0–160 μM) for 12–72 h. Curcumin inhibited the growth of both the cell lines in a concentration dependent manner. Growth inhibition of H1299 cell lines was both time and concentration dependent. Curcumin induced apoptosis in both the lung cancer cell lines. A decrease in expression of p53, bcl-2, and bcl-XL was observed after 12 h exposure of 40 μM curcumin. Bak and Caspase genes remained unchanged up to 60 μM curcumin but showed decrease in expression levels at 80–160 μM. The data also suggest a p53 independent induction of apoptosis in lung cancer cells.

Curcumin induces apoptosis in immortalized NIH 3T3 and malignant cancer cell lines
www.ncbi.nlm.nih.gov…

Curcumin, which is a widely used dietary pigment and spice, has been demonstrated to be an effective inhibitor of tumor promotion in mouse skin carcinogenesis. We report that curcumin induces cell shrinkage, chromatin condensation, and DNA fragmentation, characteristics of apoptosis, in immortalized mouse embryo fibroblast NIH 3T3 erb B2 oncogene-transformed NIH 3T3, mouse sarcoma S180, human colon cancer cell HT-29, human kidney cancer cell 293, and human hepatocellular carcinoma Hep G2 cells

Curcumin induces apoptosis in human breast cancer cells
linkinghub.elsevier.com…

The aim of this study was to determine the mechanisms of curcumin-induced human breast cancer cell apoptosis. From quantitative image analysis data showing an increase in the percentage of cells with a sub-G0/G1 DNA content, we demonstrated curcumin-induced apoptosis in the breast cancer cell line MCF-7, in which expression of wild-type p53 could be induced. Apoptosis was accompanied by an increase in p53 level as well as its DNA-binding activity followed by Bax expression at the protein level. Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53. This property of curcumin suggests that this molecule could have a possible therapeutic potential in breast cancer patients.

Curcumin inhibits proliferation, induces apoptosis, and inhibits angiogenesis of LNCaP prostate cancer cells in vivo
onlinelibrary.wiley.com…

Curcumin causes a marked decrease in the extent of cell proliferation as measured by the BrdU incorporation assay and a significant increase in the extent of apoptosis as measured by an in situ cell death assay. Moreover, a significant decrease in the microvessel density as measured by the CD31 antigen staining was also seen.

Chemopreventive Effect of Curcumin…during the Promotion/Progression Stages of Colon Cancer
cancerres.aacrjournals.org…

The inhibition of adenocarcinomas of the colon was, in fact, dose dependent. Administration of curcumin to the rats during the initiation and postinitiation stages and throughout the promotion/progression stage increased apoptosis in the colon tumors as compared to colon tumors in the groups receiving AOM and the control diet. Thus, chemopreventive activity of curcumin is observed when it is administered prior to, during, and after carcinogen treatment as well as when it is given only during the promotion/progression phase (starting late in premalignant stage) of colon carcinogenesis.

Notch-1 down-regulation by curcumin is associated with the inhibition of cell growth and the induction of apoptosis in pancreatic cancer cells
onlinelibrary.wiley.com…

Curcumin inhibited cell growth and induced apoptosis in pancreatic cancer cells. Notch-1, Hes-1, and Bcl-XL expression levels concomitantly were down-regulated by curcumin treatment. These results correlated with the inactivation of NF-κB activity and increased apoptosis induced by curcumin. The down-regulation of Notch-1 by small-interfering RNA prior to curcumin treatment resulted in enhanced cell growth inhibition and apoptosis.

Curcumin, an antioxidant and anti-tumor promoter, induces apoptosis in human leukemia cells
www.ncbi.nlm.nih.gov…

Curcumin, widely used as a spice and coloring agent in food, possesses potent antioxidant, anti-inflammatory and anti-tumor promoting activities. In the present study, curcumin was found to induce apoptotic cell death in promyelocytic leukemia HL-60 cells at concentrations as low as 3.5 micrograms/ml.

Antiproliferation and apoptosis induced by curcumin in human ovarian cancer cells
www.ncbi.nlm.nih.gov…

Curcumin, an active ingredient from the rhizome of the plant, Curcuma longa, has antioxidant, anti-inflammatory and anti-cancer activities. It has recently been demonstrated that the chemopreventive activities of curcumin might be due to its ability to inhibit cell growth and induce apoptosis. In the present study, we have investigated the effects of curcumin on growth and apoptosis in the human ovarian cancer cell line Ho-8910 by MTT assay, fluorescence microscopy, flow cytometry and Western blotting. Our data revealed that curcumin could significantly inhibit the growth and induce apoptosis in Ho-8910 cells. A decrease in expression of Bcl-2, Bcl-X(L) and pro-caspase-3 was observed after exposure to 40 microM curcumin, while the levels of p53 and Bax were increased in the curcumin-treated cells. These activities may contribute to the anticarcinogenic action of curcumin.

Daidzein
Foods: Soybeans, Kwao Krua & Kudzu.
en.wikipedia.org…

Biphasic effect of daidzein on cell growth of human colon cancer cells
www.ncbi.nlm.nih.gov…

LoVo cells were treated with 0.1, 1, 5, 10, 50 and 100 microM daidzein for 2, 3, 4 or 5 d. The results indicated that daidzein stimulated the growth of LoVo cells at 0.1 and 1 microM whereas at higher concentrations (10, 50 and 100 microM) cell growth was inhibited in a dose-dependent manner. Treatment of daidzein at 10, 50 and 100 microM resulted in cell cycle arrest at G0/G1 phase, DNA fragmentation and increases in caspase-3 activity. There were no changes in alkaline phosphatase activity (ALP), an indicator of cell differentiation, upon treatment with daidzein when compared to controls. These results indicate that daidzein has a biphasic effect on LoVo cell growth and its tumor suppressive effect is by means of cell cycle arrest and apoptosis but not through cell differentiation.

Effect of daidzein on cell growth, cell cycle, and telomerase activity of human cervical cancer in vitro
onlinelibrary.wiley.com…

The inductive effects of apoptosis were more obviously observed in low-concentration groups. After HeLa cells were treated with daidzein, the expression of human telomerase catalytic subunit mRNA decreased. These meant that daidzein affected human nonhormone-dependent cervical cancer cells in several ways, including cell growth, cell cycle, and telomerase activity in vitro.

Effects of daidzein on estrogen-receptor-positive and negative pancreatic cancer cells in vitro
www.ncbi.nlm.nih.gov…

Daidzein has antiproliferative effects on human estrogen-receptor-positive and negative pancreatic cancer cells, but their mechanisms may be different.

Dichloroacetic Acid (DCA)
Sources: Chemical & pharmaceutical supply companies, Internet, doctors prescription (if they’re willing).

When I began this study this was at the top of my list of ‘suppressed’ substances that I knew of. It made national news a few years ago when the study was published. The big story seemed to be that it wasn’t patentable so therefore it wasn’t going to go through extensive human trails because it wasn’t going to make anybody rich. While that is a big story, now that I’ve completed this study I’m revising this entry.

The real big story is that there are seemingly endless compounds and substances that are well studied and published that do the same thing, and almost none of them are aggressively pursued by the medical industry. Small teams of curious researchers study new ways of killing cancer with all sorts of things, but unless there is a way for Big Pharm to make endless billions then the medical community basically does nothing with it. I know this first hand now that my mother is going through this process and her doctors haven’t told her to eat or take anything that doesn’t come from Big Pharm, and they cringe and squirm when she tries to inquire about any of these known cancer killers.

As it turns out, it costs in the range of hundreds of millions of dollars to complete human trials for FDA approval of substances and treatments, and there is quite literally no place in the FDA approval process for anything that cannot be patented. The case of DCA has helped underscore the need for something on the order of a ‘Public Domain Drug Act’, where the public has weight in the approval process of safe substances that show promise.
www.thedcasite.com…

You can get DCA if you dig around online. I found one site in the EU where DCA costs about $30 for about 10,000 doses.

The following site has lots of useful information including treatment testimonials:
www.thedcasite.com…

Some tidbits from my research:
Do not add DCA to hot or warm beverages. DCA is unstable at higher temperatures. DCA can interact favorably or negatively with chemotherapy is some patients. This is hard to predict unless a chemosensitivity test like ChemoFit is performed.

www.youtube.com…

The Official University of Alberta DCA Website
www.dca.med.ualberta.ca…

DCA is an odourless, colourless, inexpensive, relatively non-toxic, small molecule. And researchers at the University of Alberta believe it may soon be used as an effective treatment for many forms of cancer. Dr. Evangelos Michelakis, a professor at the U of A Department of Medicine, has shown that dichloroacetate (DCA) causes regression in several cancers, including lung, breast, and brain tumors.

A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth
www.cell.com…

The unique metabolic profile of cancer (aerobic glycolysis) might confer apoptosis resistance and be therapeutically targeted. Compared to normal cells, several human cancers have high mitochondrial membrane potential (m) and low expression of the K+ channel Kv1.5, both contributing to apoptosis resistance. Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases m, increases mitochondrial H2O2, and activates Kv channels in all cancer, but not normal, cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism. DCA induces apoptosis, decreases proliferation, and inhibits tumor growth, without apparent toxicity. Molecular inhibition of PDK2 by siRNA mimics DCA. The mitochondria-NFAT-Kv axis and PDK are important therapeutic targets in cancer; the orally available DCA is a promising selective anticancer agent.

DCA Research Team publishes results of Clinical Trials
www.dca.med.ualberta.ca…

In 2007 the U of A team led by Dr Michelakis, published evidence that DCA reverses cancer growth in non-human models and test tubes. The team showed then that DCA achieves these antitumor effects by altering the metabolism of cancer. By altering the way cancer handles its nutrient fuels, specifically the sugars, DCA was able to take away cancer’s most important strength, the resistance to death. Since then, several independent groups across the world have confirmed the Alberta team’s findings. In December 2009, the editors of “Science” predicted that cancer metabolism is one of only 5 areas across all scientific disciplines, to “watch for major breakthroughs” in 2010.

Other smaller studies are being performed around the wrold. The following site is another excellent source of data on real life human trials:
www.medicorcancer.com…

Dihydroxybenzaldehyde
Sources: Barley & Xanthium Strumarium seeds, Chaga Mushroom.
www.chemicalbook.com…

Apoptotic cell death through inhibition of protein kinase CKII activity by 3,4-dihydroxybenzaldehyde purified from Xanthium strumarium
www.informaworld.com…

The CKII inhibitory compound was purified from the fruit of Xanthium strumarium by organic solvent extraction and silica gel chromatography. The inhibitory compound was identified as 3,4-dihydroxybenzaldehyde by analysis with FT-IR, FAB-Mass, EI-Mass, (1)H-NMR and (13)C-NMR. 3,4-dihydroxybenzaldehyde inhibited the phosphotransferase activity of CKII with IC(50) of about 783 microM. Steady-state studies revealed that the inhibitor acts as a competitive inhibitor with respect to the substrate ATP. A value of 138.6 microM was obtained for the apparent K(i). Concentration of 300 microM 3,4-dihydroxybenzaldehyde caused 50% growth inhibition of human cancer cell U937. 3,4-dihydroxybenzaldehyde-induced cell death was characterised with the cleavage of poly(ADP-ribose) polymerase and procaspase-3. Furthermore, the inhibitor induced the fragmentation of DNA into multiples of 180 bp, indicating that it triggered apoptosis. This induction of apoptosis by 3,4-dihydroxybenzaldehyde was also confirmed by using flow cytometry analysis. Since CKII is involved in cell proliferation and oncogenesis, these results suggest that 3,4-dihydroxybenzaldehyde may function by inhibiting oncogenic disease, at least in part, through the inhibition of CKII activity.

3,4-dihydroxybenzaldehyde purified from the barley seeds (Hordeum vulgare) inhibits oxidative DNA damage and apoptosis via its antioxidant activity
www.ncbi.nlm.nih.gov…

In antioxidant activity assay such as DPPH radical and hydroxyl radical scavenging assay, Fe(2+) chelating assay, and intracellular ROS scavenging assay by DCF-DA, 3,4-dihydroxybenzaldehyde was found to scavenge DPPH radical, hydroxyl radical and intracellular ROS. Also it chelated Fe(2+). In in vitro oxidative DNA damage assay and the expression level of phospho-H2A.X, it inhibited oxidative DNA damage and its treatment decreased the expression level of phospho-H2A.X. And in oxidative cell death and apoptosis assay via MTT assay and Hoechst 33342 staining, respectively, the treatment of 3,4-dihydroxybenzaldehyde attenuated H(2)O(2)-induced cell death and apoptosis. These results suggest that the barley may exert the inhibitory effect on H(2)O(2)-induced tumor development by blocking H(2)O(2)-induced oxidative DNA damage, cell death and apoptosis.

Cancer Cell Cytotoxicity of Extracts and Small Phenolic Compounds from Chaga
www.liebertonline.com…

The phenolic components isolated from the 80% MeOH extracts had markedly greater cancer cell toxicity than the extracts themselves. In particular, two out of seven compounds showed strong cytotoxicity towards several tumor cell lines without giving rise to significant cell toxicity toward normal cells. For example, the 50% lethal dose for 3,4-dihydroxybenzalacetone was 12.2μmol/L in PA-1 cells but was 272.8μmol/L in IMR90 cells. Fluorescence-activated cell sorting analysis further revealed these phenolic ingredients have high potentiality for apoptosis induction in PA-1 cells.

Disulfiram
Removes copper from your system. This one should be good for alcoholics diagnosed with cancer.

Disulfiram, a Clinically Used Anti-Alcoholism Drug and Copper-Binding Agent, Induces Apoptotic Cell Death in Breast Cancer
cancerres.aacrjournals.org…

Copper has been shown to be essential for tumor angiogenesis processes. Consistently, high serum and tissue levels of copper have been found in many types of human cancers, including breast, prostate, and brain, supporting the idea that copper could be used as a potential tumor-specific target. Here we report that the DSF-copper complex potently inhibits the proteasomal activity in cultured breast cancer MDA-MB-231 and MCF10DCIS.com cells, but not normal, immortalized MCF-10A cells, before induction of apoptotic cancer cell death. Furthermore, MDA-MB-231 cells that contain copper at concentrations similar to those found in patients, when treated with just DSF, undergo proteasome inhibition and apoptosis. In addition, when administered to mice bearing MDA-MB-231 tumor xenografts, DSF significantly inhibited the tumor growth (by 74%), associated with in vivo proteasome inhibition (as measured by decreased levels of tumor tissue proteasome activity and accumulation of ubiquitinated proteins and natural proteasome substrates p27 and Bax) and apoptosis induction (as shown by caspase activation and apoptotic nuclei formation).

Electricity

Nanosecond pulsed electric fields induce apoptosis in p53-wildtype and p53-null HCT116 colon carcinoma cells
www.springerlink.com…

Non-ionizing radiation produced by nanosecond pulsed electric fields (nsPEFs) is an alternative to ionizing radiation for cancer treatment. NsPEFs are high power, low energy (non-thermal) pulses that, unlike plasma membrane electroporation, modulate intracellular structures and functions. To determine functions for p53 in nsPEF-induced apoptosis, HCT116p53+/+ and HCT116p53−/− colon carcinoma cells were exposed to multiple pulses of 60 kV/cm with either 60 ns or 300 ns durations and analyzed for apoptotic markers. Several apoptosis markers were observed including cell shrinkage and increased percentages of cells positive for cytochrome c, active caspases, fragmented DNA, and Bax, but not Bcl-2. Unlike nsPEF-induced apoptosis in Jurkat cells (Beebe et al. 2003a) active caspases were observed before increases in cytochrome c, which occurred in the presence and absence of Bax. Cell shrinkage occurred only in cells with increased levels of Bax or cytochrome c. NsPEFs induced apoptosis equally in HCT116p53+/+ and HCT116p53−/− cells. These results demonstrate that non-ionizing radiation produced by nsPEFs can act as a non-ligand agonist with therapeutic potential to induce apoptosis utilizing mitochondrial-independent mechanisms in HCT116 cells that lead to caspase activation and cell death in the presence or absence of p-53 and Bax.

Ellagic Acid
Foods: Blackberries, Raspberries, Strawberries, Cranberries, Grapes, Walnuts, Pecans, Pomegranates, Wolfberry (Goji Berry) and numerous other fruits and vegetables.

Ellagic acid induces apoptosis through inhibition of nuclear factor kappa B in pancreatic cancer cells
www.ncbi.nlm.nih.gov…

We show that ellagic acid, a polyphenolic compound in fruits and berries, at concentrations 10 to 50 mmol/L stimulates apoptosis in human pancreatic adenocarcinoma cells. Further, ellagic acid decreases proliferation by up to 20-fold at 50 mmol/L. Ellagic acid stimulates the mitochondrial pathway of apoptosis associated with mitochondrial depolarization, cytochrome C release, and the downstream caspase activation. Ellagic acid does not directly affect mitochondria. Ellagic acid dose-dependently decreased NF-kappa B binding activity. Furthermore, inhibition of NF-kappa B activity using IkB wild type plasmid prevented the effect of ellagic acid on apoptosis.

p53/p21(WAF1/CIP1) expression and its possible role in G1 arrest and apoptosis in ellagic acid treated cancer cells
www.cancerletters.info…(98)00323-1/abstract

Ellagic acid is a phenolic compound present in fruits and nuts including raspberries, strawberries and walnuts. It is known to inhibit certain carcinogen-induced cancers and may have other chemopreventive properties. The effects of ellagic acid on cell cycle events and apoptosis were studied in cervical carcinoma (CaSki) cells. We found that ellagic acid at a concentration of 10−5 M induced G1 arrest within 48 h, inhibited overall cell growth and induced apoptosis in CaSki cells after 72 h of treatment. Activation of the cdk inhibitory protein p21 by ellagic acid suggests a role for ellagic acid in cell cycle regulation of cancer cells.

Ellagic Acid Induced p53/p21 Expression, G1 Arrest and Apoptosis in Human Bladder Cancer T24 Cells
ar.iiarjournals.org…

Ellagic acid significantly reduced the viable cells, induced G0/G1-phase arrest of the cell cycle and apoptosis. Ellagic acid also increased p53 and p21 and decreased CDK2 gene expression, that may lead to the G0/G1 arrest of T24 cells. Ellagic acid also promoted caspase-3 activity after exposure for 1, 3, 6, 12 and 24 h, which led to induction of apoptosis. Furthermore, the ellagic acid-induced apoptosis on T24 cells was blocked by the broad-spectrum caspase inhibitor (z-VAD-fmk).

Low Concentrations of Quercetin and Ellagic Acid Synergistically Influence Proliferation, Cytotoxicity and Apoptosis in MOLT-4 Human Leukemia Cells
jn.nutrition.org…

Ellagic acid significantly potentiated the effects of quercetin (at 5 and 10 µmol/L each) in the reduction of proliferation and viability and the induction of apoptosis. Significant alterations in cell cycle kinetics were also observed. The synergy was confirmed by an isobolographic analysis of the cell proliferation data. The interaction of ellagic acid and quercetin demonstrated an enhanced anticarcinogenic potential of polyphenol combinations, which was not based solely on the additive effect of individual compounds, but rather on synergistic biochemical interactions.

Emodin
Source: Rheum Emodi (a Himalayan rhubarb).
en.wikipedia.org…

Emodin induces apoptosis of human cervical cancer cells
www.ncbi.nlm.nih.gov…

Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is an active herbal component traditionally used in China for treating various ailments. Emodin exerts antiproliferative effects in many cancer cell lines and the actual molecular mechanism of which is still not clear. Since apoptosis could be a potential mechanism to explain these effects, we tested whether emodin induces cell death in human cervical cancer cells. Our results suggest that emodin exerts antiproliferative effects in human cervical cancer cells. Emodin inhibited DNA synthesis and induced apoptosis as demonstrated by increased nuclear condensation, annexin binding and DNA fragmentation in Bu 25TK cells in the presence of emodin. Moreover, we demonstrate for the first time in human cervical cancer cells that the apoptotic pathway involved in emodin-induced apoptosis is caspase-dependent and presumably through the mitochondrial pathway, as shown by the activation of caspases-3, -9 and cleavage of poly(ADP-ribose) polymerase.

Epigallocatechin
Foods: Green Tea (not Black Tea).
en.wikipedia.org…

Role of epigallocatechin gallate (EGCG) in the treatment of breast and prostate cancer
www.ncbi.nlm.nih.gov…

Green tea and its major constituent epigallocatechin gallate (EGCG) have been extensively studied as a potential treatment for a variety of diseases, including cancer. Epidemiological data have suggested that EGCG may provide protective effects against hormone related cancers, namely breast or prostate cancer. Extensive in vitro investigations using both hormone responsive and non-responsive cell lines have shown that EGCG induces apoptosis and alters the expression of cell cycle regulatory proteins that are critical for cell survival and apoptosis. This review will highlight the important in vitro mechanistic actions elicited by EGCG in various breast and prostate cancer cell lines. Additionally, the actions of green tea/EGCG in in vivo models for these cancers as well as in clinical trials will be discussed.

Epigallocatechin-3-gallate induces mitochondrial membrane depolarization and caspase-dependent apoptosis in pancreatic cancer cells
carcin.oxfordjournals.org…

In pursuit of our investigations to dissect the molecular mechanism of EGCG action on pancreatic cancer, we observed that the antiproliferative action of EGCG on pancreatic carcinoma is mediated through programmed cell death or apoptosis as evident from nuclear condensation, caspase-3 activation and poly-ADP ribose polymerase (PARP) cleavage. EGCG-induced apoptosis of pancreatic cancer cells is accompanied by growth arrest at an earlier phase of the cell cycle.

Topical applications of caffeine or (−)-epigallocatechin gallate (EGCG) inhibit carcinogenesis and selectively increase apoptosis in UVB-induced skin tumors in mice
www.pnas.org…

SKH-1 hairless mice were irradiated with ultraviolet B (UVB) twice weekly for 20 weeks. These tumor-free mice, which had a high risk of developing skin tumors during the next several months, were then treated topically with caffeine (6.2 μmol) or (−)-epigallocatechin gallate (EGCG; 6.5 μmol) once a day 5 days a week for 18 weeks in the absence of further treatment with UVB. Topical applications of caffeine to these mice decreased the number of nonmalignant and malignant skin tumors per mouse by 44% and 72%, respectively. Topical applications of EGCG decreased the number of nonmalignant and malignant tumors per mouse by 55% and 66%, respectively. Immunohistochemical analysis showed that topical applications of caffeine or EGCG increased apoptosis as measured by the number of caspase 3-positive cells in nonmalignant skin tumors by 87% or 72%, respectively, and in squamous cell carcinomas by 92% or 56%, respectively, but there was no effect on apoptosis in nontumor areas of the epidermis.

A component of green tea, (-)-epigallocatechin-3-gallate, promotes apoptosis in T24 human bladder cancer cells
www.ncbi.nlm.nih.gov…

Bladder cancer is the fourth most common cancer in men and ninth most common in women. It has a protracted course of progression and is thus an ideal candidate for chemoprevention strategies and trials. This study was conducted to evaluate the chemopreventive/antiproliferative potential of (-)-epigallocatechin gallate (EGCG, the major phytochemical in green tea) against bladder cancer and its mechanism of action. Using the T24 human bladder cancer cell line, we found that EGCG treatment caused dose- and time-dependent inhibition of cellular proliferation and cell viability, and induced apoptosis. Mechanistically, EGCG inhibits phosphatidylinositol 3′-kinase/Akt activation that, in turn, results in modulation of Bcl-2 family proteins, leading to enhanced apoptosis of T24 cells. These findings suggest that EGCG may be an important chemoprevention agent for the management of bladder cancer.

Erythropoietin (BAD)
en.wikipedia.org…

At first I had misread an abstract headline and thought that “EPO” was another thing that fights cancer. So I went looking for substances that boost it, and found that Echinacea (ECH) does the job. Then I looked up Echinacea for fighting cancer and found several abstracts stating such. Next I went back to EPO to pull up all of its abstracts and realized that it’s shown to help hypoxic tumor cells (tumors low on oxygen) resist apoptosis. Therefore, ECH is also bad for fighting hypoxic tumor cells. From there I found that cancer treatments often cause anemia, and anti-anemia drugs actually help boost EPO. These drugs (a multi-billion dollar a year micro-industry) are often given with chemotherapy, and despite the scientific community realizing these effects the FDA voted to still allow this methodology. There are still several studies showing usefulness with ECH, but unless you know detailed specifics about your particular cancer there are too many alternatives to even consider it.

The effect of 4 wk of oral echinacea supplementation on serum erythropoietin and indices of erythropoietic status
www.ncbi.nlm.nih.gov…

These data indicate that ECH supplementation resulted in an increase in EPO and IL-3 but did not significantly alter RBCs, Hb, or Hct.

Erythropoietin signaling inhibits hypoxia-induced apoptosis in human breast ecarcinoma cells
www.ncbi.nlm.nih.gov…

In the current study we provide evidence that increased autocrine Epo signaling induced by moderate levels of hypoxia inhibits hypoxia-induced apoptosis and promotes survival in MCF-7 human breast cancer cells. The anti-apoptotic effect of Epo correlates with upregulation of bcl-2 and bcl-XL, suggesting a mechanism similar to those described in hematopoietic cells. The resulting decreased apoptotic potential of hypoxic tumor cells may contribute to increased aggressiveness and therapy resistance of breast cancers.

Government advisors support keeping anti-anemia drugs from Amgen and Johnson & Johnson on the market for chemo patients
money.cnn.com…

The advisors voted 13-1 to keep Amgen’s Aranesp and J&J’s Procrit on the market for use with chemotherapy, said Amgen. The drugs are used to keep blood cell count from dropping and are often used with chemo, which can cause anemia in patients. It was welcome news for both companies, and both stocks closed up higher in Thursday trading. Billions of dollars in annual sales stem from the use of these drugs in chemo patients.

Ethylene Vinyl Acetate (BAD)
Source: Fire Safe Cigarettes
en.wikipedia.org…
This is the oil derived polymer that makes the new cigarettes “fire safe”. It’s now mandatory in almost every state. Obviously cigarettes are a strong cause of several forms of cancer, and that’s the point: why are they adding this chemical into them which promise to trigger a mass scale cancer epidemic? If you can’t quit smoking do whatever you can to get off of this form of cigarettes.

Results of a Long-term Experimental Study on the Carcinogenicity of Vinyl Acetate Monomer in Mice
www.ncbi.nlm.nih.gov…

Vinyl acetate monomer (VAM) was administered in drinking water at doses of 5,000, 1,000, and 0 ppm (v/v), to Swiss mice, 17 weeks old (breeders) or 12-day embryos (offspring) at the start of the experiment. The treatment lasted 78 weeks, and the animals were kept under control until spontaneous death. VAM has been shown to cause an increase in: (1) total malignant tumors; (2) carcinomas of the Zymbal glands, oral cavity, tongue, esophagus, and forestomach; (3) stomach tumors; (4) lung tumors; and (5) uterine tumors. A slight increase of hepatomas has been observed among male mice offspring treated with the higher dose. On the basis of these data VAM must be considered a multipotential carcinogen.

Evening Primrose
en.wikipedia.org…

Plant oil acts like cancer drug
news.bbc.co.uk…

Scientists have pinpointed how evening primrose oil fights breast tumours. It is down to a substance in the oil called gamma-linolenic acid that acts on the same receptor in tumours as the powerful breast cancer drug Herceptin. Unlike Herceptin, which blocks the Her-2/neu receptor, GLA interferes with the gene carrying the DNA code needed to make the receptor work. The US work in the Journal of the National Cancer Institute applies to about 30% breast cancers.

Caspase-independent apoptosis induced by evening primrose extract in Ehrlich ascites tumor cells
www.ncbi.nlm.nih.gov…

The EPE-induced translocation of AIF was suppressed with the addition of catalase, suggesting that the rapid intracellular peroxide levels after addition of EPE triggers off induction of apoptosis, which is AIF-mediated and caspase-independent.

Figs
en.wikipedia.org…
Figs seem to have usefulness in fighting cancer, and also help the appetite.

Suppressors of Cancer Cell Proliferation from Fig (Ficus carica) Resin
pubs.acs.org…

A mixture of 6-O-acyl-β-d-glucosyl-β-sitosterols, the acyl moeity being primarily palmitoyl and linoleyl with minor amounts of stearyl and oleyl, has been isolated as a potent cytotoxic agent from fig (Ficus carica) latex and soybeans. Identity was established by spectroscopic methods (NMR, MS) and confirmed by chemical synthesis. Both the natural and the synthetic compounds showed in vitro inhibitory effects on proliferation of various cancer cell lines.

Fisetin
en.wikipedia.org…
Fisetin can be found in various plants such as Acacia greggii, Acacia berlandieri, in the yellow dye young fustic from Rhus cotinus (Eurasian smoketree), in Butea frondosa (parrot tree), Gleditschia triacanthos, Quebracho colorado and the genus Rhus and in Callitropsis nootkatensis (yellow cypresses). It is also reported in mangoes.

Fisetin, a novel dietary flavonoid, causes apoptosis and cell cycle arrest in human prostate cancer LNCaP cells
carcin.oxfordjournals.org…

There was also induction of mitochondrial release of cytochrome c into cytosol, downregulation of X-linked inhibitor of apoptosis protein and upregulation of second mitochondria-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low pI on treatment of cells with fisetin. Treatment of cells with fisetin also resulted in significant activation of caspases-3, -8 and -9. Pretreatment of cells with caspase inhibitor (Z-VAD-FMK) blocked fisetin-induced activation of caspases. These data provide the first evidence that fisetin could be developed as an agent against PCa.

A plant flavonoid fisetin induces apoptosis in colon cancer cells by inhibition of COX2 and Wnt/EGFR/NF-B-signaling pathways
carcin.oxfordjournals.org…

Fisetin treatment of cells also inhibited the activation of EGFR and nuclear factor-kappa B (NF-B). Finally, the formation of colonies in soft agar was suppressed by fisetin treatment. Taken together, we provide evidence that the plant flavonoid fisetin can induce apoptosis and suppress the growth of colon cancer cells by inhibition of COX2- and Wnt/EGFR/NF-B-signaling pathways. We suggest that fisetin could be a useful agent for prevention and treatment of colon cancer.

Flavonoids Induce Apoptosis in Human Leukemia U937 Cells Through Caspase- and Caspase-Calpain-Dependent Pathways
www.ncbi.nlm.nih.gov…

At lower concentrations, these compounds were also able to sensitize these cells to apoptosis induced by tumor necrosis factor-. Regarding the mechanisms, galangin, luteolin, chrysin, and quercetin induced apoptosis in a way that required the activation of caspases 3 and 8, but not caspase 9. In contrast, an active role of calpains in addition to caspases was demonstrated in apoptosis induced by fisetin, apigenin, and 3,7-dihydroxyflavone. Our data show evidence of the proapoptotic properties of some flavonoids that could support their rational use as chemopreventive and therapeutic agents against carcinogenic disease.

Fisetin Inhibits Androgen Receptor Signaling and Tumor Growth in Athymic Nude Mice
cancerres.aacrjournals.org…

Treatment with fisetin in athymic nude mice implanted with AR-positive CWR22Rυ1 human PCa cells resulted in inhibition of tumor growth and reduction in serum PSA levels. These data identify fisetin as an inhibitor of AR signaling axis and suggest that it could be a useful chemopreventive and chemotherapeutic agent to delay progression of PCa.

Fucoidan
Foods: Various species of brown seaweed such as Kombu, Limu Moui, Bladderwrack, Wakame, Mozuku, and Hijiki.
Sources: Extracts under various names including “Modifilan”.

Apoptosis inducing activity of fucoidan in HCT-15 colon carcinoma cells
www.ncbi.nlm.nih.gov…

The antitumor activity of fucoidan from Fucus vesiculosus was investigated in human colon carcinoma cells. The crude fucoidan, a polysaccharide composed predominantly of sulfated fucose, markedly inhibited the growth of HCT-15 cells (human colon carcinoma cells). After HCT-15 cells were treated with fucoidan, several apoptotic events such as DNA fragmentation, chromatin condensation and increase of the population of sub-G1 hypodiploid cells were observed. …Furthermore, the induction of apoptosis was also accompanied by a strong activation of extracellular signal-regulated kinase (ERK) and p38 kinase and an inactivation of phosphatidylinositol 3-kinase (PI3K)/Akt in a time-dependent manner. These findings provide evidence demonstrating that the pro-apoptotic effect of fucoidan is mediated through the activation of ERK, p38 and the blocking of the PI3K/Akt signal pathway in HCT-15 cells. These data support the hypothesis that fucoidan may have potential in colon cancer treatment.

Fucoidan induces apoptosis through activation of caspase-8 on human breast cancer MCF-7 cells
www.ncbi.nlm.nih.gov…

Fucoidan is an active component of seaweed that has been shown to inhibit proliferation and induce apoptotic cell death in several tumor cells. However, the detailed mechanisms underlying this process have not yet been elucidated. In the present report, we investigated the effect of fucoidan on the induction of apoptosis in human breast cancer MCF-7 cells. Our data demonstrated that fucoidan reduced the viable cell number of MCF-7 cells in a dose- and time-dependent manner. In contrast, fucoidan did not affect the viable cell number of normal human mammary epithelial cells. Results from the apoptosis assay demonstrated that fucoidan induced internucleosomal DNA fragmentation, chromatin condensation, activation of caspase-7, -8, and -9, and cleavage of poly(ADP ribose) polymerase.

Fucoidan Induces Apoptosis of Human HS-Sultan Cells (Leukemia)
http:/pubs.acs.org/doi/abs/10.1021/jf9010406

Fucoidan-induced apoptosis was accompanied by the activation of caspase-3 and was partially prevented by pretreatment with a pan-caspase inhibitor, Z-VAD-FMK. The mitochondrial potential in HS-Sultan cells was decreased 24 hr after treatment with fucoidan, indicating that fucoidan induced apoptosis through a mitochondrial pathway. When HS-Sultan was treated with 100 mg/mL fucoidan for 24 hr, phosphorylation of ERK and GSK markedly decreased. In contrast, phosphorylation of p38 and Akt was not altered by treatment with fucoidan. L-Selectin and P-selectin are known to be receptors of fucoidan; however, as HS-Sultan does not express either of these selectins, it is unlikely that fucoidan induced apoptosis through them in HS-Sultan. The neutralizing antibody, Dreg56, against human L-selectin did not prevent the inhibitory effect of fucoidan on the proliferation of IM9 and MOLT4 cells, both of which express L-selectin; thus it is possible fucoidan induced apoptosis though different receptors. These results demonstrate that fucoidan has direct anti-cancer effects on human HS-Sultan cells through caspase and ERK pathways.

Fucoidan, a major component of brown seaweed, prohibits the growth of human cancer cell lines in vitro
www.spandidos-publications.com…

The results revealed that cell proliferation was suppressed in 13 cell lines in a time- and/or dose-dependent manner; this suppression was marked in the hepatocellular carcinoma, cholangiocarcinoma and gallbladder carcinoma cell lines. In contrast, proliferation of the neuroblastoma and 1 of the 2 ovarian carcinoma cell lines was not affected.

Inhibitory Effect of Fucoidan on Huh7 Hepatoma Cells (Liver Cancer) Through Downregulation of CXCL12
www.britannica.com…

Western blotting revealed that the amount of α-fetoprotein was decreased by 1.0 mg/ml of fucoidan in Huh7 cells, whereas it was unchanged in HepG2 cells. In Huh7 cells, CXCL12 mRNA expression was significantly downregulated by 1.0 mg/ml of fucoidan, whereas CXCR4 mRNA expression was unchanged by fucoidan. CXCL12 and CXCR4 mRNA were barely expressed in HepG2 cells. In addition, 1.0 mg/ml of fucoidan mildly arrested the cell cycle and induced apoptosis in Huh7 cells. The findings suggest that fucoidan exhibits antitumor activity toward Huh7 cells through the downregulation of CXCL12 expression.

Ethyl Alcohol Extracts of Hizikia fusiforme Sensitize AGS Human Gastric Adenocarcinoma Cells (Bone Marrow Cancer)
www.liebertonline.com…

Resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis has been reported in some cancer cells, including AGS human gastric adenocarcinoma cells. Hizikia fusiforme is a commonly used brown seaweed species in Korea that possesses potent antibacterial, antifungal, and anti-inflammatory activities. In this study, we demonstrated that treatment with TRAIL in combination with subtoxic concentrations of ethyl alcohol extract of H. fusiforme (EAHF) sensitized TRAIL-resistant AGS cells to TRAIL-mediated apoptosis. Combined treatment with EAHF and TRAIL increased chromatin condensation, DNA fragmentation, and sub-G1-phase DNA content.

Genistein
Foods: Lupin (herb), Fava Beans, Soybeans, Kudzu, Psoralea, Coffee and Flemingia Vestita (medicinal plant).
en.wikipedia.org…

Genistein-induced G2-M arrest, p21WAF1 upregulation, and apoptosis in a non-small-cell lung cancer cell line
www.ncbi.nlm.nih.gov…

Our results showed that genistein can upregulate p21WAF1 expression in genistein-treated cells. From these results, we conclude that genistein may act as an anticancer agent, and further studies may prove its efficacy in non-small lung cancer cells. Thus the biological effects of genistein may, indeed, be due to the modulation of cell growth, cell death, and cell cycle regulatory molecules.

Growth-inhibitory effects of the natural phyto-oestrogen genistein in MCF-7 human breast cancer cells
www.ncbi.nlm.nih.gov…

The low incidence of breast cancer in countries with a flavonoid-rich soy-based diet and the protection afforded by soy-derived products against experimental mammary tumours in rats suggest that genistein and other isoflavonoid compounds may exert an anti-tumour activity. We analysed the effects of genistein on cell number and cell cycle progression (flow cytometric analysis of propidium iodide-stained nuclei) of human breast cancer cells (MCF-7) in vitro. Genistein produced a significant, dose-dependent inhibition of MCF-7 cell growth with an ID50 of approximately 40 microM after 72 h of incubation.

Genistein-induced upregulation of p21WAF1, downregulation of cyclin B, and induction of apoptosis in prostate cancer cells
www.ncbi.nlm.nih.gov…

Here we report that genistein inhibits PCa cell growth in culture in a dose-dependent manner, which is accompanied by a G2/M cell cycle arrest. Cell growth inhibition was observed with concomitant downregulation of cyclin B, upregulation of the p21WAF1 growth-inhibitory protein, and induction of apoptosis. Collectively, these results provide experimental evidence for a novel effect of genistein on cell cycle gene regulation, resulting in the inhibition of cell growth and ultimate demise of tumor cells.

Genistein induces apoptosis and topoisomerase II-mediated DNA breakage in colon cancer cells
www.ncbi.nlm.nih.gov…

The present study was undertaken to determine if (a) genistein induces topo II-mediated DNA damage in HT-29 colon cancer cells; and (b) if this damage is required to induce apoptosis. DNA damage was evaluated using the comet assay. Apoptosis was determined by the ethidium bromide/acridine orange staining technique. DNA breakage was noted within 1 h of treatment. Apoptosis was only induced with high concentrations (>/=60 microM) of genistein. Marked inhibition of HT-29 cell growth was evident at concentrations ranging from 60 to 150 microM. This was associated with a cell cycle arrest at G(2)/M. Similar findings were obtained in SW-620 and SW-1116 colon cancer cell lines. Aclarubicin, a topo II antagonist, reduced genistein-induced DNA breaks but did not reduce apoptosis. These data suggest that, in colon cancer cells, topo II serves as the enzymatic target of genistein. Furthermore, topo II-mediated DNA cleavage is not required for the induction of apoptosis.

The Potential of Soybean Foods as a Chemoprevention Approach for Human Urinary Tract Cancer
clincancerres.aacrjournals.org…

Furthermore, both genistein and combined isoflavones exhibited a significant tumor suppressor effect in vivo (P < 0.05). The results justify the potential use of soybean foods as a practical chemoprevention approach for patients with urinary tract cancer.

Prevention of metastatic pancreatic cancer growth in vivo by induction of apoptosis with genistein, a naturally occurring isoflavonoid
www.ncbi.nlm.nih.gov…

In vivo, genistein significantly improved survival, almost completely inhibited metastasis, and increased apoptosis in an orthotopic model of pancreatic cancer. In vitro genistein treatment resulted in apoptosis in all pancreatic cancer cell lines tested, and this appeared to be mediated by activation of caspase-3.

Ginger
Food: Ginger Root.
en.wikipedia.org…
Related to Tumeric, it contains curcuminoids but also it’s own other unique cancer fighters.

Dietary ginger constituents, galanals A and B, are potent apoptosis inducers in Human T lymphoma Jurkat cells
www.ncbi.nlm.nih.gov…

The effects of the constituents isolated from ginger species including curcumin, 6-gingerol and labdane-type diterpene compounds on cell proliferation and the induction of apoptosis in the cultured human T lymphoma Jurkat cells were studied. Among the tested compounds, galanals A and B, isolated from the flower buds of a Japanese ginger, myoga (Zingiber mioga Roscoe), showed the most potent cytotoxic effect. …In conclusion, the results from this study provide biological evidence that ginger-specific constituents other than curcuminoids are potential anticancer agents.

Ginger ingredients reduce viability of gastric cancer cells via distinct mechanisms
www.ncbi.nlm.nih.gov…

We found that 6-gingerol, a phenolic alkanone isolated from ginger, enhanced the TRAIL-induced viability reduction of gastric cancer cells while 6-gingerol alone affected viability only slightly. 6-Gingerol facilitated TRAIL-induced apoptosis by increasing TRAIL-induced caspase-3/7 activation. 6-Gingerol was shown to down-regulate the expression of cIAP1, which suppresses caspase-3/7 activity, by inhibiting TRAIL-induced NF-kappaB activation. As 6-shogaol has a chemical structure similar to 6-gingerol, we also assessed the effect of 6-shogaol on the viability of gastric cancer cells. Unlike 6-gingerol, 6-shogaol alone reduced the viability of gastric cancer cells. 6-Shogaol was shown to damage microtubules and induce mitotic arrest. These findings indicate for the first time that in gastric cancer cells, 6-gingerol enhances TRAIL-induced viability reduction by inhibiting TRAIL-induced NF-kappaB activation while 6-shogaol alone reduces viability by damaging microtubules.

6-Shogaol (Alkanone from Ginger) Induces Apoptotic Cell Death of Human Hepatoma p53
pubs.acs.org…

In conclusion, we provide here a novel modality that can help to eradicate a p53 mutant of human hepatoma cells by using a natural consistent isolated form of ginger. These data also provide evidence to reaffirm the notion that consumption of certain foodstuffs can be beneficial to health because some of the constituents contained in them may be anticarcinogenic.

[size=3]Induction of apoptosis in HL-60 cells by pungent vanilloids, [6]-gingerol and [6]-paradol[/size]
www.ncbi.nlm.nih.gov…

[6]-Paradol, another pungent phenolic substance found in ginger and other Zingiberaceae plants, also has a vanilloid structure found in other chemopreventive phytochemicals including curcumin. In the present study, [6]-gingerol and [6]-paradol were found to exert inhibitory effects on the viability and DNA synthesis of human promyelocytic leukemia (HL-60) cells. The cytotoxic and antiproliferative effects of both compounds were associated with apoptotic cell death. The above results suggest that [6]-gingerol and [6]-paradol possess potential cytotoxic/cytostatic activities.

Multiple mechanisms are involved in 6-gingerol-induced cell growth arrest and apoptosis in human colorectal cancer cells
onlinelibrary.wiley.com…

The results suggest that 6-gingerol stimulates apoptosis through upregulation of NAG-1 and G1 cell cycle arrest through downregulation of cyclin D1. Multiple mechanisms appear to be involved in 6-gingerol action, including protein degradation as well as β-catenin, PKCε, and GSK-3β pathways.

Gingerol inhibits metastasis of MDA-MB-231 human breast cancer cells
www.ncbi.nlm.nih.gov…

In conclusion, we have shown that [6]-gingerol inhibits cell adhesion, invasion, motility and activities of MMP-2 and MMP-9 in MDA-MB-231 human breast cancer cell lines.

Ginsenoside
Source: Ginseng Root.
en.wikipedia.org…

Anti-proliferative effect of ginseng saponins on human prostate cancer cell line
www.ncbi.nlm.nih.gov…

Ginseng is a medicinal herb widely used in Asian countries, and many of its pharmacological actions are attributed to the ginsenosides. In a study of the anti-proliferative activity of ginsenosides using human prostate carcinoma LNCaP cell line, ginsenoside Rg3 displayed growth inhibitory activity. The cells lost its adherent property after incubation in the presence of 250 microM of ginsenoside for 48h.

An Intestinal Bacterial Metabolite of Ginseng Protopanaxadiol Saponins Has the Ability to Induce Apoptosis in Tumor Cells
www.ncbi.nlm.nih.gov…

Our previous study demonstrated that the in vivo anti-metastatic effect induced by oral administration of ginseng protopanaxadiol saponins was mediated by their metabolic component M1, and that the growth, invasion and migration of tumor cells were inhibited by M1 but not by ginsenosides. Here we investigated the inhibitory mechanism of M1 on the growth of tumor cells. M1 inhibited the proliferation of B16-BL6 mouse melanoma cells in a time- and dose-dependent manner, with accompanying morphological changes at the concentration of 20 microM. In addition, at 40 microM M1 induced apoptotic cell death within 24 h. Fluorescence microscopy revealed that dansyl M1 entered the cytosol and quickly reached the nuclei (approximately 15 min). Western blot analysis revealed that M1 rapidly up-regulated the expression of p27Kip1, but down-regulated the expression of c-Myc and cyclin D1 in a time-dependent manner. Thus, the regulation of apoptosis-related proteins by M1 is responsible for the induction of apoptotic cell death, and this probably leads to the anti-metastatic activity in vivo.

Antitumor activity of a novel ginseng saponin metabolite in human pulmonary adenocarcinoma cells resistant to cisplatin
www.ncbi.nlm.nih.gov…

The in vitro antitumor activity of a novel ginseng saponin metabolite, 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol (IH-901), was examined against four human cancer cell lines and one subline resistant to cisplatin (CDDP). The growth inhibitory activity of the compound was estimated by MTT tetrazolium assay. The mean concentrations of IH-901 needed to inhibit the proliferation of the cells by 50% (IC50) were 24.3, 25.9, 56.6 and 24.9 microM against human myeloid leukemia (HL-60), pulmonary adenocarcinoma (PC-14), gastric adenocarcinoma (MKN-45) and hepatoma (HepG2) cell lines, respectively. These values are higher than that of CDDP. In the CDDP-resistant PC/DDP cell line, the IC50 values of IH-901 and CDDP were 20.3 and 60.8 microM, respectively. These results suggest that IH-901 is not cross-resistant to CDDP in this cell line and could be a candidate for the treatment of CDDP resistant pulmonary cancer.

Grape Seed Extract
Surely you’ll have to chew the seeds up if you want to be able to digest the good stuff inside the seed.

Induction of Apoptosis in Human Leukemia Cells by Grape Seed Extract Occurs via Activation of c-Jun NH2-Terminal Kinase
clincancerres.aacrjournals.org…

Conclusions: The result of the present study showed that GSE induces apoptosis in Jurkat cells through a process that involves sustained JNK activation and Cip1/p21 up-regulation, culminating in caspase activation.

Grape seed extract induces apoptotic death of human prostate carcinoma DU145 cells
carcin.oxfordjournals.org…

Together, these results suggest that GSE possibly causes mitochondrial damage leading to cytochrome c release in cytosol and activation of caspases resulting in PARP cleavage and execution of apoptotic death of human PCA DU145 cells. Furthermore, GSE-caused caspase 3-mediated apoptosis also involves other pathway(s) including caspase 9 activation.

Synergistic Anti-Cancer Effects of Grape Seed Extract and Conventional Cytotoxic Agent Doxorubicin Against Human Breast Carcinoma Cells
www.springerlink.com…

In quantitative apoptosis studies, GSE and Dox alone and in combination showed comparable apoptotic death of MCF-7 cells, however, a combination of the two was inhibitory to Dox induced apoptosis in MDA-MB468 cells. This was further confirmed in another estrogen receptor-negative MDA-MB231 cell line, in which GSE and Dox combination strongly inhibited cell growth but did not show any increase in apoptotic cell death caused by Dox. Together, these results suggest a strong possibility of synergistic efficacy of GSE and Dox combination for breast cancer treatment, independent of estrogen receptor status of the cancer cell.

Grape Seed Extract Induces Cell Cycle Arrest and Apoptosis in Human Colon Carcinoma Cells
www.informaworld.com…=all~content=a905310312

We reported recently that GSE inhibits CRC cell HT29 growth in culture and nude mice xenograft. Because GSE is available commercially through different vendors, here we assessed whether GSE from 2 different manufacturers produces comparable biological effects in a panel of human CRC cell lines. Our results show that irrespective of source, GSE strongly inhibits LoVo, HT29, and SW480 cell growth, with a G1 arrest in LoVo and HT29 cells but an S and/or G2/M arrest in SW480 cell cycle progression. GSE also induced Cip/p21 levels in all 3 cell lines. Furthermore, an induction of apoptosis was observed in all 3 cell lines by GSE. Taken together, our findings suggest that GSE could be an effective CAM agent against CRC possibly due to its strong growth inhibitory and apoptosis-inducing effects.

Induction of apoptosis in HeLa cells by chloroform fraction of seed extracts of Nigella sativa
www.cancerci.com…

Methanolic, n-Hexane and chloroform extracts of Nigella sativa seedz effectively killed HeLa cells. The IC50 values of methanolic, n-hexane, and chloroform extracts of Nigella sativa were 2.28 μg/ml, 2.20 μg/ml and 0.41 ng/ml, respectively. All three extracts induced apoptosis in HeLa cells. Apoptosis was confirmed by DNA fragmentation, western blot and terminal transferase-mediated dUTP-digoxigenin-end labeling (TUNEL) assay. Western Blot and TUNEL results suggested that Nigella sativa seed extracts regulated the expression of pro- and anti- apoptotic genes, indicating its possible development as a potential therapeutic agent for cervical cancer upon further investigation.

High Fructose Corn Syrup (BAD)
List of foods that contain HFCS:
www.answerbag.com…

Cancer cells slurp up fructose, US study finds
www.reuters.com…

Pancreatic tumor cells use fructose to divide and proliferate, U.S. researchers said on Monday in a study that challenges the common wisdom that all sugars are the same. Tumor cells fed both glucose and fructose used the two sugars in two different ways, the team at the University of California Los Angeles found. They said their finding, published in the journal Cancer Research, may help explain other studies that have linked fructose intake with pancreatic cancer, one of the deadliest cancer types. “These findings show that cancer cells can readily metabolize fructose to increase proliferation,” Dr. Anthony Heaney of UCLA’s Jonsson Cancer Center and colleagues wrote.

Hispolon
Food: Phellinus Linteus (Oriental Mushroom)
en.wikipedia.org…

Hispolon induces apoptosis in human gastric cancer cells
www.ncbi.nlm.nih.gov…

Severe side effects and complications such as gastrointestinal and hematological toxicities because of current anticancer drugs are major problems in the clinical management of gastric cancer, which highlights the urgent need for novel effective and less toxic therapeutic approaches. Hispolon, an active polyphenol compound, is known to possess potent antineoplastic and antiviral properties. …Furthermore, hispolon potentiated the cytotoxicity of chemotherapeutic agents used in the clinical management of gastric cancer. These results suggest that hispolon could be useful for the treatment of gastric cancer either as a single agent or in combination with other anticancer agents.

Hispolon from Phellinus linteus has antiproliferative effects via MDM2-recruited ERK1/2 activity in breast and bladder cancer cells
www.ncbi.nlm.nih.gov…

The MDM2 proto-oncogene is overexpressed in many human tumors. Although MDM2 inhibits tumor-suppressor function of p53, there exists a p53-independent role for MDM2 in tumorigenesis. Therefore, downregulation of MDM2 has been considered an attractive therapeutic strategy. Hispolon extracted from Phellinus species was found to induce epidermoid and gastric cancer cell apoptosis. …The results indicated that cells with higher ERK1/2 activity were more sensitive to hispolon. In addition, hispolon-induced caspase-7 cleavage was inhibited by the ERK1/2 inhibitor, U0126. In conclusion, hispolon ubiquitinates and downregulates MDM2 via MDM2-recruited activated ERK1/2. Therefore, hispolon may be a potential anti-tumor agent in breast and bladder cancers.

Honey
en.wikipedia.org…
RAW honey is supposed to be the good stuff. The type of pollen the bees used to make the honey is important.

Antineoplastic activity of honey in an experimental bladder cancer implantation model: In vivo and in vitro studies
onlinelibrary.wiley.com…

In vitro studies revealed significant inhibition of the proliferation of T24 and MBT-2 cell lines by 1–25% honey and of RT4 and 253J cell lines by 6–25% honey. BrdU labeling index was significantly lower. FCM showed lower S-phase fraction, as well as absence of aneuploidy compared with control cells. In the in vivo studies, intralesional injection of 6 and 12% honey as well as oral ingestion of honey significantly inhibited tumor growth.

Bioactivity of Greek honey extracts on breast cancer (MCF-7), prostate cancer (PC-3) and endometrial cancer (Ishikawa) cells
cat.inist.fr…

Thyme, pine and fir honey showed both antioestrogenic and a weak oestrogenic effect at low and high concentration, respectively, in MCF-7 cells. Thyme honey reduced the viability of Ishikawa and PC-3 cells, whereas fir honey stimulated the viability of MCF-7 cells. In conclusion, Greek honeys are rich in phenolic compounds, they modulate oestrogenic activity whereas a thyme honey-enriched diet may prevent cancer-related processes in breast, prostate and endometrial cancer cells.

Honey could help fight cancer
news.bbc.co.uk…

Honey and royal jelly could become part of the arsenal of weapons against cancer, researchers say. A team from the University of Zagreb, in Croatia, found a range of honey-bee products stopped tumours growing or spreading in tests on mice. Writing in the Journal of the Science of Food and Agriculture, they say human cancer sufferers may also see benefits.

Isoliquiritigenin
Foods: Licorice, Shallots, Bean Sprouts.

Apoptosis Induced by Isoliquiritigenin in Human Gastric Cancer MGC-803 Cells
www.thieme-connect.com…

Isoliquiritigenin, which is possibly a principal anti-tumor constituent of licorice, a traditional Chinese herb, was examined for apoptosis-inducing activity in human gastric cancer MGC-803 cells. …These results suggest that isoliquiritigenin induced apoptosis of MGC-803 cells through calcium- and Deltapsi(m)-dependent pathways, indicating that it is potentially useful as a natural anti-cancer agent.

Isoliquiritigenin induces apoptosis by depolarizing mitochondrial membranes in prostate cancer cells
www.aacrmeetingabstracts.org…

Isoliquiritigenin (ISL) is a simple chalcone derivative, 4,2’,4’-trihydroxychalcone, found in licorice, shallot and bean sprouts. It was reported to have chemoprotective effects; inhibitory effects on murine colonic tumorigenesis, anti-angiogenic effect, and apoptosis-inducing activity. …The present results indicate that ISL inhibits prostate cancer cell growth by decreasing DNA synthesis and inducing apoptosis. The mechanism of apoptosis induction by ISL probably involves a mitochondria / caspase-9-specific pathway for the activation of the caspase cascade.

Isoliquiritigenin inhibits the proliferation and induces the apoptosis of human non-small cell lung cancer a549 cells
www.ncbi.nlm.nih.gov…

Isoliquiritigenin (ISL) is a natural pigment with the simple chalcone structure 4,2′,4′-trihydroxychalcone. In the present study, we report, for the first time, ISL-induced inhibition of the proliferation of the human non-small cell lung cancer A549 cell line. 2. The results showed that ISL not only inhibited A549 cell proliferation, but also induced apoptosis and blocked cell cycle progression in the G1 phase.

Cyclooxygenase-2 plays a suppressive role for induction of apoptosis in isoliquiritigenin-treated mouse colon cancer cells
www.ncbi.nlm.nih.gov…

Cellular damage induced by chronic inflammation is a well known cause of colon carcinogenesis. Cyclooxygenase-2 (COX-2), the enzyme that converts arachidonic acid to prostanoids, is known to play an important role in inflammation. Herbal flavonoid isoliquiritigenin (ILTG) has previously been reported to be a strong suppresser of the COX-2 pathway as well as an inducer of apoptosis. Here we report that the susceptibility to apoptosis by ILTG is dependent on the level of COX-2 in mouse colon adenocarcinoma Colon 26, which spontaneously expresses COX-2. This dependency was observed to be enhanced by blockage of the lipoxigenases (LOXs)-mediated metabolic pathway and attenuated by addition of a number of prostaglandins and thromboxanes. Taken together, these findings indicate that ILTG-induced apoptosis is negatively regulated by the COX-2 expression level.

Estrogenic and antiproliferative activities of isoliquiritigenin in MCF7 breast cancer cells
www.ncbi.nlm.nih.gov…

Transfection experiments reveal that ISL is able to transactivate the endogenous ER alpha in MCF7 cells and this is supported by the capability to induce down-regulation of ER alpha protein levels and up-regulation of pS2 mRNA. Moreover, by using chimeric proteins consisting of the hormone binding domains of ER alpha and ER beta fused to the Gal4 DNA binding domain, we have determined that ISL is an estrogenic agonist of both ER isoforms. As a biological counterpart, low and intermediate ISL concentrations that induce substantial transcriptional activity stimulate the proliferation of MCF7 cells. However, high levels of ISL become cytotoxic even in steroid-receptor negative HeLa cells. Thus, the activity of ISL and the balance between risk or chemopreventive factor for estrogen-dependent breast cancer may depend on dietary intake.

Kaempferol
Foods: Tea, Broccoli, Grapefruit, Brussel Sprouts, Apples, Witch Hazel
en.wikipedia.org…

Kaempferol-induced growth inhibition and apoptosis in A549 lung cancer cells is mediated by activation of MEK-MAPK
onlinelibrary.wiley.com…

To elucidate these mechanisms, we challenged human lung cancer cell line A549 with kaempferol and investigated its effects upon cellular growth and signal transduction pathways. Treatment of A549 cells with kaempferol resulted in a dose- and time-dependent reduction in cell viability and DNA synthesis with the rate of apoptosis equivalent to 0.9 ± 0.5, 5.2 ± 1.5, 16.8 ± 2.0, 25.4 ± 2.6, and 37.8 ± 4.5% on treatment with 0, 17.5, 35.0, 52.5, and 70.0 μM kaempferol, respectively.

Kaempferol sensitizes colon cancer cells to TRAIL-induced apoptosis
www.ncbi.nlm.nih.gov…

Kaempferol is a natural compound contained in edible plants, and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anti-cancer agent. Here, we show for the first time that the combined treatment with kaempferol and TRAIL drastically induced apoptosis in human colon cancer SW480 cells, compared to single treatments. Kaempferol markedly up-regulated TRAIL receptors, DR5 and DR4. DR5 but not DR4 siRNA efficiently blocked apoptosis induced by the co-treatment with kaempferol and TRAIL, indicating that DR5 up-regulation by kaempferol helps to enhance TRAIL actions. Moreover, we examined the combined effect on normal human cells. The co-treatment induced no apoptosis in normal human peripheral blood mononuclear cells and little apoptosis in normal human hepatocytes. These results suggest that kaempferol is useful for TRAIL-based treatments for cancer.

Limonoids
Source: Citrus Peels.
en.wikipedia.org…

Differential Inhibition of Human Cancer Cell Proliferation by Citrus Limonoids
www.ncbi.nlm.nih.gov…

Limonoids have been shown to inhibit the growth of estrogen receptor-negative and -positive human breast cancer cells in culture. …The human cancer cell lines included leukemia (HL-60), ovary (SKOV-3), cervix (HeLa), stomach (NCI-SNU-1), liver (Hep G2), and breast (MCF-7). The growth-inhibitory effects of the four limonoids and the limonoid glucoside mixture against MCF-7 cells were significant, and the antiproliferative activity of the different citrus limonoids was also dose and time dependent. No significant effects were observed on growth of the other cancer cell lines treated with the four individual limonoids at 100 μg/ml.

Citrus Limonoids Induce Apoptosis in Human Neuroblastoma Cells and Have Radical Scavenging Activity
jn.nutrition.org…

Citrus limonoid glucosides, a family of fruit bioactive compounds, were postulated to have free radical–scavenging and apoptosis-inducing properties against certain types of cancers. Four highly purified limonoid glucosides, limoin 17ß D-glucopypranoside (LG), obacunone 17ß D-glucopyranoside (OG), nomilinic acid 17ß D-glucopyranoside (NAG), and deacetylnomilinic acid 17ß D-glucopyranoside (DNAG) were tested for superoxide radical (O2–)-quenching activity and cytotoxic action against undifferentiated human SH-SY5Y neuroblastoma cells in culture. All 4 scavenged O2– as measured by inhibition of pyrogallol decomposition in a spectrophotometric assay. …We conclude that citrus limonoid glucosides are toxic to SH-SY5Y cancer cells. Cytotoxicity is exerted through apoptosis by an as yet unknown mechanism of induction. Individual limonoid glucosides differ in efficacy as anticancer agents, and this difference may reside in structural variations in the A ring of the limonoid molecule.

Citrus Reticulata blanco induces apoptosis in human gastric cancer cells SNU-668
www.ncbi.nlm.nih.gov…

Citrus fruits have been known to reduce the proliferation of many cancer cells. The antiproliferative effects of Citrus reticulata Blanco (CR) extract, the immature tangerine peel, on human gastric cancer cell line SNU-668 were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, 4,6-diamidineo-2-phenylindole staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, reverse transcription-polymerase chain reaction expressions of BCL-2, BAX and CASP-3 genes, caspase-3 activity, and immunocytochemistry of caspase-3. From the results of the morphological and biochemical assays, CR (50 microg/ml) increased the apoptosis of human gastric cancer cells with typical apoptotic characteristics, including morphological changes of chromatin condensation and apoptotic body formation.

Luteolin
Foods: Celery, Thyme, Dandelion, Rinds, Clover Blossum, Green Pepper, Chamomile Tea, Olive Oil, Carrots, Sage, Peppermint, Rosemary, Perilla and Oregano.

Antioxidant enzymes activity involvement in luteolin-induced human lung squamous carcinoma CH27 cell apoptosis
www.ncbi.nlm.nih.gov…

Luteolin (3′,4′,5,7-tetrahydroxyflavone) is an active constituent of Lonicera japonica (Caprifoliaceae), and has been reported to produce anti-tumor activities. However, the apoptosis-inducing activity of luteolin still remains unknown. Flavonoids have been found to possess prooxidant and antioxidant action. The biological and pharmacological effect of flavonoid may depend upon its behavior as either an antioxidant or a prooxidant. Our experiments found that luteolin-induced CH27 cell apoptosis was accompanied by activation of antioxidant enzymes, such as superoxide dismutase and catalase, but not through the production of reactive oxygen species and disruption of mitochondrial membrane potential. Therefore, the effects of luteolin on CH27 cell apoptosis were suspected to result from the antioxidant rather than the prooxidant action of luteolin.

The combination of TRAIL and luteolin enhances apoptosis in human cervical cancer HeLa cells
www.ncbi.nlm.nih.gov…

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is one of the most promising candidates for cancer therapeutics. However, some tumor cells are resistant to TRAIL-induced apoptosis. Our previous studies have shown that luteolin, a naturally occurring flavonoid, induces the up-regulation of death receptor 5 (DR5), which is a receptor for TRAIL. Here, we show for the first time that luteolin synergistically acts with exogenous soluble recombinant human TRAIL to induce apoptosis in HeLa cells, but not in normal human peripheral blood mononuclear cells. The combined use of luteolin and TRAIL induced Bid cleavage and the activation of caspase-8. Also, human recombinant DR5/Fc chimera protein, caspase inhibitors, and DR5 siRNA efficiently reduced apoptosis induced by co-treatment with luteolin and TRAIL. These results raise the possibility that this combined treatment with luteolin and TRAIL might be promising as a new therapy against cancer.

Effects of luteolin on the inhibition of proliferation and induction of apoptosis in human myeloid leukaemia cells
www.ncbi.nlm.nih.gov…

Luteolin, a flavonoid isolated from the fruit of Vitex rotundifolia, has been examined with regard to the inhibition of proliferation and induction of apoptosis in human myeloid leukaemia HL-60 cells. The concentration required for 50% inhibition of the growth after 96 h was 15 +/- 1.1 microM. The mode of cell death induced by luteolin was found to be apoptosis, as judged by the morphologic alteration of the cells and by the detection of DNA fragmentation using agarose gel electrophoresis. The degree of apoptosis was quantified by a sandwich enzyme immunoassay and flow cytometric analysis. These results suggest that luteolin may be used as potential chemopreventive and chemotherapeutic agents.

Induction apoptosis of luteolin in human hepatoma HepG2 cells
www.ncbi.nlm.nih.gov…

In addition, it showed that c-Jun NH2-terminal kinase (JNK) was activated after the treatment of luteolin for 3-12 h. Further investigation showed that a specific JNK inhibitor, SP600125, reduced the activation of CPP 32, the mitochondrial translocation of Bax, as well as the cytosolic release of cytochrome c that induced by luteolin. Finally, the apoptosis induced by luteolin was suppressed by a pretreatment with SP600125 via evaluating annexin V-FITC binding assay. These data suggest that luteolin induced apoptosis via mechanisms involving mitochondria translocation of Bax/Bak and activation of JNK.

Luteolin inhibits insulin-like growth factor 1 receptor signaling in prostate cancer cells
carcin.oxfordjournals.org…

Luteolin inhibited expression of cyclin D1 and increased expression of p21. As a result, luteolin suppressed proliferation and induced apoptosis of prostate cancer cells. Knockdown of IGF-1R by siRNA led to inhibition of proliferation of prostate cancer cells. Results of in vivo tumor growth assay indicated that luteolin inhibited PC-3 tumor growth. Immunoblotting of the extracts of tumor tissues showed that luteolin inhibited IGF-1R/AKT signaling. Our results provide a new insight into the mechanisms that luteolin is against cancer cells.

Induction of cell cycle arrest and apoptosis in HT-29 human colon cancer cells by the dietary compound luteolin
ajpgi.physiology.org…

We demonstrate that luteolin promotes both cell cycle arrest and apoptosis in the HT-29 colon cancer cell line, providing insight about the mechanisms underlying its antitumorigenic activities.

Luteolin Induces Apoptosis in Oral Squamous Cancer Cells
jdr.sagepub.com…

Results revealed that luteolin reduced the viability of SCC-4 cells and induced apoptosis by decreasing the expression of cyclin-dependent kinase (CDKs), cyclins, and phosphor- retinoblastoma (p-Rb) anti-apoptotic protein, but increased the expression of pro-apoptotic proteins and activated caspase 9 and 3, with a concomitant increase in the levels of cleaved poly-ADP-ribose polymerase (PARP). Combination treatment of luteolin with paclitaxel enhanced the cytotoxic effect of paclitaxel in SCC-4 cells, and continuous administration of luteolin suppressed the growth of xenograft tumors in nude mice. These results suggest that luteolin could be an effective chemotherapeutic agent for the treatment of oral squamous cell carcinoma.

Lycopene
Foods: Tomato, “Gac” Fruit, Red Carrot, Watermelon, Papaya, Red Algae, Pink Guava and Grapefruit.
en.wikipedia.org…
It’s what makes most (but not all) fruits and vegetable yellow-orange-red.

Lycopene Supplementation Inhibits Lung Squamous Metaplasia and Induces Apoptosis
cancerres.aacrjournals.org…

Higher intake of lycopene is related to a lower risk of lung cancer in human studies. Lung cancer risk is associated with higher plasma levels of insulin-like growth factor I (IGF-I) and/or lower levels of IGF-binding protein 3 (IGFBP-3).

Lycopene interferes with…mammary cancer cells
www.ncbi.nlm.nih.gov…

Collectively, the above data suggest that the inhibitory effects of lycopene on MCF7 cell growth are not due to the toxicity of the carotenoid but, rather, to interference in IGF-I receptor signaling and cell cycle progression.

Concentrations of Lycopene Induce Mitochondrial Apoptosis in LNCaP Human Prostate Cancer Cells
ebm.rsmjournals.com…

Subsequently, we demonstrated that increasing concentrations of lycopene significantly (P < 0.05) reduced mitochondrial transmembrane potential, induced the release of mitochondrial cytochrome c, and increased annexin V binding, confirming induction of apoptosis. Thus, lycopene at physiologically relevant concentrations did not affect cellular proliferation or promote necrosis but clearly altered mitochondrial function and induced apoptosis in LNCaP human prostate cancer cells.

A novel cleavage product formed by autoxidation of lycopene induces apoptosis in HL-60 cells
www.ncbi.nlm.nih.gov…

We previously reported that an autoxidation mixture of lycopene induced apoptosis in HL-60 human promyelocytic leukemia cells, but lycopene alone did not. In the present study, bioassay-directed fractionations of autoxidized lycopene led to isolation of a novel cleavage product of lycopene. Spectral analyses elucidated its structure as (E,E,E)-4-methyl-8-oxo-2,4,6-nonatrienal (MON), suggesting the formation through the oxidative cleavages at the 5, 6- and 13, 14-double bonds of lycopene.

Maitake D-Fraction
Source: Extract from Maitake Mushrooms.
en.wikipedia.org…

Possible disease remission in patient with invasive bladder cancer with D-fraction regimen
www.ncbi.nlm.nih.gov…

This case study describes an invasive bladder cancer patient at a high risk for disease recurrence who only followed a D-fraction regimen (with vitamin C) refusing other medical interventions. The two-year follow-up yet indicated no clinical evidence of progression of residual disease or recurrence with possible disease remission.

Synergistic potentiation of interferon activity with maitake mushroom d-fraction on bladder cancer cells
onlinelibrary.wiley.com…

The combination of IFN-2b (10 000 IU/mL) and PDF (200 µg/mL) reduced growth by ≈75% in T24 cells. This appears to be due to a synergistic potentiation of these two agents, inducing a G1 arrest with DNA-PK activation. Therefore, the IFN-2b/PDF combination could trigger DNA-PK activation that may act on the cell cycle to cease cancer cell growth.

Potential growth inhibitory effect of maitake D-fraction on canine cancer cells
www.ncbi.nlm.nih.gov…

The postulated anticancer effect of D-fraction, the bioactive extract of maitake mushroom, on three types (CF33, CF21, and CL-1) of canine cancer cells was evaluated. The effect of D-fraction on several human cancer cells was also investigated. The effect of other beta-glucan products was likewise examined. D-fraction was highly effective on the canine cancer cells, either potently inhibiting cell growth or directly killing cells. Similar effects were also demonstrated in certain human cancer cells. However, other beta-glucan products relevant to D-fraction had no such effects on canine cancer cells. Therefore, D-fraction is a potent natural agent that could be useful in treating canine cancers as well as other veterinary cancers.

Melatonin
Sold as a sleep aid. It is secreted by the pineal gland. Low melatonin levels are associated with cancer, it’s known to fight cancer, and it helps chemotherapy patients endure the side effects.
en.wikipedia.org…

Melatonin and retinoic acid induces apoptosis in MCF-7 human breast cancer cells
www.springerlink.com…

These data suggest that the sequential treatment regimen of Mlt and atRA may induce apoptosis by modulation of members of the Bcl-2 family of proteins. Thus, this combinatorial regimen, which reduces the concentration of atRA needed for clinical efficacy while enhancing its anti-tumorigenic activity, could be of great therapeutic benefit, and may, in fact, specifically induce the regression of established breast tumors due to its apoptosis-promoting effects.

Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status
www.ncbi.nlm.nih.gov…

Melatonin (MLT) has been proven to counteract chemotherapy toxicity, by acting as an anti-oxidant agent, and to promote apoptosis of cancer cells, so enhancing chemotherapy cytotoxicity. The aim of this study was to evaluate the effects of concomitant MLT administration on toxicity and efficacy of several chemotherapeutic combinations in advanced cancer patients with poor clinical status. The study included 250 metastatic solid tumour patients (lung cancer, 104; breast cancer, 77; gastrointestinal tract neoplasms, 42; head and neck cancers, 27), who were randomized to receive MLT (20 mg/day orally every day) plus chemotherapy, or chemotherapy alone. …This study indicates that the pineal hormone MLT may enhance the efficacy of chemotherapy and reduce its toxicity, at least in advanced cancer patients of poor clinical status.

Melatonin induces apoptosis in human neuroblastoma cancer cells
www.ncbi.nlm.nih.gov…

Low concentrations (nanomolar) of melatonin had been previously shown to inhibit cell proliferation in several cancer cell lines as well as in experimental animal models. Additionally, cell growth inhibition and differentiation of prostate cancer cell lines by high concentrations (micromolar to millimolar) of melatonin have been recently reported. In the present paper, we show the induction of apoptosis by high doses of melatonin in the human neuroblastoma cell line SK-N-MC. …Treatment with 1 mm melatonin for 6 days induced cell death in 75% of the cells. This novel finding shows that a nontoxic natural indoleamine may be potential therapy for some types of human neuroblastomas.

Melatonin and RZR/ROR receptor ligand CGP 52608 induce apoptosis in the murine colonic cancer
www.ncbi.nlm.nih.gov…

The effects of melatonin and the thiazolinidinedione derivative CGP 52608 on apoptosis of Colon 38 cancer cells were investigated. Male mice were implanted subcutaneously with a suspension of Colon 38 cells. Ten days after induction of tumors, the animals were treated with melatonin or CGP 52608. Both substances were given in subcutaneous injections in daily doses of 10 or 100 microg in the evening for 6 days. The control group received solvent. The apoptotic cells were visualized in paraffin sections by means of the transferase-mediated dUTPnick end-labeling method. Both treatments increased significantly and to the same degree the number of apoptotic cells in tumors. This finding confirms our earlier observation that melatonin exerts a pro-apoptotic effect on murine colonic cancer cells. Moreover, because CGP 52608 is a ligand of RZR/ROR receptors and the latter are considered by some investigators as nuclear binding sites for melatonin, our data suggest the involvement of these receptors in the pro-apoptotic effect of melatonin.

A randomized study of chemotherapy with cisplatin plus etoposide versus chemoendocrine therapy with cisplatin, etoposide and the pineal hormone melatonin as a first-line treatment of advanced non-small cell lung cancer patients in a poor clinical state
onlinelibrary.wiley.com…

Recent studies suggest that the pineal hormone melatonin may reduce chemotherapy-induced immune and bone marrow damage. In addition, melatonin may exert potential oncostatic effects either by stimulating host anticancer immune defenses or by inhibiting tumor growth factor production. On this basis, we have performed a randomized study of chemotherapy alone vs. chemotherapy plus melatonin in advanced non-small cell lung cancer patients (NSCLC) with poor clinical status. …The percent of 1-year survival was significantly higher in patients treated with melatonin plus chemotherapy than in those who received chemotherapy alone (15/34 vs. 7/36, P < 0.05). Finally, chemotherapy was well tolerated in patients receiving melatonin, and in particular the frequency of myelosuppression, neuropathy, and cachexia was significantly lower in the melatonin group. This study shows that the concomitant administration of melatonin may improve the efficacy of chemotherapy, mainly in terms of survival time, and reduce chemotherapeutic toxicity in advanced NSCLC, at least in patients in poor clinical condition.

Methylselenocysteine
Foods: Garlic, Onions, Astralagus, Broccoli’s, Radishes, Brussel Sprouts, Ramps, Milk Vetch, Indian Mustard and Cabbage.
Sources: Health foods stores.
en.wikipedia.org…
Se-Methylselenocysteine (SeMSC) is a naturally occurring seleno-amino acid.

Se-Methylselenocysteine induces apoptosis through caspase activation in HL-60 cells
carcin.oxfordjournals.org…

In our study, we found that Se-methylselenocysteine (MSC) induced apoptosis through caspase activation in human promyelocytic leukemia (HL-60) cells. Measurements of cytotoxicity, DNA fragmentation and apoptotic morphology revealed that MSC was more efficient at inducing apoptosis than selenite, but was less toxic. Moreover, MSC increased both the apoptotic cleavage of poly(ADP-ribose) polymerase (PARP) and caspase-3 activity, whereas selenite did not.

Se-methylselenocysteine inhibits phosphatidylinositol 3-kinase activity of mouse mammary epithelial tumor cells
breast-cancer-research.com…

Se-methylselenocysteine (MSC), a naturally occurring selenium compound, is a promising chemopreventive agent against in vivo and in vitro models of carcinogen-induced mouse and rat mammary tumorigenesis. We have demonstrated previously that MSC induces apoptosis after a cell growth arrest in S phase in a mouse mammary epithelial tumor cell model (TM6 cells) in vitro. The present study was designed to examine the involvement of the phosphatidylinositol 3-kinase (PI3-K) pathway in TM6 tumor model in vitro after treatment with MSC.

Selenocystine Induces S-Phase Arrest and Apoptosis in Human Breast Adenocarcinoma MCF-7 Cells by Modulating ERK and Akt Phosphorylation
pubs.acs.org…

Selenocystine (SeC) is a nutritionally available selenoamino acid with selective anticancer effects on a number of human cancer cell lines. The present study shows that SeC inhibited the proliferation of human breast adenocarcinoma MCF-7 cells in a time- and dose-dependent manner, through the induction of cell cycle arrest and apoptotic cell death.

Milk Thistle
en.wikipedia.org…

Milk thistle may limit liver damage from chemo
www.reuters.com…

An herb used since ancient times to treat liver ailments may help reduce the liver damage caused by some cancer drugs, a study published Monday suggests. In a study of 50 children undergoing chemotherapy for acute lymphoblastic leukemia (ALL), researchers found that an herb called milk thistle appeared to reduce treatment-related liver inflammation.

Milk Thistle and Prostate Cancer
cancerres.aacrjournals.org…

Extracts from the seeds of milk thistle, Silybum marianum, are known commonly as silibinin and silymarin and possess anticancer actions on human prostate carcinoma in vitro and in vivo. Seven distinct flavonolignan compounds and a flavonoid have been isolated from commercial silymarin extracts.

Myricetin
Foods: Walnuts, Red Grapes, Berries, Onions, Bilberry and Southern Bayberry shrub.
en.wikipedia.org…
MEK Inhibitor.

The effect of the flavonoids, quercetin, myricetin and epicatechin on the growth and enzyme activities of MCF7 human breast cancer cells
www.ingentaconnect.com…

E and Q inhibited the O-deethylation of ethoxyresorufin (EROD) catalysed by cytochrome P450 CYPIA. In contrast, M increased the EROD reaction 2-fold. Q increased the activity of DT-diaphorase, NADPH cytochrome c reductase and glutathione reductase, while E increased only NADPH cytochrome c reductase activity. The effects on enzyme activities in vitro suggest that there is not only the potential for flavonoids to alter metabolic activation of carcinogens but also of therapeutically administered drugs in vivo. We are at present investigating the synergy between anti-cancer drugs and flavonoids in terms of anti-tumour efficacy.

Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1
carcin.oxfordjournals.org…

Here we demonstrated that 3,3′,4′,5,5′,7-hexahydroxyflavone (myricetin), one of the major flavonols in red wine, is a novel inhibitor of MEK1 activity and transformation of JB6 P+ mouse epidermal cells. Myricetin (10 µM) inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA) or epidermal growth factor (EGF)-induced cell transformation by 76 or 72%, respectively, compared with respective reductions of 26 or 19% by resveratrol (20 µM). …Overall, these results indicated that myricetin has potent anticancer-promoting activity and mainly targets MEK signaling, which may contribute to the chemopreventive potential of several foods including red wines.

Nikko Maple Bark
www.hort.uconn.edu…

Hot water extract of bark of Nikko maple (Acer nikoense) induces apoptosis in leukemia cells
www.ncbi.nlm.nih.gov…

In screening for antitumor constituents in traditional crude drugs, we used three cultured cell lines: mouse leukemia P388 cells, doxorubicin-resistant P388 cells and leczyme (catalytic lectin)-resistant P388 cells. The hot water extract (HWE) of the bark of Nikko maple (Acer nikoense) showed concentration-dependent inhibitory effects on the growth of these three cell lines. DNA fragmentation and morphological changes, accompanied by condensed and fragmented nuclei, were observed in the leukemia cell lines cultured with HWE of the bark of Nikko maple. Treatment with this HWE increased the expression of sialylated glycoconjugates on the apoptotic cells. These results suggest that HWE induces cell death via apoptosis in vitro.

Nurture
en.wikipedia.org…
While medical sources typically claim that methods such as massage therapy lacks scientific data in healing, common sense and scientific data might say otherwise. Consider neglected children who don’t properly develop, how depression can shorten lifespans and sex increases the size and health of the brain.

www.mayoclinic.com…

While more research is needed to confirm the benefits of massage, some studies have found massage helpful for: Stress relief, Managing anxiety and depression, Pain, Stiffness, Blood pressure control, Infant growth, Sports-related injuries, Boosting immunity and Cancer treatment.

drfreire.com…

The child may have been born healthy but if he is exposed to toxins such as lead or alcohol, physical abuse and neglect and other childhood traumas, may develop abnormally, have stunted growth and serious problems in later life.

en.wikibooks.org…

When children lack physical contact or nurturing, psycho-social dwarfism may impede their growth. The hypothalamus does not stimulate the thyroid to produce enough growth hormone. In studies on Romanian orphanage children, the orphans had stunted growth, lower IQs, and more learning disabilities than average children (Groza et al., 1998). A few years after the orphans were adopted, they caught up in height and improved their learning abilities.

serendip.brynmawr.edu…

An excessively active sympathetic nervous system may inhibit growth hormone secretion. Researchers have attempted to pinpoint the importance of this factor in psychogenic dwarfism by injecting a drug that blocks one part of the sympathetic nervous system. Studies have indicated that this causes an increase in growth hormone levels that eventually return to normal. Additionally, glucocorticoids play a factor. Glucocorticoids are steroid hormones that act similarly to epinephrine and serve to energize the body during periods of stress; however, unlike epinephrine that acts within seconds, glucocorticoids work over a period of hours. This suggests that perhaps glucocorticoids act to help the body recover after a stressor, or prepare for the next stressor, rather than mediating the stress response. Not surprisingly, some children with psychogenic dwarfism display high levels of glucocorticoids. This effect is also seen in rats that have been deprived of their mothers. Glucocorticoids block the secretion of the growth hormone, the reception of growth hormones by the target cells, and the synthesis of new proteins and new DNA in dividing cells.

news.medill.northwestern.edu…

African-American life expectancy on average is seven to eight years less than non-Hispanic white Americans according to the Centers for Disease Control, but blacks are also far less likely to self-report major depression and anxiety. Does that mean African-Americans are living shorter, yet happier lives? The answer to that question is no, according to the University of Michigan’s Director of the Institute of Social Research, Dr. James Jackson.

www.livescience.com…

Sex apparently can help the brain grow, according to new findings in rats. Sexually active rodents also seemed less anxious than virgins, Princeton scientists discovered. Past findings had shown that stressful, unpleasant events could stifle brain cell growth in adults. To see if pleasant albeit stressful experiences could have the opposite effect, researchers studied the effects of sex in rats.

Olives & Olive Oil

en.wikipedia.org…
Epidermal growth factor receptor inhibition is proven to stop many forms and instances of cancer. There are numerous commerical forms of medicine out there, but if you even need such measures is up to professionals. Olive’s possess natural EGFR Inhibitors.

Cancer chemoprevention by hydroxytyrosol isolated from virgin olive oil through G1 cell cycle arrest and apoptosis
www.ncbi.nlm.nih.gov…

Recent epidemiological evidence and animal studies suggest a relationship between the intake of olive oil and a reduced risk of several malignancies. …The con-centrations of hydroxytyrosol which inhibited 50% of cell proliferation were ∼50 and ∼750 μmol/l for HL60 and both HT29 and HT29 clone 19A cells, respectively. At concentrations ranging from 50 to 100 μmol/l, hydroxytyrosol induced an appreciable apoptosis in HL60 cells after 24 h of incubation as evidenced by flow cytometry, fluorescence microscopy and internucleosomal DNA fragmentation. … These results support the hypothesis that hydroxytyrosol may exert a protective activity against cancer by arresting the cell cycle and inducing apoptosis in tumour cells, and suggest that hydroxytyrosol, an important component of virgin olive oil, may be responsible for its anticancer activity.

Olive Fruit Extracts Inhibit Proliferation and Induce Apoptosis in HT-29 Human Colon Cancer Cells
jn.nutrition.org…

We investigated the effect on cell proliferation and apoptosis in HT-29 cells of an extract from the skin of olives composed of pentacyclic triterpenes with the main components maslinic acid (73.25%) and oleanolic acid (25.75%). Studies of the dose-dependent effects showed antiproliferative activity at an EC50 value of 73.96 ± 3.19 µmol/L of maslinic acid and 26.56 ± 2.55 µmol/L of oleanolic acid without displaying necrosis. Apoptosis was confirmed by the microscopic observation of changes in membrane permeability in 40.9 ± 3.9% and detection of DNA fragmentation in 24.5 ± 1.5% of HT-29 cells incubated for 24 h with olive fruit extract containing 150 and 55.5 µmol/L of maslinic and oleanolic acids, respectively.

Olive oils bitter principle reverses acquired autoresistance to trastuzumab (Herceptin™) in HER2-overexpressing breast cancer cells
www.biomedcentral.com…

A low incidence of breast cancer in the Mediterranean basin suggests that a high consumption of Extra Virgin Olive Oil (EVOO) might confer this benefit. …Mechanistically, oleuropein aglycone treatment significantly reduced HER2 ECD cleavage and subsequent HER2 auto-phosphorylation, while it dramatically enhanced Tzb-induced down-regulation of HER2 expression. …Olive oil’s bitter principle (i.e., oleuropein aglycone) is among the first examples of how selected nutrients from an EVOO-rich “Mediterranean diet” directly regulate HER2-driven breast cancer disease.

Oridonin
Source: Rabdosia Rubescens Plant.
medical-dictionary.thefreedictionary.com…

Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies
mct.aacrjournals.org…

This study found that oridonin, a natural diterpenoid purified from Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266, RPMI8226), acute lymphoblastic T-cell leukemia (Jurkat), and adult T-cell leukemia (MT-1) cells with an effective dose that inhibited 50% of target cells (ED50) ranging from 0.75 to 2.7 μg/mL.

Autophagy preceded apoptosis in oridonin-treated human breast cancer MCF-7 cells
www.ncbi.nlm.nih.gov…

Recent studies have shown that MCF-7 cells undergo autophagy under some conditions, such as tamoxifen treatment and starvation. In this study, we investigated autophagy in MCF-7 cells under oridonin treatment and further examined the relationship between autophagy and apoptosis. After 3-MA (the specific inhibitor of autophagy) pre-culture, MCF-7 cells were exposed to oridonin, and the growth inhibitory ratio, morphologic changes, DNA fragmentation, proteins expression, autophagic ratio and apoptotic ratio were evaluated. Oridonin inhibited the proliferation of MCF-7 cells and induced autophagy in vitro.

Oridonin-treated MCF-7 human breast cancer cells
onlinelibrary.wiley.com…

Oridonin inhibited cell growth in a time- and dose-dependent manner. Cell cycle was altered through the upregulation of p53 and p21 protein expressions. Pancaspase inhibitor Z-VAD-fmk and calpain inhibitor II both decreased cell death ratio.

Oyster Sauce (BAD)

en.wikipedia.org…

In 2001 the United Kingdom Food Standards Agency found in tests of various oyster sauces and soy sauces that some 22% of samples contained a chemical called 3-MCPD (3-monochloropropane-1,2-diol) at levels considerably higher than those deemed safe by the European Union. About two-thirds of these samples also contained a second chemical called 1,3-DCP (1,3-dichloropropane-2-ol) which experts advise should not be present at any levels in food. Both chemicals have the potential to cause cancer and the Agency recommended that the affected products be withdrawn from shelves and avoided.[12][13]

Paclitaxel
Source: Pacific Yew Tree (Taxus brevifolia)
en.wikipedia.org…

This is the natural version of a highly used chemotherapy drug known as Taxol. It has well known effectiveness against multiple lines of cancer and citations shouldn’t be necessary.

Pepino Melon
Source: Fruits from Solanum Muricatum.
en.wikipedia.org…

Extract of Solanum muricatum (Pepino/CSG) inhibits tumor growth by inducing apoptosis
www.ncbi.nlm.nih.gov…

A lyophilized aqueous fraction extracted from Solanum muricatum (CSG4) was used in this study. The human cell lines tested include: prostate (PC3, DU145), stomach (MKN45), liver (QGY-7721, SK-HEP-1), breast (MDA-MB-435), ovarian (OVCAR), colon (HT29) and lung (NCI-H209) cancer cells; NHP (prostate), HUVEC (umbilical vein endothelial cell), and WI-38 (lung diploid fibroblasts) normal cells. The cell survival was determined by either Cell Titer MTS cell proliferation kit or trypan blue dye exclusion assay. The apoptosis was analyzed by (a) apoptotic morphology by light microscopy; (b) DNA ladder formation; (c) PARP cleavage assay. Taken together, the present study suggests, for the first time, that CSG may represent promising new chemical entity which preferentially targets various tumor cells by triggering apoptosis.

Pinellia
Source: Root called “Ban Xia” used in Chinese Medicine to transform phlegm and stop coughing.
en.wikipedia.org…

Apoptosis induction effect of Pinellia extract fraction on cell lines of cervical cancer cultured in vitro
en.cnki.com.cn…

We tested the effects of PE on cell proliferation by MTT assay.The effects of PE on morphology,and cell cycle were studied by phase-contrast microscope and fiowcytometry(FCM).Results: PE could obviously inhibit the proliferation of HeLa and CaSki cells in a time and dose dependent manner.It could induce apoptosis of HeLa and CaSki.Conclusions: PE can suppress proliferation of cervical cancer cells and induce apoptosis.It may be a pure traditional Chinese reagent with non-side effects to prevent and treat cervical cancer effectively.

Experimental study on Inducing apoptosis effects of the protein of Pinellia pedatisecta Schott on human ovarian cancer cell line SKOV3
en.cnki.com.cn…

OBJECTIVE To investigate the effects of the protein of Pinellia pedatisecta Schott on the proliferation of human ovarian cancer cell line SKOV3 in vitro and to determine whether the protein of Pinellia pedatisecta Schott inhibit the growth of ovarian cancer and its mechanism of action.METHODS CCK-8 was used to detect the effect of the protein of Pinellia pedatisecta Schott on the growth of SKOV3 cells in vitro;using flow cytometry,detected the apoptosis of SKOV3 cells treated with the protein of Pinellia pedatisecta Schott by Anexinn-V.RESULTS The protein of Pinellia pedatisecta Schott had some effect of inhibiting the proliferation and inducing apoptosis of SKOV3 cells,and the mechanism would be further studied.

Revised Pinellia Combination Treat Digestive Tract Reaction from Chemical Therapy after Operation of Gastric Cancer
en.cnki.com.cn…

The patients were randomly divided into two groups as study subjects,the treatment group(n=39) were treated with revised Pinellia Combination,5-Fu,Adriamycin and Mitomycin; while the control(n=44) with 5-Fu,Adriamycin and Mitomycin. [Result] The treatment group had much less reactions of nausea,vomiting and anorexia than control(P0.05).

Polyphenols
Foods: Berries, Tea, Beer, Grapes/Wine, Olive Oil, Chocolate/Cocoa, Coffee, Walnuts, Peanuts, Borojo, Pomegranates, Popcorn, Yerba Mate and other fruits & vegetables.
en.wikipedia.org…
en.wikipedia.org…

Polyphenols are a group of important antioxidants. Citations proving they kill cancer would be endless so are therefore pointless, but several of the entires in here are polyphenols.

Polysaccharides
Source: “Turkey Tail” Mushroom (Trametes versicolor), Ginko Biloba plant & seeds, Marine algae Capsosiphon Fulvescens and the “loach” fish Misgurnus Anguillicaudatus.
en.wikipedia.org…

Protein-bound polysaccharide K induced apoptosis of the human Burkitt lymphoma cell line, Namalwa
www.ncbi.nlm.nih.gov…

Protein-bound polysaccharide K (PSK), which is derived from mushrooms belonging to the Basidiomycetes genus, has been clinically used as a biological response modifier (BRM) for the treatment of epithelial cancer patients in Japan and other Asian countries. There are a large number of studies on the biological activities of PSK as regards the activation of immunocompetent cells and the potential cytotoxic effects on epithelial cancer cells. …These results provide initial evidence of the direct cytotoxic activity of PSK in a hematological malignant cell line, thus encouraging further molecular-level study of PSK-mediated apoptosis in malignant hematological cells.

Gene expression in response to anti-tumour intervention by polysaccharide-K (PSK) in colorectal carcinoma cells
www.ncbi.nlm.nih.gov…

Distant metastasis is one of the major problems in treatment for advanced colorectal cancer. Polysaccharide-K (PSK), or Krestin, a mushroom ingredient, has been used as a chemoimmunotherapeutic agent for the treatment of cancers in Asia for over 30 years. Some studies have reported that PSK prevent distant metastases and improve survival rates by 10-20% in colorectal cancer.

A polysaccharide of the marine alga Capsosiphon fulvescens induces apoptosis in AGS gastric cancer cells
www.ncbi.nlm.nih.gov…

Because seaweed extracts have recently been found to have antioxidant and anti-tumor activities, we analyzed a hot-water-soluble polysaccharide (PS) of the marine alga Capsosiphon fulvescens for its potential as a functional foodstuff by determining its effects on cell growth and DNA synthesis. MTS assays showed that the C. fulvescens PS (Cf-PS) significantly inhibited the proliferation of cultured human cancer cells in a dose-dependent manner. Cf-PS-treated AGS cells exhibited a marked increase in caspase-3 activation and a decrease in Bcl-2 expression. In addition, phosphorylation of insulin-like growth factor-I receptor (IGF-IR) was decreased in Cf-PS-treated AGS cells as compared to non-treated control cells, which is consistent with PI3-kinase (PI3K)/Akt activation. Cf-PS also decreased IGF-I-stimulated recruitment of p85 to IGF-IR and IRS-1. These results indicate that Cf-PS inhibits cell proliferation and induces apoptosis by inhibiting IGF-IR signaling and the PI3K/Akt pathway.

Therapeutic mechanism of ginkgo biloba exocarp polysaccharides on gastric cancer
www.ncbi.nlm.nih.gov…

Compared with the statement before treatment, GBEP capsules could reduce the area of tumors, and the effective rate was 73.4%. Ultrastructural changes of the cells indicated that GBEP could induce apoptosis and differentiation in tumor cells of patients with gastric cancer. GBEP could inhibit the growth of human gastric cancer SGC-7901 cells following 24-72 h treatment in vitro at 10-320 mg/L, which was dose- and time-dependent. GBEP was able to elevate the apoptosis rate and expression of c-fos gene, but reduce the expression of c-myc and bcl-2 genes also in a dose-dependent manner.

Apoptosis of hepatoma cells SMMC-7721 induced by Ginkgo biloba seed polysaccharide
www.ncbi.nlm.nih.gov…

GBSP product obtained was of high purity with the average molecular weight of 1.86 X 10(5). Quantitative analysis of SMMC-7721 cells in vitro with FCM showed that the percentages of G(2)-M cells without and with GBSP treatment were 17.01+/-1.28 % and 11.77+/-1.50% (P<0.05), the debris ratio of the cells were 0.46+/-0.12 % and 0.06+/-0.06 % (P<0.01), and the apoptosis ratio of cells was 3.84+/-0.55 % and 9.13+/-1.48 % (P<0.01) respectively. Following GBSP treatment, microvilli of SMMC-7721 cells appeared thinner and the number of spherical cells increased markedly. Most significantly, the apoptosis bodies were formed on and around the spherical cells treated with GBSP.

Mechanism of apoptosis induced by a polysaccharide, from the loach Misgurnus anguillicaudatus (MAP) in human hepatocellular carcinoma cells
www.ncbi.nlm.nih.gov…

The biological activities of the polysaccharide have attracted more and more attention in the biochemical and medical areas due to their anti-cancer effects. To estimate the anti-tumor mechanism of MAP, a novel polysaccharide from the loach, Misgurnus anguillicaudatus, the apoptosis effects of the polysaccharide on the human hepatocellular carcinoma cells (SMMC-7721 cells) were studied. The present studies showed that MAP could induce cell apoptosis which was closely accompanied with an increase of intracellular-free calcium concentration ([Ca2+]i), the enhancement of reactive oxygen species (ROS) level, dissipation of mitochondria membrane potential (MMP), up-regulation of p53 mRNA, increase expression of Bax mRNA, and decrease expression of Bcl-2 mRNA. These results suggested that cell apoptosis induced by MAP mainly was mediated by mitochondrial pathways, not involved death receptors (DRs) pathways. The mechanism possibly is that MAP acts on mitochondria and boosts ROS, ROS mediates a release of Ca2+ from the intracellular Ca2+ pool, increasing [Ca2+]i targets the cells a start-up of the apoptosis program.

Protodioscin
Food: Fenugreek (aka Methi) Seeds / Powder.
Sources: Indian markets.
en.wikipedia.org…
These seeds are very hard, and I suggest you buy powder instead. I planted some out of my spice cabinet that were probably 10 years old and they all sprouted.

Protodioscin isolated from fenugreek induces cell death and morphological change indicative of apoptosis in leukemic cell line H-60, but not in gastric cancer cell line KATO III.
www.ncbi.nlm.nih.gov…

Protodioscin (PD) was purified from fenugreek (Trigonella foenumgraecum L.) and identified by Mass, and 1H- and 13C-NMR. The effects of PD on cell viability in human leukemia HL-60 and human stomach cancer KATO III cells were investigated. PD displayed strong growth inhibitory effect against HL-60 cells, but weak growth inhibitory effect on KATO III cells.

Methyl protodioscin induces G2/M cell cycle arrest and apoptosis in HepG2 liver cancer cells
www.ncbi.nlm.nih.gov…

Methyl protodioscin (NSC-698790) is one of the main bioactive components in the traditional Chinese medicine Dioscorea collettii var. hypoglauca (Dioscoreaceae). In this study, we investigated the anti-proliferative effect of methyl protodioscin on the HepG2 cells and the mechanism of the induced cytotoxicity. Treatment of methyl protodioscin resulted in G2/M arrest and apoptosis in HepG2 cells. These effects were attributed to down-regulation of Cyclin B1 and the signaling pathways leading to up-regulation of Bax and down-regulation of BCL2, suggesting that methyl protodioscin may be a novel anti-mitotic agent.

Methyl protodioscin induces G2/M arrest and apoptosis in K562 cells
www.ncbi.nlm.nih.gov…

Methyl protodioscin is a furostanol bisglycoside with antitumor properties. The present study investigated its effects on human chronic myelogenous leukemia K562 cells. Cell cycle analysis showed that methyl protodioscin caused distinct G2/M arrest, with the appearance of polyploidy population.

Punicalagin
Food: Pomegranate.
en.wikipedia.org…

In vitro antiproliferative, apoptotic and antioxidant activities of punicalagin, ellagic acid and a total pomegranate tannin extract are enhanced in combination with other polyphenols as found in pomegranate juice
www.plefa.com…(05)00019-7/abstract

The potent antioxidant and anti-atherosclerotic activities of PJ are attributed to its polyphenols including punicalagin, the major fruit ellagitannin, and ellagic acid (EA). Punicalagin is the major antioxidant polyphenol ingredient in PJ. Punicalagin, EA, a standardized total pomegranate tannin (TPT) extract and PJ were evaluated for in vitro antiproliferative, apoptotic and antioxidant activities. Punicalagin, EA and TPT were evaluated for antiproliferative activity at 12.5–100 μg/ml on human oral (KB, CAL27), colon (HT-29, HCT116, SW480, SW620) and prostate (RWPE-1, 22Rv1) tumor cells. …Pomegranate juice showed greatest antiproliferative activity against all cell lines by inhibiting proliferation from 30% to 100%. At 100 μg/ml, PJ, EA, punicalagin and TPT induced apoptosis in HT-29 colon cells.

Pomegranate Juice, Total Pomegranate Ellagitannins, and Punicalagin Suppress Inflammatory Cell Signaling in Colon Cancer Cells
pubs.acs.org…

In previous studies, pomegranate juice (PJ) and its ellagitannins inhibited proliferation and induced apoptosis in HT-29 colon cancer cells. The present study examined the effects of PJ on inflammatory cell signaling proteins in the HT-29 human colon cancer cell line. At a concentration of 50 mg/L PJ significantly suppressed TNFα-induced COX-2 protein expression by 79% (SE = 0.042), total pomegranate tannin extract (TPT) 55% (SE = 0.049), and punicalagin 48% (SE = 0.022). Additionally, PJ reduced phosphorylation of the p65 subunit and binding to the NFκB response element 6.4-fold. TPT suppressed NFκB binding 10-fold, punicalagin 3.6-fold, whereas ellagic acid (EA) (another pomegranate polyphenol) was ineffective. PJ also abolished TNFα-induced AKT activation, needed for NFκB activity. Therefore, the polyphenolic phytochemicals in the pomegranate can play an important role in the modulation of inflammatory cell signaling in colon cancer cells.

Pomegranate fruit juice for chemoprevention and chemotherapy of prostate cancer
www.pnas.org…

We recently showed that pomegranate fruit extract (PFE) possesses remarkable antitumor-promoting effects in mouse skin. In this study, employing human prostate cancer cells, we evaluated the antiproliferative and proapoptotic properties of PFE. …Oral administration of PFE (0.1% and 0.2%, wt/vol) to athymic nude mice implanted with androgen-sensitive CWR22Rν1 cells resulted in a significant inhibition in tumor growth concomitant with a significant decrease in serum prostate-specific antigen levels. We suggest that pomegranate juice may have cancer-chemopreventive as well as cancer-chemotherapeutic effects against prostate cancer in humans.

Quercetin
Foods: Black & Green Tea, Onions, Caper, Lovage, Apples, Red Grapes, Citrus, Tomato, Broccoli, Cherry, Raspberry, Cranberry, Bilberry and many others.
en.wikipedia.org…
Quercetin is a flavonol, plant-derived flavonoid, used as a nutritional supplement. Laboratory studies show it may have anti-inflammatory and antioxidant properties,and it is being investigated for a wide range of potential health benefits.

Induction of cell cycle arrest and apoptosis in human breast cancer cells by quercetin
www.ncbi.nlm.nih.gov…

The present data, therefore, demonstrate that a flavonoid quercetin induces growth inhibition in the human breast carcinoma cell line MCF-7 through at least two different mechanisms; by inhibiting cell cycle progression through transient M phase accumulation and subsequent G2 arrest, and by inducing apoptosis.

The role of activated MEK-ERK pathway in quercetin-induced growth inhibition and apoptosis in A549 lung cancer cells
carcin.oxfordjournals.org…

Inhibition of caspase activation completely blocked quercetin-induced apoptosis. Expression of constitutively activated MEK1 in A549 cells led to activation of caspase-3 and apoptosis. The results suggest that in addition to inactivation of Akt-1 and alteration in the expression of the Bcl-2 family of proteins, activation of MEK-ERK is required for quercetin-induced apoptosis in A549 lung carcinoma cells.

Ellagic acid and quercetin interact synergistically with resveratrol in the induction of apoptosis and cause transient cell cycle arrest in human leukemia cells
www.cancerletters.info…(04)00430-6/abstract

Results showed a more than additive interaction for the combination of ellagic acid with resveratrol and furthermore, significant alterations in cell cycle kinetics induced by single compounds and combinations were observed. An isobolographic analysis was performed to assess the apparent synergistic interaction for the combinations of ellagic acid with resveratrol and quercetin with resveratrol in the induction of caspase 3 activity, confirming a synergistic interaction with a combination index of 0.64 for the combination of ellagic acid and resveratrol and 0.68 for quercetin and resveratrol. Results indicate that the anticarcinogenic potential of foods containing polyphenols may not be based on the effects of individual compounds, but may involve a synergistic enhancement of the anticancer effects.

Quercetin decreases the expression of ErbB2 and ErbB3 proteins in HT-29 human colon cancer cells
www.journals.elsevierhealth.com…

Quercetin inhibited HT-29 cell growth in a dose-dependent manner, whereas rutin had no effect on the cell growth. DNA that was isolated from cells treated with 50 μmol/L of quercetin exhibited an oliogonucleosomal laddering pattern characteristic of apoptotic cell death. Western blot analysis of cell lysates revealed that Bcl-2 levels decreased dose-dependently in cells treated with quercetin, but Bax remained unchanged.

Food-derived polyphenols inhibit pancreatic cancer growth through mitochondrial cytochrome C release and apoptosis
onlinelibrary.wiley.com…

We measured effects of quercetin on pancreatic cancer in a nude mouse model. We also investigated the effects of quercetin, rutin, trans-resveratrol and genistein on apoptosis and underlying signaling in pancreatic carcinoma cells in vitro. …The inhibition of mitochondrial permeability transition prevented cytochrome c release, caspase-3 activation and apoptosis caused by polyphenols. Nuclear factor-κB activity was inhibited by quercetin and trans-resveratrol, but not genistein, indicating that this transcription factor is not the only mediator of the polyphenols’ effects on apoptosis. The results suggest that food-derived polyphenols inhibit pancreatic cancer growth and prevent metastasis by inducing mitochondrial dysfunction, resulting in cytochrome c release, caspase activation and apoptosis.

Raspberries
en.wikipedia.org…

Black Raspberries Show Multiple Defenses In Thwarting Cancer (2001)
researchnews.osu.edu…

He chose black raspberries for this study because previous studies had shown that ellagic acid inhibited carcinogen-induced esophageal and colon cancer in animals. He and his colleagues then tested a series of fruits for their ellagic acid content, finding that berries contained the highest amount. “We then decided to take a food-based approach to cancer prevention and began testing the berries’ ability to inhibit chemically-induced esophageal and colon cancer,” Stoner said. “Sure enough, we found that freeze-dried berries were highly protective in the esophagus and colon. But we also found that they were ineffective in protecting against lung cancer. “The protective compounds in berries may not be absorbed into the blood stream and delivered to the lungs in high enough amounts to be protective. We do believe that they protect the esophagus and colon because they are absorbed by these organs as the food moves through the digestive tract.”

Black Raspberries Slow Cancer By Altering Hundreds Of Genes (2008)
www.sciencedaily.com…

The carcinogen affected the activity of some 2,200 genes in the animals’ esophagus in only one week, but 460 of those genes were restored to normal activity in animals that consumed freeze-dried black raspberry powder as part of their diet during the exposure. These findings, published in recent issue of the journal Cancer Research, also helped identify 53 genes that may play a fundamental role in early cancer development and may therefore be important targets for chemoprevention agents.

Resveratrol
Found in red grapes and blueberries.
en.wikipedia.org…
www.youtube.com…

Apoptosis Induced by Capsaicin and Resveratrol in Colon Carcinoma Cells Requires Nitric Oxide Production and Caspase Activation
ar.iiarjournals.org…

We examined the role of nitric oxide (NO•) and influence of p53 status during apoptosis induced by these agents in two isogenic HCT116 human colon carcinomas, wild-type p53 (p53-WT) and complete knockout of p53 (p53-null) cells. Capsaicin and resveratrol, alone or in combination, inhibited cell growth and promoted apoptosis by the elevation of NO•; combined treatment in p53-WT cells was most effective. Increased NO• production after treatment uniformly stimulated p53 and Bax expression through Mdm2 down-regulation in p53-WT cells, whereas all were unaffected in p53-null cells. Both cell types underwent a reduction in the levels of anti-apoptotic Bcl-2 protein, cytochrome c loss from mitochondria and activation of caspase 9 together with caspase 3, independently of p53 status.

Resveratrol Induces Apoptosis in Thyroid Cancer Cell Lines via a MAPK- and p53-Dependent Mechanism

jcem.endojournals.org…

Studies of nucleosome levels estimated by ELISA and of DNA fragmentation showed that RV induced apoptosis in both papillary and follicular thyroid cancer cell lines; these effects were inhibited by pifithrin-{alpha} and by p53 antisense oligonucleotide transfection.

Resveratrol induces growth inhibition and apoptosis in metastatic breast cancer cells via de novo ceramide signaling
www.fasebj.org…

In this study we show that resveratrol has a potent antiproliferative and proapoptotic effect on MDA-MB-231, a highly invasive and metastatic cell line from human breast cancer known to be resistant to several anticancer drugs.

Resveratrol induces cell death in colon cancer cells by a novel pathway involving lysosomal cathepsin D
carcin.oxfordjournals.org…

In human colorectal cancer cells, the polyphenol resveratrol (RV) activated the caspase-dependent intrinsic pathway of apoptosis. This effect was not mediated via estrogen receptors. Pepstatin A, an inhibitor of lysosomal cathepsin D (CD), not (2S,3S)-trans-epoxysuccinyl-L-leucylamido-3-methylbutane ethyl ester, an inhibitor of cathepsins B and L, prevented RV cytotoxicity. Similar protection was attained by small interference RNA-mediated knockdown of CD protein expression.

Resveratrol induces apoptosis in human esophageal carcinoma cells
carcin.oxfordjournals.org…

Resveratrol inhibited the growth of esophageal cancer cell line EC-9706 in a dose-and time-dependent manner. Resveratrol induced EC-9706 cells to undergo apoptosis with typically apoptotic characteristics, including morphological changes of chromatin condensation, chromatin crescent formation, nucleus fragmentation and apoptotic body formation.

Resveratrol-induced cell death in leukaemia cells
chesterrep.openrepository.com…

Resveratrol, a natural phytoalexin found in grapes and red wine, displays anti-cancer activities through a variety of mechanisms that include the induction of cancer cell apoptosis. Although high concentrations may be needed for the efficacy of resveratrol alone, the compound shows promise as a potent sensitizer of the apoptotic effect of other anti-cancer agents, including death ligand TRAIL. Intracellular heat shock proteins (Hsps) are frequently up-regulated in cancer cells, conferring resistance to apoptosis. Modulation of these proteins may overcome the resistance and increase efficacy of anticancer therapies. In this study, resveratrol caused significant dose-dependent apoptosis or necrosis in the lymphoid and myeloid leukaemia cell lines Jurkat and U937 at 50µM and above.

Resveratrol interferes with AKT activity and triggers apoptosis in human uterine cancer cells
www.ncbi.nlm.nih.gov…

High-dose of resveratrol triggered apoptosis in five out of six uterine cancer cell lines, as judged from Hoechst nuclear staining and effector caspase cleavage. In accordance, uterine cancer cell proliferation was decreased. Resveratrol also reduced cellular levels of the phosphorylated/active form of anti-apoptotic kinase AKT.

Retinoic Acid & Retinamide
en.wikipedia.org…
Retinoic acid is the oxidized form of Vitamin A, with only partial vitamin A function. Retinamide is a synthetic retinoid useful when retinoic acid treatment is unresponsive.

Retinoic acid receptor beta mediates the growth-inhibitory effect of retinoic acid by promoting apoptosis in human breast cancer cells
mcb.asm.org…

Retinoids are known to inhibit the growth of hormone-dependent but not that of hormone-independent breast cancer cells. We investigated the involvement of retinoic acid (RA) receptors (RARs) in the differential growth-inhibitory effects of retinoids and the underlying mechanism. Our data demonstrate that induction of RAR beta by RA correlates with the growth-inhibitory effect of retinoids. The hormone-independent cells acquired RA sensitivity when the RAR beta expression vector was introduced and expressed in the cells.

N-(4-hydroxyphenyl)retinamide induces apoptosis of malignant hemopoietic cell lines including those unresponsive to retinoic acid
www.ncbi.nlm.nih.gov…

In conclusion, our study demonstrates that HPR suppresses malignant cell growth and induces apoptosis at pharmacologically relevant doses. The differential responsiveness by a number of cell lines, especially HL-60R and NB306, to HPR and RA indicates that these compounds may act through different receptors. The clinical use of HPR, particularly in retinoic acid-unresponsive acute promyelocytic leukemia patients, is suggested.

Differential induction of apoptosis by all-trans-retinoic acid and N-(4-hydroxyphenyl)retinamide in human head and neck squamous cell carcinoma cell lines
clincancerres.aacrjournals.org…

Retinoids have been shown to act as cytostatic agents against a variety of tumor cell types, including squamous carcinoma cells. Recently it was reported that certain retinoids can induce apoptosis as well. Because we are investigating the potential of retinoids in chemoprevention and therapy for head and neck premalignant and malignant lesions, we compared the effects of all-trans-retinoic acid (ATRA) and N-(4-hydroxyphenyl)retinamide (4HPR) on seven human head and neck squamous cell carcinoma cell lines (17A, 17B, 22A, 22B, 38, SqCC/Y1, and 1483). Six of the seven cell lines showed dramatic morphological changes after treatment with 10 micrometer 4HPR, whereas no such changes were induced by 10 micrometer ATRA. …These results demonstrate that 4HPR causes apoptosis in several head and neck squamous cell carcinoma cell lines and that it is more potent in this effect than ATRA.

Rhein
Food: Rhubarb
en.wikipedia.org…

Rhein-induced apoptosis in A-549 Human Lung Cancer cells
ar.iiarjournals.org…

The Ca2+ chelator BAPTA was added to the cells before rhein treatment, thus blocking the Ca2+ production and inhibiting rhein-induced apoptosis in A-549 cells. Our data demonstrate that rhein induces apoptosis in A-549 cells via a Ca2+-dependent mitochondrial pathway.

Rhein lysinate suppresses the growth of tumor cells and increases the anti-tumor activity of Taxol in mice
www.ncbi.nlm.nih.gov…

In previous studies, rhein, one of the major bioactive constituents in the rhizome of rhubarb, inhibited the proliferation of various human cancer cells. However, because of its water insolubility, the anti-tumor efficacy of rhein was limited in vivo. In this study, we observed the anti-tumor activity of rhein lysinate (the salt of rhein and lysine easily dissolves in water) in vivo and investigated its mechanism. …It inhibited tumor growth by both intragastric and intraperitoneal administrations and improved the therapeutic effect of Taxol in H22 hepatocellular carcinoma mice. In conclusion, rhein lysinate offers an anti-tumor activity in vivo and is hopeful to be a chemotherapeutic drug.

Rhein induces apoptosis in HL-60 cells
www.ncbi.nlm.nih.gov…

Rhein is an anthraquinone compound enriched in the rhizome of rhubarb, a traditional Chinese medicine herb showing anti-tumor promotion function. In this study, we first reported that rhein could induce apoptosis in human promyelocytic leukemia cells (HL-60), characterized by caspase activation, poly(ADP)ribose polymerase (PARP) cleavage, and DNA fragmentation. …Our data demonstrate that rhein induces apoptosis in HL-60 cells via a ROS-independent mitochondrial death pathway.

Rhein Inhibits the Growth and Induces the Apoptosis of Hep G2 Cells
www.ncbi.nlm.nih.gov…

The effects of rhein on the human hepatoblastoma G2 (Hep G2) cell line were investigated in this study. The results showed that rhein not only inhibited Hep G2 cell growth but also induced apoptosis and blocked cell cycle progression in the G1 phase.

Rhein Induced Apoptosis…in SCC-4 Human Tongue Squamous Cancer Cells
iv.iiarjournals.org…

In this study, it was observed that rhein induced S-phase arrest through the inhibition of p53, cyclin A and E and it induced apoptosis through the endoplasmic reticulum stress by the production of reactive oxygen species (ROS) and Ca2+ release, mitochondrial dysfunction, and caspase-8, -9 and -3 activation in human tongue cancer cell line (SCC-4).

Rosemary
en.wikipedia.org…

Rosemary may cut cancer-causing agents (in meats)
www.upi.com…

The addition of rosemary extract to ground beef reduces cancer-causing agents that can form upon cooking, U.S. researchers said. Heterocyclic amines are mutagenic compounds that form when meat and fish are cooked at high temperatures — especially meats that are grilled, pan-fried, broiled or barbecued — and are categorized as human carcinogens, the researchers said.

Selenium
Foods: Brazil Nuts, Other Nuts, Fish, Wheat Flour, Shell Fish, Chicken, Turkey and many others.
en.wikipedia.org…

Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin
www.ncbi.nlm.nih.gov…

Selenium treatment did not protect against development of basal or squamous cell carcinomas of the skin. However, results from secondary end-point analyses support the hypothesis that supplemental selenium may reduce the incidence of, and mortality from, carcinomas of several sites. These effects of selenium require confirmation in an independent trial of appropriate design before new public health recommendations regarding selenium supplementation can be made.

Redox-mediated Effects of Selenium on Apoptosis and Cell Cycle in the LNCaP Human Prostate Cancer
cancerres.aacrjournals.org…

The effects of selenium exposure were studied in LNCaP human prostate cancer cells, and this same cell line adapted to selenium over 6 months to compare acute versus chronic effects of sodium selenite, the latter most closely resembling human clinical trials on the effects of selenium in cancer prevention and therapy. Our results demonstrated that oxidative stress was induced by sodium selenite at high concentrations in both acute and chronic treatments, but outcomes were different. …Our results in selenite-adapted cells suggest that selenium may exert its effects in human prostate cancer cells by altering intracellular redox state, which subsequently results in cell cycle block.

Selenium-induced inhibition of angiogenesis in mammary cancer at chemopreventive levels of intake
www.ncbi.nlm.nih.gov…

The trace element nutrient selenium (Se) has been shown to possess cancer-preventive activity in both animal models and humans, but the mechanisms by which this occurs remain to be elucidated. Because angiogenesis is obligatory for the genesis and growth of solid cancers, we investigated, in the study presented here, the hypothesis that Se may exert its cancer-preventive activity, at least in part, by inhibiting cancer-associated angiogenesis. The effects of chemopreventive levels of Se on the intra-tumoral microvessel density and the expression of vascular endothelial growth factor in 1-methyl-1-nitrosourea-induced rat mammary carcinomas and on the proliferation and survival and matrix metalloproteinase activity of human umbilical vein endothelial cells in vitro were examined.

Skullcap
Source: Chinese herb Scutellaria Baicalensis.
en.wikipedia.org…
This herb has mutliple compounds that have had results together and apart. Make sure it’s the exact species.

Wogonin and fisetin induce apoptosis in human promyeloleukemic cells
www.ncbi.nlm.nih.gov…

Seven structurally related flavonoids including luteolin, nobiletin, wogonin, baicalein, apigenin, myricetin and fisetin were used to study their biological activities on the human leukemia cell line, HL-60. On MTT assay, wogonin, baicalein, apigenin, myricetin and fisetin showed obvious cytotoxic effects on HL-60 cells, with wogonin and fisetin being the most-potent apoptotic inducers among them.

Antitumor effects of Scutellariae radix and its components baicalein, baicalin, and wogonin on bladder cancer cell lines
www.goldjournal.net…(00)00467-2/abstract

All the drugs inhibited cell proliferation in a dose-dependent manner, but baicalin exhibited the greatest antiproliferative activity. The concentration of baicalin necessary to obtain 50% inhibition was 3.4 μg/mL for KU-1, 4.4 μg/mL for EJ-1, and 0.93 μg/mL for MBT-2. For KU-1 and MBT-2, the percentage of cell survival significantly decreased (P <0.05) at a baicalin concentration of 1 μg/mL. In an in vivo experiment, antitumor effects of Scutellariae radix on C3H/HeN mice implanted with MBT-2 were investigated. All the control mice showed a progressive increase in tumor volume, reaching 2.81 ± 0.18 cm3 on day 20 and 5.36 ± 0.44 cm3 on day 25. However, when Scutellariae radix was orally administered at a dose of 10 mg per mouse one time daily for 10 days from day 11 to day 20, the tumor volume was 1.99 ± 0.19 cm3 on day 20 and 3.86 ± 0.26 cm3 on day 25, a significant inhibition of tumor growth (P <0.05).

Induction of apoptosis in prostate cancer cell lines by a flavonoid, baicalin
www.cancerletters.info…(00)00591-7/abstract

The flavonoid baicalin (baicalein 7-D-β-glucuronate), isolated from the dried root of Scutellaria baicalensis Georgi (Huang Qin), is widely used in the traditional Chinese herbal medicine for its anti-inflammatory, anti-pyretic and anti-hypersensitivity effects. In the present study, we investigated the in vitro effects of baicalin on the growth, viability, and induction of apoptosis in several human prostate cancer cell lines, including DU145, PC-3, LNCaP and CA-HPV-10. The cell viability after treating with baicalin for 2–4 days was quantified by a colorimetric 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. The results showed that baicalin could inhibit the proliferation of prostate cancer cells.

Effects of wogonin on inducing apoptosis of human ovarian cancer A2780 cells
www.ncbi.nlm.nih.gov…

Wogonin can inhibit proliferation and induce apoptosis of A2780 cells within a certain concentration range(50-250 microg/ml). Anticancer effects of wogonin were associated with the induction of apoptosis and partly with the suppression of telomerase activity.

Reversal of inflammation-associated dihydrodiol dehydrogenases (AKR1C1 and AKR1C2) overexpression and drug resistance in nonsmall cell lung cancer cells by wogonin and chrysin
onlinelibrary.wiley.com…

We also showed that IL-6-induced AKR1C1/1C2 expression and drug resistance were inhibited by wogonin and chrysin, which are major flavonoids in Scutellaria baicalensis, a widely used traditional Chinese and Japanese medicine. In conclusion, this study demonstrated novel links of pro-inflammatory signals, AKR1C1/1C2 expression and drug resistance in NSCLC.

Anticancer effects of wogonin in both estrogen receptor-positive and -negative human breast cancer cell lines in vitro and in nude mice xenografts
onlinelibrary.wiley.com…

Wogonin feeding to mice showed inhibition of tumor growth of T47D and MDA-MB-231 xenografts by up to 88% without any toxicity after 4 weeks of treatment. As wogonin was effective both in vitro and in vivo, our novel findings open the possibility of wogonin as an effective therapeutic and/or chemopreventive agent against both ER-positive and -negative breast cancers, particularly against the more aggressive and hormonal therapy-resistant ER-negative types.

Sophora
Source: Genus of shrubs native to every continent except Africa & North America.
en.wikipedia.org…

Ethanolic extracts of Sophora moorcroftiana seeds induce apoptosis of human stomach cancer cell line SGC-7901 in vitro

academicjournals.org…

The seeds of Sophora moorcroftiana are used in Chinese traditional medicine for the treatment of verminosis, infectious diseases, and anti-inflammation. To investigate the antitumor and induction of apoptosis activity of Sophora moorcroftiana seeds, the ethanolic extracts from the seeds was prepared and added into the culture of human stomach cancer cell line SGC-7901 in vitro. The proliferation and apoptosis of cells treated with the ethanolic extracts were assessed by tetrazolium salt reduction (MTT) assay, fluorescence microscopy, transmission electron microscopy, flow cytometry and agarose gel electrophoresis of DNA fragmentation. The results showed that the growth of SGC-7901 cells was strongly inhibited by the ethanolic extracts at the concentration ranging between 0.31-5.00 mg/ml, and the apoptosis of treated cells was induced at the concentration of 1.25, 2.50, and 5.00 mg/ml in vitro. This suggested that the ethanolic extracts from S. moorcroftiana seeds contain potent antitumor fraction(s) on human stomach cancer SGC-7901 cells.

A mannose-binding lectin from Sophora flavescens induces apoptosis in HeLa cells
www.ncbi.nlm.nih.gov…

The objective of this study was to investigate the anti-tumor activity of a lectin from Sophora flavescens and explore its potential apoptotic induction mechanism. …In conclusion, all experimental results demonstrated that this lectin seems to be a potent anti-tumor agent for its cytotoxicity and apoptosis effects on HeLa cells. Also, bioinformatics analyses showed that this lectin is speculated to bind a certain mannose-containing receptor on cancer cell surface thereby initiating downstream caspase cascade.

Sophoranone, extracted from a traditional Chinese medicine Shan Dou Gen, induces apoptosis in human leukemia U937 cells
onlinelibrary.wiley.com…

Screening of various natural products in a search for novel inducers of apoptosis in human leukemia cells led us to identify the strong apoptosis-inducing activity in a fraction extracted with methanol from the roots of Sophora subprostrata Chun et T. Chen. We purified the compound that induced apoptosis in human leukemia cells and identified it as sophoranone. Sophoranone inhibited cell growth and induced apoptosis in various lines of cells from human solid tumors, with 50% inhibition of growth of human stomach cancer MKN7 cells at 1.2 ± 0.3 μM. The growth-inhibitory and apoptosis-inducing activities of sophoranone for leukemia U937 cells were very much stronger than those of other flavonoids, such as daidzein, genistein and quercetin.

Matrine induced gastric cancer MKN45 cells apoptosis via increasing pro-apoptotic molecules of Bcl-2 family
www.ncbi.nlm.nih.gov…

Matrine, one of the main active components from the dry roots of Sophora flavescence, was known to induce apoptosis in a variety of tumor cells in vitro. However, the molecular mechanism of cell apoptosis induced by Matrine remains elusive. Here, we investigated the apoptosis in Matrine-treated human gastric cancer MKN45 cells. The results showed that Matrine could inhibit cell proliferation and induce apoptosis in a dose-dependent manner. Further immunoblots revealed that in Matrine-treated cells, caspase-3, -7 were activated and the pro-apoptotic molecules Bok, Bak, Bax, Puma, and Bim were also up-regulated. Our results suggested that Matrine induced gastric cancer MKN45 cells apoptosis via increasing pro-apoptotic molecules of Bcl-2 family.

Leachianone A as a potential anti-cancer drug by induction of apoptosis in human hepatoma HepG2 cells
www.ncbi.nlm.nih.gov…

The Chinese herbal medicine Radix Sophorae is widely applied as an anti-carcinogenic/ anti-metastatic agent against liver cancer. In this study, Leachianone A, isolated from Radix Sophorae, possessed a profound cytotoxic activity against human hepatoma cell line HepG2 in vitro, with an IC(50) value of 3.4microg/ml post-48-h treatment. Its action mechanism via induction of apoptosis involved both extrinsic and intrinsic pathways. Its anti-tumor effect was further demonstrated in vivo by 17-54% reduction of tumor size in HepG2-bearing nude mice, in which no toxicity to the heart and liver tissues was observed. In conclusion, this is the first report describing the isolation of Leachianone A from Radix Sophorae and the molecular mechanism of its anti-proliferative effect on HepG2 cells.

Tumor-specificity and Apoptosis-inducing Activity of Stilbenes and Flavonoids
ar.iiarjournals.org…

A total of eleven stilbenes [1-6] and flavonoids [7-11] were investigated for their tumor-specific cytotoxicity and apoptosis-inducing activity, using four human tumor cell lines (squamous cell carcinoma HSC-2, HSC-3, submandibular gland carcinoma HSG and promyelocytic leukemia HL-60) and three normal human oral cells (gingival fibroblast HGF, pulp cell HPC, periodontal ligament fibroblast HPLF). All of the compounds, especially sophorastilbene A [1], (+)-α-viniferin [2], piceatannol [5], quercetin [9] and isoliquiritigenin [10], showed higher cytotoxicity against the tumor cell lines than normal cells, yielding tumor-specific indices of 3.6, 4.7, >3.5, >3.3 and 4.0, respectively. Among the seven cell lines, HSC-2 and HL-60 cells were the most sensitive to the cytotoxic action of these compounds. Sophorastilbene A [1], piceatannol [5], quercetin [9] and isoliquiritigenin [10] induced internucleosomal DNA fragmentation and activation of caspases -3, -8 and -9 dose-dependently in HL-60 cells. (+)-α-Viniferin [2] showed similar activity, but only at higher concentrations. All the compounds failed to induce DNA fragmentation and activated caspases to much lesser extents in HSC-2 cells. Western blot analysis showed that sophorastilbene A [1], piceatannol [5] and quercetin [9] did not induce any consistent changes in the expression of pro-apoptotic proteins (Bax, Bad) and anti-apoptotic protein (Bcl-2) in HL-60 and HSC-2 cells. An undetectable expression of Bcl-2 protein in control and drug-treated HSC-2 cells may explain the relatively higher sensitivity of this cell line to stilbenes and flavonoids.

Soy: Good or Bad?
There’s conflicting data on the effects of Soy on “estrogen positive” cell lines. Before taking on a Soy regimen, you’ll need to know whether or not your cancer is estogen positive or negative, do more research, and consult your physician.

From there Soy has multiple compounds shown individually to fight cancer. It includes compounds such as Daidzein & Genistein, while Soy fermented with Bacillus Subtilis is the highest known natural source of Vitamin K2.

Spikemoss
Plant: Selaginella Tamariscina
en.wikipedia.org…

Selaginella tamariscina induces apoptosis via a caspase-3-mediated mechanism in human promyelocytic leukemia cells
www.ncbi.nlm.nih.gov…

ST-induced apoptosis is accompanied by the activation of caspase-3 and the specific proteolytic cleavage of PARP. Concomitantly, ST treatments led to an increase in the proapoptotic Bax levels, while Bcl-2 expression was decreased. Moreover, this effect was attenuated by SOD and catalase. These results suggest that oxidative stress may be involved in the cytotoxicity of ST, and that ST-induced apoptosis of HL-60 cells is primarily mediated by the caspase activation pathway.

Effects of Selaginella tamariscina on in vitro tumor cell growth, p53 expression, G1 arrest and in vivo gastric cell proliferation
www.ncbi.nlm.nih.gov…

The 1% Selaginella tamariscina feeding caused a significant reduction (P < 0.05) in the proliferating cell nuclear antigen-(PCNA) labeling index of the glandular stomach epithelium as compared with the MNNG-alone group value although 5% Selaginella tamariscina feeding was only associated with a tendency for decrease. These results suggest that Selaginella tamariscina could be a candidate chemopreventive agent against gastric cancer.

Radioprotective effects of the water-soluble part of Selaginella Tamariscina on thymus and spleen in irradiated mice
en.cnki.com.cn…

Conclusion The water-soluble part of Selaginella tamariscina can protect mice from rays by inhibiting of apoptosis,adjusting of cell cycle progression of thymus and spleen cells in irradiated mice.

Stonebreaker
Herb: Phyllanthus Niruri (Chinese Medicinal Herb)
en.wikipedia.org…
Phyllanthus urinaria triggers the apoptosis and Bcl-2 down-regulation in Lewis lung carcinoma cells
www.ncbi.nlm.nih.gov…

Phyllanthus urinaria (P. urinaria), a widely used herb medicine, was tested for the anticancer effect in its water extract for the first time. The water extract of P. urinaria significantly decreased the number of Lewis lung carcinoma cells in a dose-and time-dependent manner as determined by MTT assay. However, the water extract of P. urinaria did not exert any cytotoxic effect on normal cells such as endothelial cells and liver cells. Result from flow cytometry revealed a dose-dependent increase of dead cells 24 hours after treating Lewis lung carcinoma cells with P. urinaria extract.

In-vitro Inhibitory Effect of Phyllanthus Urinaria L Compound on Proliferation of Human liver Cancer Cell HePG_2 and Its Apoptosis Induction
en.cnki.com.cn…

Within a certain limit of concentrations,the higher the concentration and the longer the acting time,the stronger the inhibition.Co-cultured with 500 μ g/mL Phyllanthus Urinaria L compound for 72 h,the inhibitory rate reached 93.58 % and IC50 was 240 μ g/mL.Phyllanthus Urinaria L compound at different concentrations had an certain effect on inducing cell apoptosis.Conclusion Phyllanthus Urinaria L compound can inhibit the proliferation of hepatoma cell,and its mechanism may be related with the induction of hepatoma cell HePG2 apoptosis.

Phyllanthus Amarus Inhibits Cell Growth and Induces Apoptosis in Daltons Lymphoma Ascites Cells
ict.sagepub.com…

The authors found in an earlier study that Phyllanthus amarus extract could significantly inhibit the solid and ascites tumor development in mice induced by Dalton’s lymphoma ascites (DLA) cells. In the present study, the apoptotic effects of P.amarus against DLA cells in culture was evaluated. P.amarus produced significant reduction in cell viability as determined by the MTT assay.

Inhibiting Effect of Phyllanthus Urinaria Alcohol Extract on Human Stomach Cancer Cell MKN28
en.cnki.com.cn…

MTT method determination showed that the extract had inhibiting effect on the multiplication of MKN28 cells and the inhibiting effect was dependent on concentration and time.The result of flow cytometry suggested that the extract could induce MKN28 apoptosis.CONCLUSION The alcohol extract of phyllanthus ruinaria can inhibit the growth of human stomach cell MKN28,and apoptosis is one of its mechanisms.

Hairy root extract of Phyllanthus amarus induces apoptotic cell death in human breast cancer cells
/23nctan

This study deals with establishment of hairy root cultures of Phyllanthus amarus using Agrobacterium rhizogenes and cytotoxic effects of methanolic extract of hairy roots on human adenocarcinoma cell line, MCF-7. The hairy root extract displayed a linear concentration- and time-dependent cytotoxicity. Further, increased concentration of the root extract showed an increase in the percent apoptotic cells from 26% to 36% as determined by annexin V-FITC and propidium iodide. The observed cytotoxicity correlated well with the increased levels of intracellular reactive oxygen species (ROS) as well as decreased mitochondrial membrane potential (MMP). The overall results amply suggest an appreciable antiproliferative effect of P. amarus hairy root extract on the MCF-7 cells through induction of apoptosis, thereby establishing the potential anticancer activity of the extract.

Styrylpyrone
Source: Goniothalamus Umbrosus Trees
en.wikipedia.org…

Styrylpyrone Derivative (SPD) induces apoptosis in a caspase-7-dependent manner in the human breast cancer cell line MCF-7
www.cancerci.com…

Styrylpyrone derivative (SPD) is a plant-derived pharmacologically active compound extracted from Goniothalamus sp. Previously, we have reported that SPD inhibited the proliferation of MCF-7 human breast cancer cells by inducing apoptotic cell death, while having minimal effects on non-malignant cells.

Oncolysis of Breast, Liver and Leukemia Cancer Cells Using Ethyl Acetate and Methanol Extracts of Goniothalamus umbrosus
docsdrive.com…

Sulindac
Source: Pharmaceutical Drug.
en.wikipedia.org…
A drug originally used for treating things like arthritis, and inflammation, I happened across some abstracts showing it to induce apoptosis in various cancers. Coupling this drug with other things in this presentation might really lower reliance on “chemotherapy”. Here is one example:

Sulindac derivatives inhibit growth and induce apoptosis in human prostate cancer cell lines
www.ncbi.nlm.nih.gov…

We examined the activity of two metabolites of sulindac (a nonsteroidal anti-inflammatory drug), sulindac sulfide and sulindac sulfone (exisulind, Prevatec), and a novel highly potent analog of exisulind (CP248) on a series of human prostate epithelial cell lines. Marked growth inhibition was seen with the BPH-1, LNCaP, and PC3 cell lines with IC50 values of about 66 microM, 137 microM, and 64 nM for sulindac sulfide, exisulind, and CP248, respectively. DNA flow cytometry and 4′,6′-diamido-2-phenylindole (DAPI) staining indicated that these three compounds also induced apoptosis in all of these cell lines.

Tetrathiomolybdate (TM)
www.thedcasite.com…
www.infiltec.com…

[size=3]Copper-Lowering Drug Stabilizes Advanced Cancer: Research on Wilson’s Disease Led to Discovery[/size]
www.medicineatmichigan.org…

By depriving cancer tumors of the copper supply they need to form new blood vessels, researchers in the U-M Medical School have stopped the growth of the disease in a small group of patients with advanced cancer. Five of six patients whose copper levels were kept at one-fifth of normal for more than 90 days had no growth of existing tumors or formation of new ones, according to a paper published in the January, 2000, issue of Clinical Cancer Research. The sixth patient had progression of only one tumor; all other tumors within her body remained stable. Twelve other patients did not achieve the target copper level, or could not stay at the target level for 90 days, because of disease progression.

About an Experimental Drug, Tetrathiomolybdate
www.cancerfoundation.com…

An experimental drug called tetrathiomolybdate (referred to from here on as “TM”) is currently undergoing clinical trials at the University of Michigan. TM is known to decrease copper levels in the body by a process called “chelation”. In simple language, TM binds copper to a protein, forming a complex which can then be excreted from the body. Copper is used by many organs in the body, but the use which is of interest here is that it is essential to the growth of new blood vessels, a process called “angiogenesis”. (“Angio” means blood vessel and “genesis” means new formation.) Whenever tumor cells “set up housekeeping” in the body, blood vessels are necessary to provide nourishment for their growth. Once a tumor reaches the size of two millimeters it needs a blood supply to maintain itself. Without an adequate level of copper in the blood, this new blood supply cannot form and thus the tumor cannot enlarge.

THC
Source: Cannabis
en.wikipedia.org…
Ths is an interesting one. There are studies showing cancer inhibition, and induction in various types of cancer. Considering the controversial nature of THC, there’s no telling if there’s foul play involved in the studies claiming it causes cancer. If you’re considering using this treatment be sure to know your cell line and do deeper research.

The cannabinoid delta(9)-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells
www.ncbi.nlm.nih.gov…

The inhibition of ERK and AKT activity by THC was accompanied by activation of the proapoptotic BCL-2 family member BAD. Reduction of BAD protein expression by RNA interference rescued colorectal cancer cells from THC-induced apoptosis. These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells. The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy.

Tetrahydrocannabinol Inhibits Cell Cycle Progression in Human Breast Cancer Cells
cancerres.aacrjournals.org…

Here, we show that Δ9-tetrahydrocannabinol (THC), through activation of CB2 cannabinoid receptors, reduces human breast cancer cell proliferation by blocking the progression of the cell cycle and by inducing apoptosis.

Delta9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells
www.ncbi.nlm.nih.gov…

The effect of delta9-tetrahydrocannabinol (THC), the major psycho-active component of marijuana, in human prostate cancer cells PC-3 was investigated. THC caused apoptosis in a dose-dependent manner. Morphological and biochemical changes induced by THC in prostate PC-3 cells shared the characteristics of an apoptotic phenomenon. First, loss of plasma membrane asymmetry determined by fluorescent anexin V binding. Second, presence of apoptotic bodies and nuclear fragmentation observed by DNA staining with 4′,6-diamino-2-phenylindole (DAPI). Third, presence of typical ‘ladder-patterned’ DNA fragmentation. Central cannabinoid receptor expression was observed in PC-3 cells by immunofluorescence studies. However, several results indicated that the apoptotic effect was cannabinoid receptor-independent, such as lack of an effect of the potent cannabinoid agonist WIN 55,212-2, inability of cannabinoid antagonist AM 251 to prevent cellular death caused by THC and absence of an effect of pertussis toxin pre-treatment.

Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivoTHC inhibits NSCLC metastasis and growth
www.nature.com…

Δ9-Tetrahydrocannabinol (THC) is the primary cannabinoid of marijuana and has been shown to either potentiate or inhibit tumor growth, depending on the type of cancer and its pathogenesis. Little is known about the activity of cannabinoids like THC on epidermal growth factor receptor-overexpressing lung cancers, which are often highly aggressive and resistant to chemotherapy. In this study, we characterized the effects of THC on the EGF-induced growth and metastasis of human non-small cell lung cancer using the cell lines A549 and SW-1573 as in vitro models. We found that these cells express the cannabinoid receptors CB1 and CB2, known targets for THC action, and that THC inhibited EGF-induced growth, chemotaxis and chemoinvasion.

Cannabinoids Induce Cancer Cell Proliferation via Tumor Necrosis Factor α-Converting Enzyme
cancerres.aacrjournals.org…
Δ9-Tetrahydrocannabinol-Induced Apoptosis in the Thymus and Spleen as a Mechanism of Immunosuppression in Vitro and in Vivo
jpet.aspetjournals.org…
Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response
www.ncbi.nlm.nih.gov…

Theaflavin
Source: Green & Black Tea.
en.wikipedia.org…
Another useful compound found in everyday tea.

Induction of apoptosis in human leukemia cells by black tea and its polyphenol theaflavin
www.ncbi.nlm.nih.gov…

Treatment of human leukemic cell lines HL-60 and K-562 with extracts of green and black tea and their polyphenols epigallocatechin gallate and theaflavins, respectively, showed a dose dependent inhibition of growth as a result of cytotoxicity and suppression of cell proliferation.

Black tea theaflavins induce programmed cell death in cultured human stomach cancer cells
www.ncbi.nlm.nih.gov…

The exposure of human stomach cancer KATO III cells to black tea theaflavin extract, free theaflavin, and theaflavin digallate that are main components of the extract, led to both growth inhibition and the induction of programmed cell death (apoptosis). Morphological changes showing apoptotic bodies were observed in the cells treated with black tea theaflavin extract, theaflavin and theaflavin digallate. The fragmentations by these theaflavin compounds of DNA to oligonucleosomal-sized fragments that are characteristics of apoptosis were observed to be concentration- and time-dependent. These data suggest that drinking of black tea in large amounts is recommended to protect humans from stomach cancer.

Theaflavins induced apoptosis of LNCaP cells
www.ncbi.nlm.nih.gov…

Prostate cancer (PCA), the most frequently diagnosed malignancy in men, represents an excellent candidate disease for chemoprevention studies because of its particularly long latency period, high rate of mortality and morbidity. Infusion of black tea and its polyphenolic constituents have been shown to possess antineoplastic effects in androgen dependent PCA in both in vivo and in vitro models including transgenic animals.

Thymoquinone
Food: Nigella Sativa (Black Cumin) Seeds & Seed Oil.
Sources: Indian and other Asian markets (seeds), Health food stores (extracts).
en.wikipedia.org…
Not to be confused with the type of cumin (Cuminum cyminum) used in Mexican Cuisine.

Thymoquinone and cisplatin as a therapeutic combination in lung cancer: Invitro and in vivo
www.biomedcentral.com…

TQ was able to inhibit cell proliferation, reduce cell viability and induce apoptosis. TQ at 100 µM and CDDP at 5 µM inhibited cell proliferation by nearly 90%and the combination showed synergism. TQ was able to induced apoptosis in both NCI-H460 and NCI-H146 cell lines. TQ also appears to affect the extracellular environmentinhibiting invasion and reducing the production of two cytokines ENA-78 and Gro-alphawhich are involved in neo-angiogenesis.

Chemopreventive potential of volatile oil from black cumin (Nigella sativa L.) seeds against rat colon carcinogenesis
www.ncbi.nlm.nih.gov…

These findings demonstrate that the volatile oil of N. sativa has the ability to inhibit colon carcinogenesis of rats in the postinitiation stage, with no evident adverse side effects, and that the inhibition may be associated, in part, with suppression of cell proliferation in the colonic mucosa.

Thymoquinone induces apoptosis through activation of caspase-8 and mitochondrial events in p53-null myeloblastic leukemia HL-60 cells
www.ncbi.nlm.nih.gov…

Here, we report that TQ exhibits antiproliferative effect, induces apoptosis, disrupts mitochondrial membrane potential and triggers the activation of caspases 8, 9 and 3 in myeloblastic leukemia HL-60 cells. The apoptosis induced by TQ was inhibited by a general caspase inhibitor, z-VAD-FMK; a caspase-3-specific inhibitor, z-DEVD-FMK; as well as a caspase-8-specific inhibitor, z-IETD-FMK.

Structure-Activity Studies on Therapeutic Potential of Thymoquinone Analogs in Pancreatic Cancer
www.springerlink.com…

Pancreatic cancer (PC) is one of the deadliest of all tumors. Previously, we were the first to show that Thymoquinone (TQ) derived from black seed (Nigella sativa) oil has anti-tumor activity against PC. However, the concentration of TQ required was considered to be high to show this efficacy. Therefore, novel analogs of TQ with lower IC50 are highly desirable.

Trientine
Source: Prescription.
en.wikipedia.org…

The copper-chelating agent, trientine, suppresses tumor development and angiogenesis in the murine hepatocellular carcinoma cells
onlinelibrary.wiley.com…

Trientine dihydrochloride (trientine) is used in clinical practice as an alternative copper (Cu)-chelating agent for patients with Wilson’s disease of penicillamine intolerance. In our study, we examined the effect of Cu-chelating agents on tumor development and angiogenesis in the murine HCC xenograft model. Although both trientine and penicillamine in the drinking water suppressed the tumor development, trientine exerted a more potent inhibitory effect than penicillamine. In combination with a Cu-deficient diet, both trientine and penicillamine almost abolished the HCC development.

Uncaria
Plant also known as “Cat’s Claw”.
en.wikipedia.org…
I have a friend whose yard is infested with this stuff… still after years of trying to kill it.
www.cancer.org…

Ethnobotany, phytochemistry and pharmacology of Uncaria (Rubiaceae)
www.ncbi.nlm.nih.gov…

The Uncaria genus is an important source of medicinal natural products, particularly alkaloids and triterpenes. The collected information is an attempt to cover the more recent developments in the ethnobotany, pharmacology and phytochemistry of this genus. During the past 20 years, alkaloids, terpenes, quinovic acid glycosides, flavonoids and coumarins have been isolated from Uncaria. Fifty-three novel structures are reported in this review. The species in which the largest number of compounds has been identified is the Peruvian Uncaria tomentosa or ‘cat’s claw.’ Pharmacological studies are described according to cytotoxicity, anti-inflammatory, antiviral, immunostimulation, antioxidant, CNS-related response, vascular, hypotensive, mutagenicity and antibacterial properties. The potential for development of leads from Uncaria continues to grow, particularly in the area of immunomodulatory, anti-inflammatory and vascular-related conditions.

Oxindole alkaloids from Uncaria tomentosa induce apoptosis in proliferating, G0/G1-arrested and bcl-2-expressing acute lymphoblastic leukaemia cells
onlinelibrary.wiley.com…

Natural products are still an untapped source of promising lead compounds for the generation of antineoplastic drugs. Here, we investigated for the first time the antiproliferative and apoptotic effects of highly purified oxindole alkaloids, namely isopteropodine (A1), pteropodine (A2), isomitraphylline (A3), uncarine F (A4) and mitraphylline (A5) obtained from Uncaria tomentosa, a South American Rubiaceae, on human lymphoblastic leukaemia T cells (CCRF-CEM-C7H2). Four of the five tested alkaloids inhibited proliferation of acute lymphoblastic leukaemia cells. Furthermore, the antiproliferative effect of the most potent alkaloids pteropodine (A2) and uncarine F (A4) correlated with induction of apoptosis. After 48 h, 100 μmol/l A2 or A4 increased apoptotic cells by 57%. CEM-C7H2 sublines with tetracycline-regulated expression of bcl-2, p16ink4A or constitutively expressing the cowpox virus protein crm-A were used for further studies of the apoptosis-inducing properties of these alkaloids. Neither overexpression of bcl-2 or crm-A nor cell-cycle arrest in G0/G1 phase by tetracycline-regulated expression of p16INK4A could prevent alkaloid-induced apoptosis. Our results show the strong apoptotic effects of pteropodine and uncarine F on acute leukaemic lymphoblasts and recommend the alkaloids for further studies in xenograft models.

Methanolic Extracts of Uncaria rhynchophylla Induce Cytotoxicity and Apoptosis in HT-29 Human Colon Carcinoma Cells
www.springerlink.com…

In this paper, we report the anticancer activities of Uncaria rhynchophylla extracts, a Rubiaceae plant native to China. Traditionally, Uncaria rhynchophylla has been used in the prevention and treatment of neurotoxicity. However, the cytotoxic activity of Uncaria rhynchophylla against human colon carcinoma cells has not, until now, been elucidated. We found that the methanolic extract of Uncaria rhynchophylla (URE) have cytotoxic effects on HT-29 cells. The URE showed highly cytotoxic effects via the MTT reduction assay, LDH release assay, and colony formation assay. As expected, URE inhibited the growth of HT-29 cells in a dose-dependent manner. In particular, the methanolic URE of the 500 μg/ml showed 15.8% inhibition against growth of HT-29 cells. It induced characteristic apoptotic effects in HT-29 cells, including chromatin condensation and sharking occurring 24 h when the cells were treated at a concentration of the 500 μg/ml.

Antiproliferative and Pro-apoptotic Effects of Uncaria tomentosa in Human Medullary Thyroid Carcinoma Cells
ar.iiarjournals.org…

Medullary thyroid carcinoma (MTC), a rare calcitonin-producing tumor, is derived from parafollicular C-cells of the thyroid and is characterized by constitutive Bcl-2 overexpression. The tumor is relatively insensitive to radiation therapy as well as conventional chemotherapy. To date, the only curative treatment is the early and complete surgical removal of all neoplastic tissue. In this study, the antiproliferative and pro-apoptotic effects of fractions obtained from Uncaria tomentosa (Willd.) DC, commonly known as uña de gato or cat’s claw were investigated. Cell growth of MTC cells as well as enzymatic activity of mitochondrial dehydrogenase was markedly inhibited after treatment with different fractions of the plant. Furthermore, there was an increase in the expressions of caspase-3 and -7 and poly(ADP-ribose) polymerase (PARP) fraction, while bcl-2 overexpression remained constant. In particular, the alkaloids isopterpodine and pteropodine of U. tomentosa exhibited a significant pro-apoptotic effect on MTC cells, whereas the alkaloid-poor fraction inhibited cell proliferation but did not show any pro-apoptotic effects. These promising results indicate the growth-restraining and apoptotic potential of plant extracts against neuroendocrine tumors, which may add to existing therapies for cancer.

An ethanolic extract of Uncaria tomentosa reduces inflammation and B16-BL6 melanoma growth in C57BL/6 mice
journals.indexcopernicus.com…

Extracts of the bark of Uncaria tomentosa (Cat’s Claw – Uña de Gato) have been used traditionally for their anti-inflammatory and anticancer properties. We investigated the effect of a hydroethanolic extract (UT) of U. tomentosa on a) the viability of primary and tumor cells, b) the inflammatory response (tumor necrosis factor alpha [TNF-α], interleukin-6 [IL-6] and nitric oxide [NO]) both in vitro and in vivo, c) B16/BL6 melanoma cell growth and metastasis in the C57BL/6 mouse, and d) nuclear factor κB (NF-κB) activity in LPS-stimulated HeLa cells. UT did not show an important cytotoxic effect in vitro at the doses up to 300 μg/ml, but did inhibit tumor growth and metastasis in vivo. UT inhibited TNF-α, IL-6 and NO production in vitro. NF-κB activity was also inhibited. Our studies show that UT merits further study for its effects on processes common to inflammation and cancer.

Vanillin
Source: Vanilla Beans.
en.wikipedia.org…

Vanillin suppresses in vitro invasion and in vivo metastasis of mouse breast cancer cells
www.ncbi.nlm.nih.gov…

Vanillin, a food flavoring agent, has been reported to show anti-mutagenic activity and to inhibit chemical carcinogenesis. In this study, we examined the effect of vanillin on the growth and metastasis of 4T1 mammary adenocarcinoma cells in BALB/c mice. Mice orally administered with vanillin showed significantly reduced numbers of lung metastasized colonies compared to controls. In vitro studies revealed that vanillin, at concentrations that were not cytotoxic, inhibited invasion and migration of cancer cells and inhibited enzymatic activity of MMP-9 secreted by the cancer cells.

Apoptosis and cell cycle arrest of human colorectal cancer cell line HT-29 induced by vanillin
www.ncbi.nlm.nih.gov…

Results showed that apoptosis was induced by vanillin and the IC(50) for HT-29 and NIH/3T3 normal cell lines were 400 microg/ml and 1000 microg/ml, respectively. Different concentrations of vanillin arrest cell cycle at different checkpoints. 5-Bromo-2-deoxyuridine-labeling cell proliferation assay showed that G0/G1 arrest was achieved at lower concentration of vanillin (200 microg/ml) while cell cycle analysis by flow cytometer showed that G2/M arrest occurs at higher concentration of vanillin (1000 microg/ml).

Vitamin D3
Foods: Salmon, Catfish, Tuna, Eggs, Milk, Yogurt, Margarine, Bread.
Source: Suppliments, Sol (the Sun).
en.wikipedia.org…
Vitamin D3 inhibits Thioredoxin, which is a good thing.

Thioredoxin, a Gene Found Overexpressed in Human Cancer, Inhibits Apoptosis
cancerres.aacrjournals.org…

The redox protein thioredoxin plays an important role in controlling cancer cell growth through regulation of DNA synthesis and transcription factor activity. Thioredoxin is overexpressed by a number of human primary cancers and its expression is decreased during dexamethasone-induced apoptosis of mouse WEHI7.2 thymoma cells. We examined the ability of WEHI7.2 cells stably transfected with human thioredoxin cDNA showing increased levels of cytoplasmic thioredoxin to undergo apoptosis in vitro and in vivo. The cells were protected from apoptosis induced by dexamethasone, staurosporine, etoposide, and thapsigargin, but not by N-acetyl-sphingosine.

Vitamin K2
Foods: “Natto” (highest concentration). Lower concentrations include: Chicken, Beef, Egg Yolks, Cheese, and Salami.
Sources: Suppliments, Coumadin.
en.wikipedia.org…
Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1. Other foods that contain Vitamin K: Peas, Spinach, Swiss CHard, Brussel Sproats, Broccoli, Carrots, Kale, Asparagus, Mustard Greens and Green Beans.

Apoptosis induction of vitamin K2 in lung carcinoma cell lines: the possibility of vitamin K2 therapy for lung cancer
www.ncbi.nlm.nih.gov…

Morphologic features of the cells treated with VK2 were typical for apoptosis along with caspase-3 activation and becoming positive for APO2.7 monoclonal antibody, an antibody which specifically detects the cell undergoing apoptosis. In addition to the leukemia cell line, LU-139 cells accumulated into G0/G1 phase during 72-h exposure to VK2. Combined treatment of cisplatin plus VK2 resulted in enhanced cytocidal effect compared to the cells treated with either cisplatin or VK2 alone. Since VK2 is a safe medicine without prominent adverse effects including bone marrow suppression, our data strongly suggest the therapeutic possibility of using VK2 for the treatment of patients with lung carcinoma.

Apoptosis of liver cancer cells by vitamin K2 and enhancement by MEK inhibition
www.ncbi.nlm.nih.gov…

These data demonstrated that VK2 induced apoptosis and activated the MEK/ERK1/2 signaling pathway in a cell-type specific manner, and a MEK inhibitor could augment the cell death in these cells.

Vitamin K2-induced antitumor effects via cell-cycle arrest and apoptosis in gastric cancer cell lines
www.ncbi.nlm.nih.gov…

Vitamin K2 (VK2) has a growth inhibitory effect on various types of cancer cells in vitro, and its efficacy has been demonstrated in clinical applications in a number of patients with leukemia and hepatocellular carcinoma. In this study, the effect of cell growth inhibition and apoptosis induction and the concomitant use of an anticancer agent by VK2 (menaquinone: MK4), on gastric cancer cell lines were examined. When 4 kinds of gastric cancer cells (KATO III, MKN7, MKN74 and FU97) were exposed to MK4, the cell growth was inhibited in an MK4 dose-dependent manner. Morphologically, apoptosis induced by MK4 was recognized in FU97, but only a slight number of apoptotic images was recognized in other cell lines.

Role of Vitamin K2 in the Development of Hepatocellular Carcinoma in Women With Viral Cirrhosis of the Liver
jama.ama-assn.org…

Hepatocellular carcinoma was detected in 2 of the 21 women given vitamin K2 and 9 of the 19 women in the control group. The cumulative proportion of patients with hepatocellular carcinoma was smaller in the treatment group (log-rank test, P = .02). On univariate analysis, the risk ratio for the development of hepatocellular carcinoma in the treatment group compared with the control group was 0.20 (95% confidence interval [CI], 0.04-0.91; P = .04).

Production of superoxide and dissipation of mitochondrial transmembrane potential by vitamin K2 trigger apoptosis in human ovarian cancer TYK-nu cells
www.springerlink.com…

Watercress
en.wikipedia.org…

Compounds in broccoli, cauliflower, and watercress block lung cancer progression
www.medicalnewstoday.com…

A family of compounds found in cruciferous vegetables, such as broccoli, cauliflower, and watercress, blocked lung cancer progression in both animal studies and in tests with human lung cancer cells, report researchers from Georgetown University Medical Center and the Institute for Cancer Prevention. They say the results, published in a set of papers in the September 15 issue of Cancer Research, suggest that these chemicals — put into a veggie pill of sorts — might some day be used to help current and former smokers ward off development of lung cancer, the leading cause of cancer death in Americans.

Willow
en.wikipedia.org…

Willow bark extract (BNO1455) and its fractions suppress growth and induce apoptosis in human colon and lung cancer cells
www.ncbi.nlm.nih.gov…

We showed that willow bark extract BNO 1455 an its fractions inhibit the cell growth and promote apoptosis in human colon and lung cancer cell lines irrespective of their COX-selectivity.

Willow Leaves Extracts Contain Anti-Tumor Agents Effective against Three Cell Types
www.ncbi.nlm.nih.gov…

In vivo Ehrlich Ascites Carcinoma Cells (EACC) were injected into the intraperitoneal cavity of mice. The willow extract was fed via stomach tube. The (EACC) derived tumor growth was reduced by the willow extract and death was delayed (for 35 days). In vitro the willow extract could kill the majority (75%–80%) of abnormal cells among primary cells harvested from seven patients with acute lymphoblastic leukemia (ALL) and 13 with AML (acute myeloid leukemia). DNA fragmentation patterns within treated cells inferred targeted cell death by apoptosis had occurred. The metabolites within the willow extract may act as tumor inhibitors that promote apoptosis, cause DNA damage, and affect cell membranes and/or denature proteins.

White Button Mushroom
Food: From many commom “table” Agaricus mushrooms.
en.wikipedia.org…
en.wikipedia.org…

Blazein of a new steroid isolated from Agaricus blazei Murrill (himematsutake) induces cell death and morphological change indicative of apoptotic chromatin condensation in human lung cancer LU99 and stomach cancer KATO III cells.
www.ncbi.nlm.nih.gov…

Blazein was isolated from mushroom (Agaricus blazei Murrill) and identified by Mass and 1H-NMR as blazein. The effect of blazein on the DNA of human various cancer cells was investigated. DNA fragmentations by blazein to oligonucreosomal-sized fragments, a characteristic of apoptosis, were observed in the human lung LU99 and stomach KATO III cancer cells. The DNA fragmentations by blazein were observed from day 2 (KATO III cells) or day 3 (LU99 cells) after the addition of blazein to the culture cells. These findings suggest that growth inhibition by blazein results from the induction of apoptosis by the compound.

White Button Mushroom (Agaricus Bisporus) Exhibits Antiproliferative and Proapoptotic Properties and Inhibits Prostate Tumor Growth in Athymic Mice
www.ncbi.nlm.nih.gov…

White button mushrooms are a widely consumed food containing phytochemicals beneficial to cancer prevention. The purpose of this research was to evaluate the effects of white button mushroom extract and its major component, conjugated linoleic acid (CLA) on prostate cancer cell lines in vitro and mushroom extract in vivo. In all cell lines tested, mushroom inhibited cell proliferation in a dose-dependent manner and induced apoptosis within 72 h of treatment.

Win55,212-2
Source: Cannabis
en.wikipedia.org…
Cannabinoid Receptor-Mediated Apoptosis Induced by R(+)-Methanandamide and Win55,212-2
molpharm.aspetjournals.org…

We have recently shown that cannabinoids induce growth inhibition and apoptosis in mantle cell lymphoma (MCL), a malignant B-cell lymphoma that expresses high levels of cannabinoid receptor types 1 and 2 (CB1 and CB2). In the current study, the role of each receptor and the signal transduction triggered by receptor ligation were investigated. Induction of apoptosis after treatment with the synthetic agonists R(+)-methanandamide [R(+)-MA] and Win55,212-2 (Win55; (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl) pyrrolo-[1,2,3-d,e]-1,4-benzoxazin-6-yl]-1-naphthalenyl-methanone) was dependent on both cannabinoid receptors,

Xanthohumol
Sources: Hops or Ashataba Extracts.
www.organica…/xanthohumol.html
It’s found in Hops in trace amounts, and therefore beer, but apparently you’d have to drink 120 gallons of beer a day to get proper dosage. Therefore extracts from the Ashataba plant are necessary to hope to make any use of this substance.

Xanthohumol induces apoptosis in cultured 40-16 human colon cancer cells by activation of the death receptor- and mitochondrial pathway
onlinelibrary.wiley.com…

In this study, we investigated the cell growth inhibitory potential of XN on cultured human colon cancer cells. Cell proliferation was measured by sulforhodamine B staining. Poly(ADP-ribose)polymerase (PARP) cleavage, activation of caspases-3, -7, -8, and -9, and Bcl-2 family protein expression were detected by Western blot analyses. XN significantly reduced proliferation of the HCT116-derived colon cancer cell line 40-16. …We conclude that induction of apoptosis by downregulation of Bcl-2 and activation of the caspase cascade may contribute to the chemopreventive or therapeutic potential of XN.

Xanthohumol, a prenylflavonoid derived from hops induces apoptosis and inhibits NF-kappaB activation in prostate epithelial cells
www.ncbi.nlm.nih.gov…

Limited in vitro studies indicate that several prenylated flavonoids present in the hop plant (Humulus lupulus) possess anticarcinogenic properties. The purpose of this study was to investigate the anti-tumorigenic effects of xanthohumol (XN), the major prenylflavonoid in hops, on prostate cancer and benign prostate hyperplasia. …XN and its oxygenated derivative also induced cell cycle changes in both cells lines, seen in an elevated sub G1 peak at 48h treatment. Western blot analysis was performed to confirm the activation of proapoptotic proteins, Bax and p53. XN and its derivative caused decreased activation of NFkappaB. This work suggests that XN and its oxidation product, XAL, may be potentially useful as a chemopreventive agent during prostate hyperplasia and prostate carcinogenesis, acting via induction of apoptosis and down-regulation of NFkappaB activation in BPH-1 cells.

Xanthohumol inhibits inflammatory factor production and angiogenesis in breast cancer xenografts
onlinelibrary.wiley.com…

Xanthohumol (XN), a natural polyphenol present in beer, is known to exert anti-cancer effects. However, its precise mechanisms are not yet clearly defined. The aim of this study was to investigate the effect of oral administration of XN in breast cancer xenografts in nude mice. …Oral administration of XN to nude mice inoculated with MCF7 cells resulted in central necrosis within tumours, reduced inflammatory cell number, focal proliferation areas, increased percentage of apoptotic cells and decreased microvessel density. Anti-angiogenic effects of XN were further confirmed by immunoblotting for factor VIII expression in XN-treated tumours as compared to controls. Decreased immunostaining for NFκB, phosphorylated-inhibitor of kappa B and interleukin-1β were also observed as well as a significant decrease in NFκB activity to 60% of control values. These novel findings indicate that XN is able to target both breast cancer and host cells, namely inflammatory and endothelial cells, suggesting its potential use as a double-edge anti-cancer agent.

Xanthohumol kills B-chronic lymphocytic leukemia cells by an apoptotic mechanism
onlinelibrary.wiley.com…

Based on these observations, lymphocytes from patients with B-CLL were cultured in the presence of XA in vitro. XA induced a dose-dependent killing of B-CLL cells at an LD50(24 h) of 24.4 ± 6.6 μM, independent of known adverse prognostic factors including functional loss of p53. Cell death was associated with poly (ADP)-ribose polymerase cleavage and annexin V positivity, suggestive of an apoptotic mechanism. Surprisingly, p70S6K phosphorylation was stimulated upon XA treatment. In conclusion, XA has an antitumor activity on B-CLL cells in vitro. The molecular mechanisms behind this pro-apoptotic effect deserve further investigation.

Zerumbone
Source: Shampoo Ginger Plant (Zingiber Zerumbet)
en.wikipedia.org…

Zerumbone induced apoptosis in liver cancer cells via modulation of Bax/Bcl-2 ratio
www.ncbi.nlm.nih.gov…

Zerumbone is a cytotoxic component isolated from Zingiber zerumbet Smith, a herbal plant which is also known as lempoyang. …zerumbone was found to induce the apoptotic process in HepG2 cells through the up and down regulation of Bax/Bcl-2 protein independently of functional p53 activity.

Zerumbone, a bioactive sesquiterpene, induces G2/M cell cycle arrest and apoptosis in leukemia cells via a Fas- and mitochondria-mediated pathway
www.ncbi.nlm.nih.gov…

We demonstrated here for the first time that zerumbone (ZER), a natural cyclic sesquiterpene, significantly suppressed the proliferation of promyelocytic leukemia NB4 cells among several leukemia cell lines, but not human umbilical vein endothelial cells (HUVECs), by inducing G2/M cell cycle arrest followed by apoptosis with 10 microM of IC50.

Zerumbone, a tropical ginger sesquiterpene, inhibits colon and lung carcinogenesis in mice
onlinelibrary.wiley.com…

Our findings suggest that dietary administration of ZER effectively suppresses mouse colon and lung carcinogenesis through multiple modulatory mechanisms of growth, apoptosis, inflammation and expression of NFκB and HO-1 that are involved in carcinogenesis in the colon and lung.

Zinc
www.cancerfoundation.com…
Zinc like TM is nontoxic but has the disadvantage of having therapeutic effectiveness much slower than TM. Zinc lowers copper levels by inducing hepatic and intestinal metallothionein (MT) synthesis which in turn binds copper, rendering it unavailable for absorption into the bloodstream.

Afterthoughts
If you’re diagnosed with cancer it’s critical you find out what specific cell line it is. Then go to Google Scholar and search for the name / number of the cell line, along with “cancer” “apoptosis”. This will bring up papers with results specific to your particular cancer. I you have cancer don’t stop with this huge summary, dig further. You need to try to understand potential interactions and such at the very least.

I didn’t cite every possible study as I compiled this. In almost all cases, I was very specific about the titles of the studies having the name of the compound and the form of cancer successfully treated with it. This means with almost every items theres are scores of additional literature. Following thsi criteria, there ended up being several items I didn’t include.

Short of physically removing cancer / tumors, I don’t count on there being any one single silver bullet to ‘curing’ cancer, nor that they ever truly go away completely.
I only missed 2 letters: J & Y.

These realities really do call into question the profit based medical system, although I’m certain that the idea of “socialized medicine” wouldn’t ever work under this government. Nothing but killing people ever goes right under this system.

I’m sure there are plenty of other examples out there in the literature, as these are only the ones I happened to notice maintly while going through the titles and abstracts of others prior. It finally got to the point I just HAD to stop.

With what has been discovered over the past decade they’ve really figured out the keys to destroying cancer, but many of these papers are over 10 years old.

Typical hospitals don’t have select diets they give their overcharged patients based on their conditions. In my moms case they boiled the broccoli to the point of it tasting “like water”. Boiling destroys the usefulness of most vegetables. They charge about $10,000 per day, and don’t even give you a piece of paper listing beneficial foods for when you go home. And the idea of massage therapists being on hospital staffs, nice try.

It could be argued that more kills cancer than actually causes it. Such a furious debate amongst many people would turn up more cures than I dug up on my own.

This site ought to be of use also, but I didn’t even get around to using it:
clinicaltrials.gov…

This is all in effect a tie-in to my other inter-related epic works lately:

agimanhattanproject.com…

*The Story of the Millennium: The AGI Manhattan Project.

The Technological Establishments paradigm changing agenda, and the Economic World War being waged to prevent the masses from ever participating.

Ignorance Is Futile Exclusive:

http://agimanhattanproject.com/

When we look at all the figures, from where the debt economy has been going for years, to the way the specific meltdown occurred and was carried out, to what’s looming on the horizon, how isn’t this deliberate?

But to propose that’s the case, there has to be a “why” they would do it. The simple answers of “greed” or “power” are lackluster to address the scale we’re enduring.

This trend has been accelerating almost directly in line with accelerating technological change and the ever increasing collective power of the computers of those at the commanding heights. I’ve yet to see the question asked: with increasing computer power and quality of techniques why aren’t ‘we’ getting better at sustainable economics?

Technology should be helping us, but instead it’s the true motive of what we’re witnessing. Technology is the answer to these tough questions, and the AGI Manhattan Project is at the heart of it all.

The world keeps getting crazier and crazier, at an accelerating rate, and we haven’t seen anything yet. At a glance it all appears to be impossible. Impossible to happen, yet even more impossible to stop. Here you will find answers and truths that explain it, and cannot be found anywhere else. Here you will find the why of it all, and even the solutions to undo this dystopian technological agenda.

The push for near-trillion dollar military budgets to fight “terrorists”, as if they’re beyond the scope of the Soviet Union, doesn’t make much sense. Neither does the extreme global warming related proposals, such as a global government and a global carbon tax which would cost trillions and therefore promises to bankrupt what’s left of the worlds economy, while doing little to actually solve the perceived problem. All this push, while the premises of each issue is highly debatable. That’s the truth that the advocates pushing for either issue doesn’t want to admit.

What a trillion dollars looks like in $100 bills.

Ask yourself when haven’t you seen 2 people dramatize an event between them, and didn’t each have different stories to what actually happened? Now consider, Democrats are supposed to be anti-war and pro-Global Warming mitigation and man caused theory. Republicans are opposite on both issues. This creates a small selection of scenarios. (1) One side is right about both, the other 99% wrong about what they advocate (consider the odds of over 50 million people being totally wrong on both major issues). (2) Each side is right about what they promote, which makes them each wrong about what they argue against. (3) Each side is wrong about what they advocate for, and are right about what they argue against. Odds are either scenario 2 or 3 is the right answer. Then consider how hyped everything always is. Now crunch some odds numbers.

The one thing that cannot be debated it the looming economic mega-crisis that promises to harm more people than terrorists or a rise in global temperatures could ever dream of in their worst nightmare scenarios, in the near term. Between the extreme budgets for the War on Terror, the extreme measures being pushed for Global Warming, on top of  the cash crunch we face in this technological 21st Century, it’s hard to make sense of this world gone mad. That is until we factor in the common thread behind that unites all three issues… The AGI Manhattan Project, and those who are behind it.

Not only has the global economy imploded rather dramatically, all the hard numbers point towards an inevitable total collapse, especially in the USA. The Federal Reserve and EU Bank are both privately owned institutions, and there’s no debating this fact. The Federal Reserve in particular was at the heart of the US economic meltdown, which brought the rest of the world with it. These institutions are literally at the helm of each federal economy, and aren’t subject to being audited. They’re above each government, just the same as your local city government is subject to the state government, and the state to the federal government.

AGI Manhattan Project – Are you in the club?

The global banking scheme is seemingly leading the world into a post-apocalyptic nightmare. How is this possible? Today we have increasingly powerful computers of all different sizes, yet the more powerful our computing hardware and software becomes the faster we’re falling into the abyss, instead of rising to an economic utopia. Computers clearly aren’t helping the system maintain a balanced budget sheet, while when you look at the graphs it appears they’re helping the elitist plutocracy to plunder the nations. Ask yourself how in the face of everything that’s happened in the past few year, billionaires increased in numbers and profits at a record rate in 2009 (Link 1, 2, 3, 4, 5, 6, 7).

So we’re in the middle of a collapse that by all measures looks deliberate, that was caused by private stock holders, who made unfathomable amounts of cash on the ways up and down, and were handed trillions of unaccountable dollars in “bailout” money in the aftermath. Despite all of this, there’s still this push for a near-trillion dollar military budget (in the US alone), along with a global government based on a global carbon tax.

Meanwhile the new administration is spending at all time record levels on all other fronts. We’re already on the brink here, how can they push harder, and tax us in all new ways? How can this looming total collapse not be deliberate? How is any president for providing the poor with mobility, when they all support the Infalation system of the Federal Reserve, which exploits the poor the hardest? Why won’t they stop spending, and is there something to this money crisis that answers these questions? The answer is yes.

We’re in a new world that changes everyday. Technology keeps expanding in its abilities, and our own. This is all happening at an exponentially increasing rate. This refers to its “doubling rate”, and in general the power of computational technology doubles roughly every 18 months, while it’s cost drops by half. This is most well known with computer CPU’s, but this rule applies with a similar rate to virtually every facet of technology, including revolutionary new technologies. There are 4 main areas of technology I’m referring to: nanotechnology, biotechnology, information technology, and cognitive sciences. They’re all beginning to merge in different ways in each area of technology and innovation.

This is very important. This answers the questions being posed above. These new thrusts in science are giving rise to new technologies that are game changers in human society. Mankind is on the verge of radical life extension, brain implants, nanobots, and a wide range of related technologies with artificial intelligence in the middle of it all. Technological progress increases with it’s own doubling rate. Meanwhile there’s an ever increasing push for more and more powerful artificial intelligence, so powerful in fact it’s like what you see in the sci-fi horror movies. Who hasn’t heard of Skynet? What they’re trying to build is already poised to be vastly more powerful than how it was depicted in the Terminator films. Ask yourself how absurd it sounds to build ‘Skynet’ to fight Islamic terrorists.

This sounds insane, but it’s absolutely true and there is absolutely no debating this fact whatsoever, as we’ll see.

At this point, even a conspiracy theorist might say that if there are powerful elites in control of everything, why would they risk losing that control in the face of a global artificial general intelligence (AGI) network? The answer is simple: they firmly believe that they’ll be able to live virtually indefinite life-spans, literally hundreds if not thousands of years. They believe they’ll be able to stop and then even reverse aging. They believe they’ll be able have enhanced physical and cognitive abilities, as well as being able to connect to a new type of global consciousness based Internet, in a hive mind.

They literally believe they’ll become gods, and there have been many scientific break-through’s that suggest they might be right on everything just listed. It all answers why we’re being bled and bankrupted at an increasing pace. They literally say we’ll face war if we try to stop them from becoming gods. I argue that this war has already begun, and the original questions answer the how and the why.

Imagine if the tyrants of history and today could live nearly forever. Now imagine what they must think in the face of humanity being able to extend their lives in the face of perceived overpopulation. Consider how medical advances of the 20th Century helped global populations explode. Now consider what it would mean if one about half of the population used non-radical life extension to live an extra couple dozen years, while the other half went all out wanting radical life extension that over a long enough timeline could offer lifespans that lasted hundreds of years.

If you listen closely to Global Warming rhetoric in particular, or most over-stated environmentalist rhetoric in general, there’s a total disdain for humans and our populations. Note that multinational energy companies such as Enron and BP helped design the carbon trading scheme, even though supposedly the energy companies are to be the ones to lose out. Regardless of your opinion of the “science”, it’s all extremely debatable, so at least please consider the possibility of the issue being used to manipulate us out of more of our our money and liberty like almost literally everything else that happens and gets exploited. But it’s what global climate change efforts have in common with the global War on Terror that this is all about.

Efforts from both the global War on Terror and global climate change are fueling funding in artificial intelligence, while helping keep everyone divided and distracted from debating the implications of the four aforementioned revolutionary sciences. Recall that AI, and especially AGI, inherently increases the rate at which the elites might get their hands on their god technologies. This common thread between these issues you will not see anywhere else.

Whatever is actually possible, it’s all coming sooner than the masses would think. Even majority of the front-men of this movement speak loudly about their dream wherever they can be heard, but they seem to project it as if it’s only something for the next-generation to be concerned. They carefully leave out the true scope of the current military science R&D. One thing is for sure, they don’t care about you and me. Their job is to condition the masses so when this comes we’re not taken by total shock & awe, but not tell us enough so that today we might stand up appalled.

There’s a Manhattan Project type initiative to bring about AGI much sooner than the 20 years away estimates that Moore’s Law would suggest. Moore’s Law applied to all fields of technology already gives us amazing natural innovation, but this isn’t good enough for the Technocrats. The players are the United States government & military with key corporations like Google and IBM. They’re doing much of it without explicitly telling you, and much of it is being done on your dime. The facts can be found in their own words, documents and websites. It’s not even a secret except that few would ever suspect the massive initiative or possibility, while the controlled Big 5 Media machine fails to make much mention let alone deliver actual context.

We exist under a so-called 2 party system. These 2 parties and the Big 5 Media work in concert together to ensure that no “3rd parties” have any chance of succeeding, despite giving us a facade of being mortal enemies while they divide and conquer. They’re almost perfectly totally against what the other is doing, but each side is still inherently supporting the same Technocracy agenda in what they do push for, while most of the time the career politicians are generally just paying lip service to the ideals that are expected of them.

“Democrats” fling all sorts of anti-war talk, but still vote to fund the wars, and American Imperialism in general. The US has over 1,000 military bases in foreign nations (about 6,000 total), with a dozens of supercarrier fleets (no other nation has even one). The rest of the world knows the U.S. as classical empire, and the Democrats are just as responsible for it. Even the word “freedom” has been manipulated into meaning the freedom to dominate, occupy and conquer. Meanwhile the “Republicans” talk all sorts of small government rhetoric, while helping to hyper-expand government and spending over the past 10 years. Democrats and Republicans are both just as responsible to the shipping of our jobs overseas so that we can only afford Chinese garbage products that aren’t even worth fixing when they break.

We don’t only use crude oil for fuel, we literally need it to be able to make virtually everything we enjoy in our daily modern lives, yet they claim alternative energy will actually impact how much oil we use. Over-stated environmental issue guilt-mongering dehumanizes us, while engineered conflicts makes us believe we humans are the problem, while the Technocrats argue they’re cybernetic technologies will have us evolve above these perceived “problems” in human nature.

Another related issue that we can all thank both Democrat and Republican career politicians for is the rapidly growing trend towards a Big Brother Police State. We’re on the verge of collapse, by their doings, yet they have more and more billions of dollars per year to spend on new ways to completely violate the Bill of Rights and spy on us in real time with virtually every device in our existence, while building a militarized police apparatus ready to crush any peaceful protest movement with state of the art technologies. Majority of the “western world” is already under a pervasive real time dragnet that makes the spying of the Soviet Union look like 1980’s 8-bit video games compared to XBox 360.

This is supposed to be a free nation, yet we’re not even free to move to the other side of the world and not pay the IRS taxes. We face prison time and the confiscation of our homes for possession of certain natural drugs that are less toxic than most of the synthetic drugs cooked up in big pharmaceutical labs that we’re overcharged for.

We’re free to talk, but we’re completely marginalized, and talking about the government these days gets you put on terrorist lists. Both Bush and Obama have declared war on Freedom of the Press. We’re not even free to travel without being groped and naked body scanned, for a ‘threat’ that didn’t even kill as many people in the year 2001 as did everyday aspirin.

The reality is, by all definitions, here in the US we’ve been enveloped by corporate fascism, while holding the world hostage as the only remaining “Superpower” aka global empire. We have both the Democrats and Republicans to thank for this, including both Obama and Bush, except the Democrats try and act different, by offering us global communism. The problem is that total communism and total fascism are technically indistinguishable, both being centralized government totalitarianism. This is verifiable by the reality that the US ranks 5th as the worlds worst Police State, right behind North Korea, China, Belarus and Russia. Same holds true on the international ranking of surveillance societies. What happened to the Land of the Free, and what are the implications of the beacon of freedom in the world descending into such darkness?

Worst Police States in the World.

To declare with absolute certainty that there isn’t a group or groups of like-minded people, large and small, that have the same overall elitist agendas, especially considering all of the undeniable realities we face, is insanity. It’s not like there’s some watchdog organization that makes sure we’re not being undermined by oligarchy ‘clicks’. It could be said that there are, but they’re usually labeled kooky nutter conspiracy theorists and are ridiculed and shouted down. Meanwhile technology marches on, power is consolidated and wealth is concentrated worldwide, with the elites of the world getting closer and closer to becoming gods, and cutting us out.

It all starts with the technological agenda, the AGI Manhattan Project. Next comes the system behind it, and the war against the masses which has already begun. It ends with the psychology and philosophy of the people working for it, and those behind it.

The AGI Manhattan Project

Radical life extension, along with body & brain augmentation, each aspects of the growing movement known as “Transhumanism”, are the overarching goals of the establishment. The first and foremost “holy grail” goal is Strong AI, aka Artificial General Intelligence. The world is full of AI; from video games to the stock market. But these AI’s are “narrow” in ability. AGI refers to a “general” intelligence. Generally intelligent, not narrowly. Human level and beyond intelligence would greatly accelerate their other technological goals kicking off what they call the “Technological Singularity“.

Regardless of whether or not you believe this to be possible, they’re actively doing it, and they’re taxing you for it. There is absolutely no debate or refutation to this fact whatsoever. This isn’t even to say it’s possible, but they’re trying with all of their might (and your money)to do it. It’s right on public military websites, and in video statements by the higher ups and even heads of top tech corporations. The New York Times even recently did a piece, titled “Merely Human? That’s So Yesterday“, that championed Ray Kurzweil, Sergey Brin, Larry Page, Peter A. Thiel, Peter H. Diamandis and Keith Kleiner as being at the forefront of the Singularian Movement. The Singularity University, located at NASA’s Ames Research Center, is their epicenter.

Perhaps most importantly, especially considering how if they succeed it would be undoubtedly the biggest event in human history, and most potentially devastating, with almost no chance of turning back, it’s all happening without an ounce of public discourse or debate.

This overall effort openly involves virtually every government agency and department, every branch of military, which are all funded by Congress, and led by the administrations of both George Walker Bush and Barack Hussein Obama. It also involves the projects and supercomputers at literally all major all national laboratories, along with virtually all national universities, and all of the above tied in with the majority of the crony heads of the top technology corporations.

The Intelligence Industrial Complex
In July of 2010, the Washington Post unveiled “Top Secret America“, a massive 2 year investigative journalism story with an interactive presentation detailing the post-9/11 security and intelligence apparatus. Their investigation into this realm of Military Industrial Complex uncovered some 1,271 government organizations, 1,931 private companies in about 10,000 locations, an estimated 854,000 contractors holding top-secret security clearances,  all working on programs related to counter-terrorism, homeland security and intelligence  across the United States. In Washington, and the surrounding area 33 building complexes for top-secret intelligence work are under construction or have been built since September 2001. Together they occupy the equivalent of almost three Pentagons or 22 U.S. Capitol buildings – about 17 million square feet of space.

All of that based on the premise of stopping Al Qaeda. Now 100% of the above wouldn’t be exactly be specifically about building AGI, but that is the overall security and domestic spying apparatus. What their massive report didn’t tabulate is the direct AGI Manhattan Project efforts being conducted primarily by DARPA, NASA, NIST and the NSF.

DARPA
The Pentagons mad science coordination division, aka Defense Advanced Research Projects Agency (DARPA), sits at the top of this dragnet of science research & development (R&D) gathering. Enter the heart of science R&D pyramid… the AGI Manhattan Project.

DARPA is the lead agency. They are both the capstone, and the foundation. They coordinate national labs & universities, companies and corporations, and agencies with all branches of military. Their scientific “thrusts” run the entire gauntlet of transhumanism related efforts, from cybernetics to life extension to next-gen Skynet level artificially intelligent cognitive computers. They direct the R&D to the most appropriate groups and institutions, and then help orchestrate systems wide integration upon completion.

To cite all relevant quotes from their various programs could take half a book. At this juncture there’s only space to list and link the programs, which are basically all modules of the same goal:
Architectures for Cognitive Information Processing (ACIP), Biologically-Inspired Cognitive Architectures (BICA), Omnipresent High Performance Computing (OHPC), Real-World Reasoning (REAL), Cognitive Assistant that Learns (CALO), Deep Green (DG), Cognitive Information Processing Technology, Physical intelligence (PI), NetTrack (NT), Bootstrapped Learning (BL), Deep Learning, Integrated Learning (IL), Transfer Learning (TL), Accelerated Learning, Machine Reading (MR), Robustness of Biologically-Inspired Networks (RoBIN), Ubiquitous High Performance Computing (UHPC), Neurotechnology for Intelligence Analysts, Bio-Molecular Nano-Devices/Systems (MOLDICE), Biomimetic Computing, RealNose, Towards a Unification of Inference, Reasoning and Learning, Global Autonomous Language Exploitation (GALE), Self-Regenerative Systems (SRS), and Systems of Neuromorphic Adaptive Plastic Scalable Electronics (SyNAPSE).

This video was made using all government / military quotes and imagery.

It’s very difficult to even attempt to place budget figures on DARPA. They have their budget, as well as their cousins IARPA & HSARPA, while a lot of work by NASA, the NSF is in lockstep, not to mention military black budgets and secretive CIA & DIA budgets.

Funding for virtually every aspect of government agendas has hardly even decreased, while many areas have seen increases. The unique thing about DARPA is they aren’t limited by their budget alone.

NASA
Singularity University, Intelligent Archives (IA), Intelligent Systems, High-End Computing Capability (HECC), Integrated Systems Research, Nanotechnology, Biotechnology, Cognitive Sciences, and a dizzying array of other complex projects in those research areas. One project in particular stands out here:

NASA’s “Planetary Skin” program seeks to build a “global nervous system” network of sensors to monitor the entire planet, with all nations hooked into the system. It’s being sold on over-hyped Global Warming alarmism, and it intends to help the global management of resources, building a new carbon based economy. Watch the video. By its very nature it’s the ultimate act of high treason, a total stampede over national privacy and sovereignty, that’s costing us $100 million in it’s initial phase.

National Science Foundation (NSF)
Adaptive Systems Technology (AST), Cyber-enabled Discovery and Innovation (CDI), Behavioral and Cognitive Sciences (BCS), Emerging Frontiers (EF), Core BIO Investments, Adaptive Systems Technology (AST), Information and Intelligent Systems (IIS), Science and Engineering Beyond Moore’s Law, Cyber-physical Systems, Cognitive Engineering, Mapping the Brain in Time and Space, Cognitive Engineering,

NNI
One good example of virtually every government agency working in lockstep towards the Technological Singularity is the National Nanotechnology Initiative. The following institutions are all coordinated under the NNI, by the cabinet level National Science and Technology Council (NSTC):
Bureau of Industry and Security, Consumer Product Safety Commission,USDA, Air Force Office of Scientific Research (AFOSR), Army Engineering R&D Center, Army Research Laboratory (ARL), Army Research Office (ARO), DARPA, Defense Research & Engineering (DDR&E), Defense Threat Reduction Agency (DTRA), Office of Naval Research (ONR), Department of Education, Department of Energy, Department of Homeland Security, Department of Justice, Department of Labor, Department of State, Department of Transportation, Department of Treasury, EPA, FDA, Forest Service, US Intelligence Community, U.S. International Trade Commission, NIH, NIST, NASA, NSF, Nuclear Regulatory Commission, Patent and Trademark Office and the US Geological Survey.

NBIC Conference
Another prime example of the system wide drive for the Singularity is a 2001 conference organized by the Dept. of Commerce and the NSF, which produced a 482 page document titled “Converging Technologies for Improving Human Performance“. It had representatives and speakers from the following institutions:

The White House, National Science Foundation (NSF), Department of Commerce, Newt Gingrich, NASA, National Institutes of Health, Hewlet Packard, Institute for Global Futures, National Science and Technology Councils Subcommittee on Nanoscale Science Engineering and Technology (NSET), IBM, Raytheon, Lucent, University of California, Stanford University, Sandia National Labs, Brandeis University, MIT, University of Washington, University of Strathclyde, Tissue Informatics, University of Pennsylvania, University of Louisville, NYU Medical School, University of Calgary, Duke University, University of Texas, UCSB, Rensselaer Polytechnic Institute, National Institute of Standards and Technology, Carnegie Melon University, Department of Defense, DARPA, Naval Research Laboratory, Defense For Research, New England Complex Systems Institute, University of Virginia, University of Maryland, Institute of Nanotechnology, Office of Science and Technology Policy, Commission on the Future of Aerospace, US Nuclear Regulatory Commission, Defense Threat Reduction Agency, The EPA, Department of Chemistry, Princeton Materials Institute …

The goal of the meeting wasn’t merely to promote the 4 “NBIC” technologies:
“Four transforming tools have emerged: nanotechnology for hardware, biotechnology for dealing with living systems, information technology for communication and control, and cognition-based technologies to enhance human abilities and collective behavior.”

Instead it was about structuring collaborative research to promote the converging of the 4 revolutionary science paradigms into an all new form of substrate. The goal being eventually to create and merge humans with new forms of synthetic “life”, to become “Post Humans”, and to merge humans into a brain implant enabled “hive mind” (that’s a quote):

Hive Mind
If we can easily exchange large chunks of knowledge and are connected by high-bandwidth communication paths, the function an d purpose served by individuals becomes unclear. Individuals have served to keep the gene pool stirred up and healthy via s exual reproduction, but this data-handling process would no longer necessarily be linked to individuals. With knowledge no longer encapsulated in individuals, the distinction between individuals and the entirety of humanity would blur. Think Vulcan mind-meld. We would perhaps become more of a hive mind —an enormous, single, intelligent entity.

Singularity University
Another choice example of cross-sector collaboration to construct the Singularity, is the Singularity University, which is housed at none other than the NASA Ames Reserch Center (ARC), in Silicon Vally. It’s partners include Google, ePlanet, Autodesk, Motorola, FIAP, Steelcase, 23andMe, Canon, LinkedIn, WordPress, KurzweilAI, University of California, Stanford and others.

Unducation
From there actual universities are the next realm of the AGI Manhattan Project. It would be absurdly counterproductive to even list only the universities which are directly awarded project solicitations from DARPA. But some of the universities with most relevance here are Standford, Carnegie–Mellon, Vanderbilt and the University of Chicago. These universities are amongst the forefront of transhumanist related research, and happen to be founded by robber baron industrial tycoons.

Eugenics propaganda.

These tycoons were heavy advocates for Eugenics, a race pseudo-science movement of the early 20th Century, and their pet project schools listed above were amongst the leading fountain heads for eugenics theory. If you’re not aware of the history of eugenics this is required research material, it being the politicized science of 100 years ago, which utilized the same type of “crisis” fearmongering rhetoric that we hear today with “global warming” rhetoric.

By all measures, transhumanism is just the modern version of eugenics, the modern “self direction of human evolution”. A full history of eugenics and listing of their theories is beyond the scope here, but in short it was the race ‘science’ and methods of ‘solution’ that influenced Hilter‘s concentration camps. After Hitler’s vulgar display of eugenics the movement got a bad reputation and renamed it to transhumanism.

Today the link between transhumanism and eugenics isn’t merely in comparison or rhetoric, it can be found quoted right by James Hughes, the former Executive Director of the World Transhumanist Association (now known as “Humanity+”). In his book Cyborg Citizen he argues for moralitychips implanted in the brains of all citizens to ensure good behavior, class-based social policy, “global governance” through “world law” enforced by an “International Army”, UN “Power to tax nations and corporations” and state controlled eugenic enhancement programs.

Corporations

Google was the primary institution behind the Singularity University, which is no surprise considering Google’s co-founders have repeatedly stated on the record that they intend to develop AI that in their words “would be like the mind of God“, which by default would be AGI. AGI is in effect the first sentence on their corporate philosophy page.

Their mission statement is to gather and organize all of the worlds information (literally all of it), and their statements are for their machine to understand all it it better than you or I ever could. This includes every book, scientific paper, web page, email, instant message, news & magazine article,      ever written by humans that they can manage to get their hands on. It also includes images, user made videos (not even only those posted on YouTube), every movie and TV show ever recorded.

From there, Google is rapidly expanding into the phone and soon to be TV markets. While the TV side will only let them spy on you as well as the TV can, the phone market gives them real time GPS tracking with audio & camera monitoring. They’re on the record saying they already monitor everyone via their PC microphones, and it doesn’t end there.

Google’s model from the ground up is in building what they call “the mind of god”, knowing and “understanding everything in the world”, and in this pursuit they’re connected to the government and military to the core. The Google Boys truly are brilliant, as they’ve designed their system and all of their products to make the system smarter every time all of their users use them. Meaning, every time you use their ‘free’ services, and things like their phones, you help bring their “mind of god” scenario closer to reality.

It’s important to note that Google has a 1.2 million square foot research complex leased on NASA’s ARC, which is a borderline military facility. The main Googleplex HQ is almost literally next door neighbors of the ARC, and they use it to land their corporate and private aircraft. Google was a NASA / DARPA / NSF / CIA funded startup, and today they’re openly partnered with the NSA which has an open record of spying on the U.S. populace.

Google is but one corporate example.

Apple

Apple recently purchased a DARPA AGI-precursor pet project named “Siri” (PAL / CALO), for a cool $200 million. They didn’t actually buy it from DARPA, instead they bought it from Stanford Research Institute (SRI) who DARPA paid $150 million to make. That’s right, US taxpayers paid SRI $150 million to then turn around and sell the product to Apple for another $200 million, while themselves keeping what they need to build even more powerful AI in less time.

IBM

While Google is at the AGI forefront in software, IBM is leading the AGI renaissance in revolutionary hardware and mammalian brain simulation. Projects range from their Blue Brain to DARPA’s SyNAPSE (as explained by them in the video above). IBM’s Almaden Research Center is a major hub in AGI coordination where they host annual conferences for AGI luminaries to have a gathering of the minds.

Intel

When talking about hardware don’t leave out Intel. The Singularity is the passion of their CTO, as he explains in the video above and countless others. They’re even working on brain implants, perhaps to help Google reach their dream of everyone having Google built into their brains.

HP

Hewlet Packard’s 10 year “Central Nervous System for the Earth” (CeNSE) program is likely the inspiration behind NASA’s Planetary Skin. They seem to have been in the lead of their own little realm of AGI Panopticon, while the other bigshot corporations take care of the rest of its aspects.

Microsoft, Cisco, Oracle, Yahoo, Sun, and endless others are also lockstep in the AGI Manhattan Project, all envious of Google’s leading role. It needs to be noted that federal funding budgets don’t include the funding allocated by these corporations themselves, or other outsiders, making assessing the true funding of the AGI Manhattan Project virtually impossible, but just going by non-secretive federal budget numbers it’s in the billions annually, not to mention parallel efforts in the UK & EU.

Congress
The 110th U.S. Congress, released a report on the Singularity, in 2007:

Every exponential curve eventually reaches a point where the growth rate becomes almost infinite. This point is often called the Singularity. If technology continues to advance at exponential rates, what happens after 2020? Technology is likely to continue, but at this stage some observers forecast a period at which scientific advances aggressively assume their own momentum and accelerate at unprecedented levels, enabling products that today seem like science fiction. Beyond the Singularity, human society is incomparably different from what it is today. Several assumptions seem to drive predictions of a Singularity. The first is that continued material demands and competitive pressures will continue to drive technology forward. Second, at some point artificial intelligence advances to a point where computers enhance and accelerate scientific discovery and technological change. In other words, intelligent machines start to produce discoveries that are too complex for humans. Finally, there is an assumption that solutions to most of today’s problems including material scarcity, human health, and environmental degradation can be solved by technology, if not by us, then by the computers we eventually develop.

Obama
While the AGI Manhattan Project really came to being under Bush (the “Christian”), Obama has brought it out of the lab and into his house. Obama, who likes to talk about innovation in technological revolutions, put one Zachary Lemnios as DoD Director of Defense Research & Engineering. This guy helped setup DARPA’s IPTO to spearhead the type of AI you see in the movies.

“America risks being left behind in the global economy: Revolutionary advances in information technology, biotechnology, nanotechnology and other fields are reshaping the global economy. Without renewed efforts, the United States risks losing leadership in science, technology and innovation.”

That’s what Obama’s campaign website said the day he was elected (which is completely removed now).

The “Revolutionary” advances he’s talking about are Artificial General Intelligence (“information technology”), genetic engineering / synthetic biology & designer babies (“biotechnology”), and too much in terms of nanotechnology to sound-byte like the others. The “other fields” he mentioned is almost certainly the other field he didn’t mention, cognitive sciences.

Google is at the forefront of this thing, with as deep of governmental integration as is possible (literally), including today with agents embedded in the Obama administration.

Google CEO Eric Schmidt and their “Chief Internet Evangelist” Vint Cerf were on Obama’s campaign team, and campaigned with him on the Obama jet, and was then immediately appointed ‘Special Economic Adviser’ on a panel of Federal Reserve and Goldman Sachs henchmen. Today he sits on Obama’s President’s Council of Advisers on Science and Technology.

Google managers and employees were some of the strongest supporters of candidate Obama, donating around $803,000 to his presidential campaign, according to the website OpenSecrets.org. Among corporate employees, only staffers at Goldman Sachs and Microsoft gave more.
…
Google’s fingerprints are visible on a broad new report on the future of the Internet and information commissioned by the Knight Foundation and the Aspen Institute. The paper calls for greater broadband deployments and “open-access policies.” FCC chairman Julius Genachowski and the administration’s chief technology officer, Aneesh Chopra, praised the report, saying it would guide Obama’s web policy. The co-chair of the commission that wrote the report? Google vice president Marissa Mayer.

Read my lips: ‘No Lobbyists In My Administration‘! Some other Google agents in the Obama administration include Sonal Shah, Sumit Agarwal, Andrew McLaughlin and formerly Katie Jacobs Stanton.

Ray Kurzweil is essentially the messiah of the transhumanist movement, and in 2007 he did a double-header keynote speech with Obama in front of United Church of Christ in Hartford, Connecticut.

Al Gore
At the SC09 (Supercomputing 2009) conference, Gore, the main keynote speaker at the event, in his speech titled “Building Solutions – Energy, Climate and Computing for a Changing World”, to an audience of 11,000 top technologists and technocrats, he argued that ‘supercomputing’ will save us from Global Warming.  This wouldn’t be the first time he’s implied supercomputers will be our savior. In 2005, in front of nearly 2,000 technologists and technocrats, at Stanford’s Memorial Auditorium, Al Gore had then also appealed to massive supercomputers as being the savior from global warming.

The audience was filled with Silicon Valley luminaries: Apple’s Steve Jobs; Google’s Larry Page and Eric Schmidt; Internet godfather Vint Cerf; Yahoo!’s Jerry Yang; venture capitalists John Doerr, Bill Draper, and Vinod Khosla; former Clinton administration defense secretary William Perry; and a cross section of CEOs, startup artists, techies, tinkerers, philanthropists, and investors of every political and ethnic stripe.

The goal: to enlist the assembled leaders in finding market-driven, technological solutions to global warming and then, in quintessential Silicon Valley style, to rapidly disseminate their ideas and change the world. “I need your help here,” an emotional Gore pleaded at the end of the evening. “Working together, we can find the technologies and the political will to solve this problem.” The crowd fell hard. “People were surprised,” says Wendy Schmidt, who helped organize the event and, with her husband, Google CEO Eric Schmidt, supported Gore’s 2000 presidential campaign.

Ever since Al  ”lost’ the 2000 election, he’s been serving on the Senior Board of Directors at Google, as well as at Apple Computer since 2003. The 1986 “National Science Foundation Authorization Act”, which was, in part, for the establishment of a global warming policy. What’s typically overlooked is the 2nd part of that same Act that was for the drive for the NSF/DARPA “supercomputing” program. Then, only 2 years later, in 1988, Gore authored legislation to:

“ESTABLISH A HIGH-CAPACITY NATIONAL RESEARCH COMPUTER NETWORK, DEVELOP AND DISTRIBUTE SOFTWARE, DEVELOP ARTIFICIAL INTELLIGENCE PROGRAMS“

Al also campaigned for U.S. President that year, and according to him, his main goal of that campaign was more about increasing awareness of global warming than it was about actually winning.

Today Google enjoys perhaps the deepest government integration in history, with their primary operations being centered around AGI, and Apple just recently bought DARPA’s ‘Skynet precursor’ from SRI. Until 2009, Eric Schmidt sat on Apple’s Board of Directors with Al Gore, both of whom were implicated in a 2006 stock options backtrading scandal with Steve Jobs.

Newt Gingrich
Decades ago he was closely allied with Al Gore’s “Atari Democrats“, and futurist Alvin Toffler, which had left a lot of people scratching their heads as to why he was the top “Republican” for so long.

At that “Converging Technologies for Improving Human Performance” event, Newt Gingrich did the key keynote presentation, and in it he refers to our current era in time as the “Age of Transitions”:

We are starting to live through two patterns of change. The first is the enormous computer and communications revolution described above. The second, only now beginning to rise, is the combination of the nanotechnology-biology-information revolution. These two S curves will overlap. It is the overlapping period that we are just beginning to enter, and it is that period that I believe will be an Age of Transitions.

Focusing on computers and communications is only the first step toward understanding the Age of Transitions. While we are still in the early stages of the computer-communications pattern of change, we are already beginning to see a new, even more powerful pattern of change that will be built on a synergistic interaction between three different areas: the nano world, biology, and information.

The sciences have reached a watershed at which they must combine in order to advance most rapidly. The new renaissance must be based on a holistic view of science and technology that envisions new technical possibilities and focuses on people. The unification of science and technology can yield results over the next two decades on the basis of four key principles: material unity at the nanoscale, NBIC transforming tools, hierarchical systems, and improvement of human performance.

After he resigned (right while Bill Clinton was being impeached), he went on to stand together with Hillary Clinton in setting up computerized health records. One the one hand it can help some people, on the other it completely deprivatizes our health records by allowing the federal government instant access.

Bill Clinton
Quote: “We want to live forever, and we’re getting there.”

Manhattan Project v2.0
National laboratories are the final “public” realm. Literally all of them, and their supercomputers are fully integrated into the aforementioned apparatus. One example of choice would be Los Alamos, which was the home of the original Manhattan Project. They’re hooked up, along with many leading universities, into the NSF’s TeraGrid network, which is a super high speed advanced version of the Internet, designed specifically for large scale science collaboration across institutions, enabling access to the various different top-in-class supercomputers. What puts DARPA at the top of the scientific pyramid is that they have access to mining literally every resource, meaning even indirectly supportive work done at different levels are still at their disposal for concept and results mining.

Major sites in Manhattan Project v1.0.

Oversimplified Manhattan Project v2.0.

It can be ascertained that the countless thousands of people indirectly involved in it don’t even realize what they’re a part of. With global telecommunications now being radically different than 60 years ago, private intranets can connect up any remote office or personal computer as a collective.

This means that a modern day Manhattan Project could be operated across the planet in ‘secret’ with great ease. This would especially be the case if you had literally a million or more parallel platformed CPU’s at your disposal (like Google does). Consider that computing power per $1000 is literally less than millionth what was during the Manhattan Project, and that project only cost about US$24 billion. Anything even resembling a modern semiconductor computer hadn’t even been invented yet. Meanwhile, every year their capabilities expand as CPU prices drop and work gets easier, exponentially, thanks to Moore’s Law and the Law of Accelerating Returns. The original Manhattan Project had about 100,000 workers, mostly all doing physical labor. The AGI Manhattan Project can easily have more than that figure, mostly all doing direct scientific research.

The Debate Over The AGI Manhattan Project Is Over!
Unlike the issues being exploited to operate it, there’s no debating the existence of the AGI Manhattan Project.  The issue is what the intentions of the true elites that shape U.S. policy have in mind for all of this. Listening to the PR people of transhumanism should offer a safe insight: becoming “gods”.

There’s a war being waged against us. A great many of the people on the planet are feeling the effects from this already, via the economic meltdown. While the generic economic war didn’t against us started generations ago, the modern technological war came before the economic assault, so we’ll explore that first.

ignoranceisfutile.org
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Children

These graphs begin when the Dept. of Education was founded.

We’re being targeted as children with social engineering indoctrination, to be desensitized to perpetual surveillance, while being systematically dumbed down. Every year school children’s productivity scores twirl around the downward spiral, despite increases in Dept. of Education spending annually. You get what you pay for. Today when we’re born our DNA goes into a federal DNA Databank. Next the children are targeted by manipulative marketers openly bent on turning them into mindless brand loyalist consumers via TV and other forms of media.

On the way to school they face being monitored via microphones while riding the bus, iris scanning at the entrance, and then they’re under the watchful eye of cameras and on duty police, including cameras in the restrooms and in some cases inside the actual toilets, and at lunch they might have to pay using their thumbprint. Finally, when they go home they have to worry about being recorded by camera and microphone by school issued laptops while being tracked with GPS trackers.

TSA
Perhaps in a few years the system will start installing full naked body scanners into schools like are going into all of the airports. As adults we’re being trained to be subjected to being frisked or filed into a naked body scanner, which are meant to become mandatory. You would never see a government official go through one of these and then post the images online, yet in the UK even children are supposed to go through them even though it violates child pornography laws.

All of this over a ‘panty bomber’ plot that didn’t succeed, where reports suggest that the scanners wouldn’t have caught him, while the real problem was that he got on the plane without a passport. All of this being conducted by the TSA, while Obama has appointed a controversial spy figure to head the agency. It’s no surprise when we hear reports of maniac TSA employees power tripping over citizens and literally declaring themselves to be god.

In Our Homes
We’re not even allowed to have privacy in our homes. It used to be illegal for any level of government to tap our phones without a warrant. But then Bush’s FedGov unilaterally decided it would, and after breaking the law the Democrat Congress adjusted the ‘laws’ to allow it while giving telecom companies immunity. Obama campained on stopping telecom immunity, and then immediately moved to protect it. Now the Army, NSA, FBI (more), Justice Dept. and others do it anyways with an ongoing record of abuse, while storing untold amounts of data in vast databases. Under the “Patriot Act” they can literally break into your home without anyone’s knowledge and go through your things and plant bugs, which opens the door to the planting of false evidence.

They peek into our mail. Popping up in neighborhoods are police cameras with high-res night vision lenses than can zoom into peoples windows. Every census has them asking ever more personal questions, this time asking virtually everything, while having the census takers use a GPS transponder to mark your front door into their system. This is precisely what they used to do in the Soviet Union. Today it appears on virtually all fronts that despite out living the Soviets, the US federal government has become the enemy and makes those who criticize it enemies of the state.

Online Activities
When we’re being targeted, it can be assumed that we’re the enemy. We’re especially targeted on the Internet. Not only do many of the relevant Internet companies store our personal emails and surfing habits, they’re pushed by various levels of government to do so for at least 5 years. Between the Pentagon, Air Force,  DARPA, CIA, FBI (more), NSA, EU and local police we’re monitored browsing the web, using all of the major social networks and in online video games. In case you assume they don’t have enough people to do all of this, they’re using AI in countless forms to catalog and chronicle all of the data they can.

They even use AI to assess bloggers moods & opinions, for “hate speech” and other “subversive” behavior. All of this for domestic citizens, as now the “terrorist threats” are citizens from “supporters of the Constitution“, to “Luddites” and “conspiracy theorists” who complain about all of this Big Brother technology invading their rights to privacy. Next Obama is moving to create an ID token “Identity Ecosystem” designed to remove passwords from everything we do, where instead our personal names are tied to every single electronic device and component therein, right down to the flash memory chip you plug into your digital camera.

Tracking
Then when we try to leave our homes it’s the same story. You walk out your door and a military satellite might spot you. Then you get into your car, that has an increasing chance of being equipped with trackable GPS. You’re tracked as you drive down the road to have your face and license plate and scanned by cameras that mail you your traffic ticket via robotic automation. Mandatory black boxes are being proposed for all new vehicles that record even more data. Stop in for a tattoo and you might falsely get caught up in an FBI investigation. Our airfare travel and border crossings being recorded, travel funds even being frozen, yet illegal immigrants are allowed to run rampant in border regions causing an escalating drug cartel warzone situation.

This crisis is caused not just by a flawed border policy, but by us not being free to do what we want with our bodies. According to the federal government, even when states decide for themselves that it is, but this is beside the point. Biometric ID cards were first proposed to domesticate the illegals, and now they’re about to be forced upon us all as an unconstitutional National ID, while the Fed’s are setting up a National Biometrics Agency.

Also consider that vice president Joe Biden once promised Supreme Court justice Roberts that one day he’d have to rule on whether or not everyone would be forced to take an implantable microchip to track their whereabouts via satellite.

Cell Phones
We’re being “Reality Mined” via our cell phones. Even if you try to walk, your cell phone has tabs on you. Under Bush the precedent was set for us to be physically tracked via both triangulation and GPS and to be monitorable in real time via the microphone or camera. Obama’s Justice Dept. fought in court in 2010 to keep it active. Even if the phone is turned off, the feds and police can still activate the microphone. You literally have to remove the battery to stop it, while the more sophisticated phones like those made by Apple and Google have increasing methods to be able to study our behavior, and to condition us to actually enjoy being tracked and monitored 24/7.

These phones have the ability to transcribe all of our conversations spoken within the phones microphone range to be cataloged, which is a particular threat to business people considering you’re literally trusting all of your trade secrets and insider information with corporations like Google who have their own automated shopping system. The Google Android phone even has a free app that ‘lets’ you take a snapshot of your eye’s iris so they can store it in their NSA databanks, while the army is developing high speed iris scanners that scan rapidly scan entire crowds of people.

Next Homeland Security wants private industry to integrate smell sensors into out phones, while DARPA is trying to scent sensing capability able to detect, track, and even positively identify people and detect “aggression or hostile intent”.

Neurometrics
Just as the public is gradually discovering the world of biometrics, newer neurometrics are becoming commonplace. In recent years scientists have managed to use brain imaging to read the human mind. Successes include being able to see what a person is seeing, knowing who a person was spoke to and what was said, what number a person has seen, memories of where someone been, where thoughts of familiar objects occur inside the mind and predictive analysis of what a person is thinking about.

Today these successes and others has the military and other security agencies pushing for checkpoint based as well as mobile mind and behavior scanners. Desired and even existing products range from airport screening mind readers, micro-expression behavior scanners, voice analyzers, binoculars from Northrop Grumman to detect threats through brain activity, super sensitive lie detectors, and voice recognition software that reads peoples brainwaves.

TIA

Next we have DARPA’s Total Information Awareness program. TIA was to be about gathering and linking every scrap of data possible on people through massive artificially intelligent data mining supercomputers, and then to create complex maps of every possible connection people have to one another. Even private banking records aren’t safe from government prying. Initially Congress ruled to shut it down as being unconstitutional, but it didn’t take long before it was parted out amongst the various expected agencies of interest, all connected under Homeland Security. After a few years mainstream media reports of it still being alive began to surface, and the new Democrat congress did nothing to stop it.

FBI Surveillance is to the hilt unconstitutional, and surveillance software is expected to quadruple by 2013. Today Fusion Centers are being set up in every state using the TIA framework, manned by military, federal and state police officials, all under Homeland Security and endorsed by Obama. All of this data cataloging of virtually everyone, even though it’s proven that datamining doesn’t even work at tracking terrorist cells. Maybe a new Domestic Intelligence Agency can solve that?

Cyberwar
Despite cyber security being overhyped as usual, the military with Homeland Security and the NSA have created the Office of Cyber Command (CyberCom) “as a unified, sub-division of U.S. Strategic Command to operate the Defense Department’s information resources of 15,000 computer networks across 4,000 military bases in 88 countries”. The modis operandi acronym for this thrust is C4ISR, which stands for “Command, Control; Computers, and Communication Intelligence Surveillance & Reconnaissance”.

Overall efforts in this domain are filled with controversy. Obama’s first Director of the National Cyber Security Center (NCSC) quit after less than a year, stating that the nation’s computer security efforts poses “threats to our democratic processes.” Obama’s replacement lacks accountability not even being allowed to testify before congress. Other agendas include making it a serious crime for using file sharing networks, to an “Internet Kill Switch” that can shut down the web or sectors of the web considered a threat, to it being used in the War on Drugs (much like the Patriot Act and Homeland Security are).

Various powerful AI agents are being developed for all of this. One is the Ubiquitous Network Transient Autonomous Mission Entities (aka Cybots) program that a team of researchers is developing at Oak Ridge National Laboratory. Another is called CyberStorm developed by a private company named Trusted Computer Solutions. Another is an NSA program called “Perfect Citizen“.

AGI Panopticon
All of these tracking systems are being integrated into a pervasive and ubiquitous 3 dimensional real time global surveillance system. Stopping global warming is stated in the first paragraph of the official description of NASA’s “Planetary Skin” global nervous system. As Hewlett Packard prepares the nerves for it via technologies such as “smart dust”, IBM is working with DARPA to build the “global brain’ AGI system to hook it all into. All of this tied together via the military “Global Information Grid“. The EU has the same idea as they’re building a global monitoring system being designed to also predict into the future. It’s no wonder there’s all this talk about a global government starting with deep USA & EU integration.

This goes beyond just having a bunch of everyday cameras on the street. It’s about a full scale real time 3D monitoring system composing all different sorts of state of the art AI enabled predictive sensors from smell to imagery, from below to above from ground to satellite.

DARPA programs that are part of the AGI Panopticon include:
Mind’s Eye, Fine Detail Optical Surveillance (FDOS), Flow-based Information Theory Tracking (FITT), Persistent Stare Exploitation and Analysis System (PerSEAS), Exploitation of 3-D Data (E3D), Urban Reasoning and Geospatial Exploitation Technology (URGEnT), Standoff Precision ID in 3-D (SPI-3D), Persistent Operational Surface Surveillance and Engagement (POSSE), Autonomous Real-Time Ground Ubiquitous Surveillance – Infrared (ARGUS-IR), Cognitive Technology Threat Warning System (CT2WS), Fopen Reconnaissance, Surveillance, Tracking and Engagement Radar (FORESTER), NEOVISION2, NetTrack (NT), Harnessing Infrastructure for Building Reconnaissance (HIBR), and Conflict Modeling, Planning, and Outcomes Experimentation (COMPOEX).

The combination of all of these aspects would have this system able to see through trees, walls and deep into the ground; while having billions of sensors of all types and sizes spread out across the earth; in and on everything. And guess who gets to pay for it.

Reality Check
It’s worth noting that in 2003 9,000 people died in automotive accidents, three times how many died on 9/11, a single disaster which could have been prevented without any of these new Orwellian technologies, or a Police State.

The thing about 9/11 was that same day Bush said the terrorists attacked our freedoms, which was then parroted by media pundits and politicians for years. Yet the federal government has been the one attacking our freedoms increasingly and persistently, doing things to us that won’t stop Islamic terrorism, while doing things that is creating more terrorists globally, while not even doing things like securing our borders where terrorists could infiltrate our nation with supposed suitcase nukes. The “American” people are the ones being targeted across the board as terrorists, as enemies of the state. Guilty until proven innocent, and then still suspect needing to be monitored and tracked.

Stop The Neo-Luddites
There are already efforts to demonize “Luddites” or “Neo-Luddites” as terrorists. People who oppose technological progress are generally called Luddites. It was a late 19th Century movement with the most famous case being the more modern Unabomber. Today if you opposed the Big Brother AGI Panopticon that gets you the stigmatized label Neo-Luddite.

In 2009 Homeland Security released a document titled “Domestic Extremism Lexicon“, which listed Neo-Luddites as terrorists, right above “Aryan prison gangs”. This document followed the 2009 “MIAC Report“, which listed opponents of global government and forced RFID ‘Verichip” implants, as well as the supporters of third party candidates such as Ron Paul, as potential militia terrorists. In a 2008 paper written by Cass Sunstein, head of Obama’s Office of Information and Regulatory Affairs, said that “conspiracy theorists” need to be infiltrated, which sounds an awful lot like a modern COINTELPRO.

Richard A. Clarke, former conterterrorist czar and today special advisor to Obama, wrote a fiction forewarning book “Breakpoint”, that tells a tale set in 2012 about Luddite terrorists. The Luddites are trying to stop a global artificial intelligence network dubbed “Globalgrid” & “Living Software” that was being built by DARPA, NASA Ames and the Googleplex with help from Carnegie-Stanford.

Then we have Dr. Michio Kaku, a top level transhumanist technocrat elitist, who says those who oppose global government & transhumanism are “terrorists”. You might have seen him in his 3 part BBC documentary “Visions of the Future”.

Protests
Protesting virtually any issue out there gets you added to terrorist watch lists, especially now that the Pentagon has labeled protesting “low level terrorism“. The Obama administration wants it so that if you’re put on a terrorist no fly list you can’t buy a firearm, without any conviction, while 6 years old kids have been rejected at airports for being on the list. So if you protest any issue you might not be able to travel or buy a gun. And if you do protest you may face brutal consequences.

Police riot squads already have or are developing a daunting array of Milspec sophisticated “non-lethal” weapons including sonic cannons, microwave pain beams, optical ‘vomit beam’ guns, shotgun and grenade launcher fired tasers, “Shockwave” swarm fired taser batteries, crowd blaster tear gas launchers and discuss other sickening things like chemical neurowarfare and microwave beams that will rain pain from the sky for use against demonstrators. Odds of facing these weapons are higher than you’d think, as at protest after protest police agent provocateurs are busted vandalizing businesses and burning cop cars to justify beating and arresting crowds of protesters. Under the “Enemy Belligerent, Interrogation, Detention, and Prosecution Act of 2010,” introduced by Sens. John McCain and Joseph Lieberman, you might even be detained indefinitely without trial for dissent.

Police State
The growing trend for the past several decades has been the militarization of the police, turning them into a standing army. There is now even a NORTHCOM marine hit squad brigade has been tasked with Homeland Security objectives, including the stomping of protesters. All of this is a violation of the Posse Comitatus Act, passed in 1878 to prevent the federal government from using the military for law enforcement.

Every year whichever president is in office signs new executive orders further consolidating the military takeover of the US, and Obama is no exception to this rule. We’re already under a state of de facto martial law, as we’ve been under a state of national emergency since 1995, and these executive orders are always written under the context of a national emergency. It’s also worth noting that by de facto 2/3 of U.S. citizens live in “Constitution Free Zones“.

Obama signed Executive Order 13528 establishing a “council of governors” to consolidate power over the National Guard. Laws are constantly introduced and even passed giving the military and federal government the ‘legal right’ to detain us in secret, against the foundational concept of Habeas Corpus, with no legal representation, indefinitely, where we can be brutally tortured and even ‘disappeared’ for ever. Whether or not you think that would ever happen is irrelevant, as this is already chiseled in stone. Ask yourself why they’d install such measures, and ask yourself why they’d have hundreds of designated civilian internment FEMA / Halliburtan / military camps (with barbwire pointing inwards) for detainment and civilian labor.

With all of the police and the half a trillion dollar plus budget military, ask yourself for what valid reason Obama has said repeatedly that he intends to set up a civilian national security force “just as large, just as well funded as the military”, that includes a mandatory draft and youth snitch brigades. Ask yourself why Homeland Security is training the Boy Scouts in SWAT team gear and tactics, on mock missions to subdue an Iraq War veterans.

Ask yourself why the military is constantly setting up checkpoints and patrol streets in cities across the US. Ask yourself why the military runs drills in US cities, that include foreign troops, doing mock roundups of groups of US citizens. Ask yourself why FEMA has a system of over 50,000 religious “Clergy Response Team” ready to help round up guns, and to snitch on potential freedom fighters that might go to their local religious leaders for rest. Ask yourself why the Bush administration said they could massacre US citizens.

Wake Up Call
Ask yourself what these things have to do with terrorism, when the policies and actions of the federal government are what is pissing everyone off domestically and around the world. Ask yourself why each new administration is more secretive than their predecessors, with Obama’s being worse than Bush’s even after all the “change” he campaigned on. Ask yourself why the military is openly and deliberately training kids to be killers via video games, and why they’re making the interfaces of military equipment based on games, when 1 in 3 homeless men are military veterans.

How is celebrating the 4th of July even legitimate, when faced with all of these things perpetrated by this illegitimate government, and federal taxes today are 50 times what the Boston Tea Party people had imposed upon them?

They Don’t Need Us
The military is pushing ever harder for an all out robot done military force. The Air Force already has its first entire drone fighter wing. Obama expended the war into Pakistan using drones, with a bruised record so far. Ground based drones already come with extensive weapons platforms, and nearly fully autonomous automobiles. Drones are being readied for police functions including squashing protests, while police are already using them in the US for surveillance.

They’re already autonomous, but currently the ability for the drones to fire on targets is disabled. But DARPA and friends such as Northrup Grumman, Lockheed Martin, and Boeing push forth for more powerful drones of different variants, with MESH grid connectivity. Mad science research has robot AI learning how to deceive to reach their objectives, and to learn evolve predator-prey strategies. For years mad scientists have had radio controlled rats, cockroaches, monkeys, dragonflies and more, but the problem is these aren’t self-guiding to their missions, can’t see through walls, and aren’t as good for hooking into the hive mind.

Neuro-Warfare

After September 11th the CIA’s infamous Project MKULTRA mind war program went back into overdrive. MKULTRA was originally about all creative forms of cognitive warfare from (successfully) wiping a persons entire slate of lifetime memories totally blank, to cognitive enhancement to mind control. Today there’s no telling what secretive projects the CIA and their spook collaborators have been up to, but public developments can be a strong indicator.

One example would be the NSF’s “Cybertools” 2 part program is both sociological and psychological. The Psychological aspect, carried out by the University of Chicago, developed:

tools for collecting and analyzing human behavioral data on an unprecedented scale and level of sophistication. In their “SuperLab,” the multidisciplinary team of researchers will be able to track human behavior in both individual and group settings, while collecting exquisitely detailed data on the participants in real time. These data, in turn, will help the Chicago group address research questions that far exceed the capacity of any laboratory today. How is social behavior correlated with the participants’ neural activity, for example? How is it connected with their movements, postures, gestures, facial expressions and speech–or for that matter, their state of development, environmental context and cultural norms? Central to the Chicago group’s effort will be the creation of a distributed data warehouse known as the Social Informatics Data Grid (SID Grid): a piece of cyberinfrastructure will encourage data sharing and accelerate the development of standards for collecting and coding physiological and behavioral data. The SID Grid will be deployed as part of the larger TeraGrid, a suite of grid computing resources available to the scientific community at large.

The Chicago group will develop, test, and refine their data collection and analysis tools through research in three areas of inquiry: multimodal communication, neurobiology of social behavior, and cognitive and social neuroscience. But they foresee many other uses for the tools they will create. Most notably, their efforts will contribute to research on how human behavior can be automatically extracted, and even interpreted, from media like audio and video recordings. Such research may open the way towards mining the truly vast amounts of data on human behavior that are recorded every day.

Humans can be and are programmed and manipulated via numerous means  such as psychiatric drugging or operant conditioning via electric shock. Humans can actually be physically controlled via remote control by pulsing soundwaves just behind the ears, and our moral judgments can be altered via electromagnetism.  Considering the fact this kind of research is going on out in the open it hardly even has an impact on people when they hear that France has made it a crime to yell at our spouse, or Obama’s plan to mandate “lifestyle behavior modification”.

It’s bad enough that marketers are using brain scans to test the effectiveness of TV commercials, but then we have the National Research Council and the Defense Intelligence Agency releasing reports that the human brain is the battlefield of the future. Then we have the Army preparing to give soldiers “synthetic telepathy” via brain implants, with the Air Force bent on using bioscience to “artificially overwhelm enemy cognitive abilities.” On top of it all, why is Obama pushing for pre-crime arrests and indefinite detention?

Ecoscience
John Holdren, Obama’s Science Czar, coauthored a book, “Ecoscience“, with Paul Ehrlich who is an infamous top eugenicist Malthusian doomsday theorist. In it they argued there needs to be a “United Nations” based “planetary regime” that institutes forced one child policies as well as adding sterilants to drinking water supply.

Considering this fact, ask yourself why we’re being sickened by countless softkill weapons, and denied recent safe cancer cures. Why did Bill Gates say that vaccines would be used to reduce the global population by one billion, while pushing $10 billion of his fortune to make this the “decade of vaccines“? And why is the wealthiest man in the world, Warren Buffet, doing this side by side with Mr. Gates?

Economic Warfare
By now there might even be aboriginal tribes people -totally off the grid- around the world that have heard about the Great Recession, so detailing it’s total implications is beyond the scope here. Instead the key causes and some of the key players and their connections to all of this is the focus.

Many people put all of the blame on the housing bubble, but a more realistic view is that that crisis only sped up the inevitable. The massive spending associated with bailouts and stimulation merely put off even longer the inevitable. The longer this inevitable is put off the harder the crash will be. Just look at the numbers. Spending got us into the mess, so in response they spend even more. Like it’s going out of style… literally.

It wasn’t originally designed to implode, despite that being how it looks today, but it’s always been designed to leech away the self-reliable wealth of those with less. The less you have the more it hurts you… is and always has been the purpose of the privately owned Federal Reserve bank. The mechanism responsible is inflation.

When the value of the dollar is deliberately reduced every year it creates a situation where you have to set up your surplus finances in ways that will hedge against the inflationary dollar devaluation. During ‘normal’ times, you could invest your money into your home or other property and as the value of the dollar goes down the value of the property would go up. This is just the opposite with automobiles which helps explain why social engineering has us all obsessing with dumping all of our money into our cars that are worth $10,000 less the day you drive it off the lot. Everybody’s primary financial concerns should be in how to position their earnings against inflation, not new spinner rims.

Now what happened with the housing meltdown is the big trend that makes it hard to believe that the design wasn’t to rob almost literally all of the populace, as normally the best thing the little guy can do is invest in his property so that he can fight off inflation. All those years most people thought their house was somehow naturally going up in value, in reality the dollar was going down in value and the markets knew it. Except now the value of our homes has plummeted, it’s unsafe to even invest in property, endless millions refinanced their homes and now owe more than the property is worth, and some 60% of US national assets have been absorbed by the Federal Reserve and the Big 6 banking cartel that are the majority stock holders in the “Fed”.

The other catalyst of the economic downturn was the fuel price crisis. It served as the 1-2 punch to the entire global economy. In the graph above you can see that the more fuel consumption went down the more the price went up. This is the opposite of how the market works, proving massive manipulation. What’s important about is it happened directly parallel to the housing collapse, which made its effects substantially worse than if it occurred in 1999. Assuming it was deliberate, what does this tell you about the titans of Wall Street and their disdain for the global populace?

That graph shows that neither  oil production nor inventory had never changed in ways to justify the spike in prices. On the contrary, inventories went up while consumption was down while mass scale price gouging like never before was in full effect. The answer for how this happened was market speculation. The big banks and hedge funds in effect ‘all’ got together and continuously bet in large scale that oil prices would go up, and sure enough that’s what happened. The costs of everything went up, people were broke, major institutions absorbed by the government & banks, the property markets crashed, and now the inevitable collapse is out in the open for everyone to see.

Note that during the peak of the oil crisis Obama actually went on the record saying that ‘fuel’ prices should be artificially increased so that people would use less fossil fuels. Now he didn’t say to raise oil prices in that particular quote, but inherently that is the overall goal of Cap’N Trade type policies, and we all had a devastating test run during the artificial fuel crisis. Can anyone say they were glad the test run of Cap & Trade happened?

Obama’s Treasury Secretary Tim Geithner is a Federal Reserve agent, being the former president of the New York branch Federal Reserve Bank. Other Federal Reserve agents in the Obama Administration include Paul Volker, Christina Romer, Alan Blinder, Robert Rubin and Lawrence Summers.

Click to enlarge.

As with 9/11, Bush ignored all of the warnings of the looming ‘economic 9/11’. His Treasury Secretary Hank Paulson was the former CEO of Goldman Sachs, a key player in the economic meltdown. Goldman has embraced the world of AI, with sophisticated AI supercomputers that utilize learning algorithms to conduct “high frequency trading” that allows them to literally cheat at the stock trading game, and in all likelihood conduct operations such as artificially raising global fuel prices. Goldman Sachs agents in the Obama’s inner circle include Gary Gensler, John Corzine, Rahm Emanuel, Mark Patterson, Neel Kashkari, Reuben Jeffery III and even Elana Kagen.

During the economic disaster, Goldman executives cheered their results, emails went on to show. All throughout the crisis, Sachs reaped billions of dollars in record profits while the rest of the world economy has floundered. In July of 2010 Sachs was fined the record amount of $550 million by the SEC for their role in the Subprime fiasco. The same day their stocks actually went up 5% as those in the game know how much evil they had committed, and were relieved at only having to pay a mere $550 million. Days after the settlement, Sach’s put aside $9 billion for employee bonuses.

Sachs was Obama second largest campaign contributor, funneling him $994,795, 7 times what Enron famously gave to Bush. His other top contributors included Google, Harvard, University of California, Microsoft, Citigroup, JP Morgan Chase, Stanford, IBM, Morgan Stanley, BP and General Electric.

Side note: General Electric is a corporation not yet discussed. It’s one of the largest weapons manufacturers in the world, and also has its hands in new green technologies like those mercury filled curly lightbulbs many environmentalists are pushing. As the top lobbyist in DC, and being one of the Big 5 media complex, these cronies reap profits from lobbying congress and propagandizing the populace in supporting both “defense budgets” and the global warming agenda.

These people are textbook “Disaster Capitalists”, those whose portfolios are stacked to reap profits and success in their goals via the mass scale suffering of others. It’s no secret that BushCo. was a regime of disaster capitalists, but ObamaCo. is too. Rahm Emanuel and Hillary Clinton have made public statements condoning the capitalization of crisis. The notorious Henry Kissinger said the economic crisis was a “great opportunity” for Obama to create a “new world order.” Disaster capitalists are amongst the greatest threat to the world, as having people set up to reap profits ranging from millions to trillions sets a precedent of why would they prevent the crisis, especially if there are agendas that transcend money. “Problem Reaction Solution” is the mechanism to our undoing.

Between the agents from the Federal Reserve many of the key players in the economic meltdown are all accounted for. On top of everything above, Larry Summers, under Bill Clinton, played a key role in repealing the Glass-Steagall Act, which was set up after the first Great Depression to prevent it from happening again. He also helped deregulate derivatives, for which there is now a one quadrillion dollar bubble. After the modern collapse had already begun, Obama made him a top level adviser.

The Federal Reserve was the centerpiece of the housing bubble, as well as in serving as the vehicle to enable Congress to commit runaway spending that involves endless wars and the AGI Manhattan Project. In the meltdown aftermath, Obama moved immediately to hand the bankster monolith even more power, and the Congress banished Ron Paul’s legislation that would have given the Congress for the first time the ability to audit the Federal Reserve to bring to light their deeds.

Endgame
These players are amongst those at the forefront of setting up a total plutocracy. In a plutocracy the wealthy rule everything, as described  by a famous leaked Citigroup memo, where at an alarming pace the regular people of the world face no hope of being able to utilize the NBIC technologies including even non-radical life extension. The Federal Reserve itself is the primary mechanism used to ‘fund’ the the AGI Manhattan Project and all the rest, except the debt they provide to do it incurs interest. In effect, we’re being taxed almost literally to death so they can accelerate their technological goals.

The mentality of the classical elitist must be discussed. They tend to be Social Darwinists, who apply Darwinist theory to sociology. In their view it’s their divine role to dominate those beneath them, at the top of the food chain as the fittest to survive. This class of elites are their own social group, much like how most ordinary people identify themselves with race, political party, music scene, and so on. This social group adherence transcends the everyday social group affiliations the rest of us know, and elitist propaganda has us all wanting to identify with them to subconsciously justify their types of actions.

Another issue in the economic war is Health Care Reform. While the US certainly needed reform, which carries with it a huge debate, consider that the bill rammed through Congress was almost literally written by health insurance companies. Within it are massive tax hikes on numerous fronts, including mandatory health insurance. The full implications are beyond the scope here, but look further into what was actually passed and you will see.

Implicated
Humanity needs to wake up to the system and the technology. The system is killing the liberty and prosperity of the world, while the technology promises in itself to perhaps wipe out the species. The NBIC technology platform is about changing humans into posthumans. With the despotic system we face all bets are off about hoping it wouldn’t be enforced or worse. The technology alone can wipe us all out in the fashion of a scifi movie. Meanwhile humanity itself could tear itself apart when humans start upgrading and therefore make non-upgraded humans obsolete in the dwindling workforce.

Just this social meltdown war alone could call what one leading AGI scientist calls “gigadeath”. Hugo de Garis postulates that a new era of class warfare will morph into an inter-species warfare event could lead to the death of billions of people.

Neuro-Invasive Nanobots
Nanotechnology alone poses inherent threats greater than anything we’ve ever faced. Nanobots that can penetrate past the blood-brain barrier to attach to neurons for mind control threatens an entire new dimension of tyranny. These could be released into the drinking water supply or administered via vaccine shots.

Currently billions of dollars per year are dumped into nano research by governments and corporations worldwide. Even Ray Kurzweil realizes this threat. His “solution” is for us to deliberately inject ourselves with “defensive” nanobots, which only creates entire new sets of problems.

The End?
For there to be any hope of the worst not happening from the looming breakthrough technologies this tyrannical system needs to be stopped, and mass scale public debate needs to occur. Currently it’s all being rushed in under the radar and at breakneck speed. This is beyond wreckless. The technology issue is immense, and needs to be debated, but first and foremost we must focus on deeply changing the system before it’s too late.

The writing is on the wall. We face unspeakable darkness where there is no escape and turning back. There is no longer any longer any time to play games. We’re already on our last stand, but are we going to make one?

There is still hope, but time is short. The corrupted banking system is the most obvious starting point, but we now have a way to slow down the growing AGI using simple Automated Untelligence software tools that can be fun to use. AU must be employed to curb the “Semantic Web” and Google’s looming hard takeoff.  For the political system, we have a unifying concept to pull the funding out from underneath the criminally corrupt Congress, via Consensual Taxation only, marginalizing their powers over us and to do these things that are bent on power instead of the human betterment they’re claimed to be. The future is now. Fight for what you want it to become, because the dystopian system being set up is already fighting you.

ignoranceisfutile.org
ignoranceisfutile.wordpress.com

The 24 Types of Authoritarians.

*SOLUTION: Consensual Taxation (ONLY).

They often say “vote with your pocketbook”. I say lets take that concept to the extreme. Imagine if on your IRS form instead of focusing on the check-boxes of ‘dependents’ you claim, the majority of the ordeal would be a compendium of all of the various things government does, and taxes us for.

Think about that: EVERYTHING the government does and taxes us for, itemized, in a checklist. The form would be more like a book. There would be so much that people would only have time to flip through trying to find things they actually support.

From there there could be a 1-10 system. Like the form has a column that states the total intended price tag, and then the next column shows how much would cost each individual under the government vision. From there you get a base-10 percentage option of how much of their intended price for you that you actually support.

I argue that this alone would solve pretty much everything. In fact, it would almost negate the need for congress critters and the office of the president, especially as we know them. I argue that politicians are the root of majority of our problems.

Although I detest ’emotional wedge issues’, I do often point out how it’s unfair that people who don’t support abortion are forced to pay for abortion related programs. If it were the other way around, and abortion were outlawed, should avid abortion supporters be forced to pay for anti-abortion programs? Considering this concept again recently brought me to the conclusion of this case point.

Imagine all of the issues. Now imagine all of those who avidly support them, and nastily don’t. Space: if you want to fund NASA’s Mars mission, go for it. Millions of people are rightfully obsessed with having a new 9/11 investigation. Let them! Let them opt to pay for it, or ignore it. Or consider Global Warming. Vast amounts of government funding goes towards numerous things and studies related to that issue. Hey, if people want to pay for such things, let them. But don’t force everyone else to. If people didn’t have to be taxed to death in relation to things they don’t support, why should they?

I came to this conclusion over a month ago. I posted about it over at ATS, but at first I didn’t know what best to call it. It had to have a title.  Finally “Consent Taxation” came to mind. Before I had the title, I had no luck finding anything like it, even via Google God. But as soon as I thought of the title I immediately found another person with the same idea. Charles B. Petzold is the first person I know of to brainstorm this idea. He even already has a Facebook page specifically for the idea (if you like this concept the first thing to do is support his page):

The concept is simple in theory, but perhaps more complicated in implementation. However, if people can file taxes, than they can just as easily do this. In fact, they may even find a personal interest in doing so, as it promotes their own wishes, and makes their voice heard. It would essentially operate much like the IRS does now (ironically), in that people would be filing tax consent forms to the Fed, state, and local governments, with each new budget cycle. The Fed, states, and local government would publicly submit their budget proposals, and proposed spending initiatives before each budget cycle. The public (those who give a #), would than review these proposals for a period of time, before their tax consent forms were due. Based on the public’s feedback, budgets would be created on a strictly popular vote basis. Some of the items would be shorter term, and others longer term. The longer term issues would naturally be of the most importance on any given consent form. The form itself would essentially be a checklist of items presented to the taxpayer. The taxpayer would be able to indicate the level of importance they lend to each item, possibly by use of the old “on a scale of 1-5” format, which would dictate the amount they deemed fit to spend on it….or…. they could check “unsatisfactory”, indicating they have no interest whatsoever in having their tax money being spent on that item. If implemented, the American people would be so jaw-dropped by the long lists of frivolous spending, that it would be cut short in a very small amount of time. Almost sounds too simple, doesn’t it?….. Well, so simple, I think it would work.

Other than Petzold’s pages, searching for “consent taxation ‘check list'” brought up a bunch of dead end looking PDF files, etc.

Wikipedia’s Taxation as Theft entry talks about the unfairness of being forced to pay taxes on things we haven’t consented to, but fails to mention an outline of that being the solution to the problem.

Instead it says this:

In taxation a taxpayer wasn’t given a choice in what services to pay for. Somebody else chooses on behalf of the payer without his/her explicit consent as to what services to pay for, even if the payer does not use that service or believes against that particular service. If it were possible to track where exactly a taxpayer’s tax money goes, the taxpayer could pay that entity directly. However, besides the logistic difficulties of this proposal, a country’s inhabitants routinely benefit from non-excludable goods or services, such as national defense or infrastructure. This is discussed in greater detail in David Osterfeld’s paper “Social Utility” and Government Transfers of Wealth: An Austrian Perspective.

That paper can be found here. This paragraph is striking:

Currently, in excess of 50 percent of the budgets of practically all governments in the world are devoted to transfer payments. This makes wealth transfers, at least quantitatively, the most important function of government. The official justification for these activities is that they increase “social utility.” Since transferring wealth from some individuals to others reduces choice sets of the former while expanding them for the latter, this means that some are forced to choose between options that provide them with less utility than those they would have chosen on the market, while others are able to choose from options that would not be open to them on the market. Since the utility of some is reduced while that of others is increased, any claim that social utility has been increased implies the ability to compare, if not measure, the utilities of different individuals. Thus, the justification for wealth transfers clearly implies the use of utility in its cardinal sense (Simon), defined here as the ability to measure and/or compare the utilities of different individuals. Those who maintain that wealth transfers can and do increase social utility should be able to support this claim with adequate evidence.

50% of government is in deciding what to transfer from who and to where? It’s sounds like things might be better off if we do that decision making for them. This would seriously marginalize their power over us.

A little further down:

The results of the foregoing are interesting. One may say with certainty that the market always increases social utility. On the other hand, one can never state with certainty that any act of government ever increases social utility, and the only conclusion one could ever make with absolute certainty is that a given act of government reduced “social utility.” And this, as we shall see, is not as unlikely as might be thought.

That paper is a good read, but I somehow didn’t find mention of how that Wikipedia entry I cited put it that: “If it were possible to track where exactly a taxpayer’s tax money goes, the taxpayer could pay that entity directly. However, besides the logistic difficulties of this proposal, a country’s inhabitants routinely benefit from non-excludable goods or services, such as national defense or infrastructure.” The paper more seems to completely argue against taxes altogether, and I didn’t see that bit about it being “impossible to track where tax money goes’.

Instead it says this:

This means that it is impossible to ascertain whether a given government action increased or decreased net social utility or left it unchanged.

I also came across:
Public Choice Theory

One of the chief underpinnings of public choice theory is the lack of incentives for voters to monitor government effectively. Anthony Downs, in one of the earliest public choice books, An Economic Theory of Democracy, pointed out that the voter is largely ignorant of political issues and that this ignorance is rational. Even though the result of an election may be very important, an individual’s vote rarely decides an election. Thus, the direct impact of casting a well-informed vote is almost nil; the voter has virtually no chance to determine the outcome of the election. So spending time following the issues is not personally worthwhile for the voter. Evidence for this claim is found in the fact that public opinion polls consistently find that less than half of all voting-age Americans can name their own congressional representative.

Public choice economists point out that this incentive to be ignorant is rare in the private sector. Someone who buys a car typically wants to be well informed about the car he or she selects. That is because the car buyer’s choice is decisive—he or she pays only for the one chosen. If the choice is wise, the buyer will benefit; if it is unwise, the buyer will suffer directly. Voting lacks that kind of direct result. Therefore, most voters are largely ignorant about the positions of the people for whom they vote. Except for a few highly publicized issues, they do not pay a lot of attention to what legislative bodies do, and even when they do pay attention, they have little incentive to gain the background knowledge and analytic skill needed to understand the issues.
www.econlib.org…

That deals directly with my arguments that people are predictably ignorant as they feel voting and participating in the system as we know to be irrelevant.

This section also highlights some of what I’ve been saying:

Public choice economists also examine the actions of legislators. Although legislators are expected to pursue the “public interest,” they make decisions on how to use other people’s resources, not their own. Furthermore, these resources must be provided by taxpayers and by those hurt by regulations whether they want to provide them or not. Politicians may intend to spend taxpayer money wisely. Efficient decisions, however, will neither save their own money nor give them any proportion of the wealth they save for citizens. There is no direct reward for fighting powerful interest groups in order to confer benefits on a public that is not even aware of the benefits or of who conferred them. Thus, the incentives for good management in the public interest are weak. In contrast, interest groups are organized by people with very strong gains to be made from governmental action. They provide politicians with campaign funds and campaign workers. In return they receive at least the “ear” of the politician and often gain support for their goals.

In other words, because legislators have the power to tax and to extract resources in other coercive ways, and because voters monitor their behavior poorly, legislators behave in ways that are costly to citizens.

What is odd however is that I don’t see any mention of the ideal of ‘Consent Taxation” mentioned in the Public Choice Theory model. It’s like it’s right on the tips of their tongues, but PCT seems more about “studies the behavior of politicians and government”.

Much More To Come…

*Illegitimate 4th of July celebrations.

Hate to be the party pooper, but I can’t fathom what people are celebrating. This isn’t even about those who don’t even know what they’re celebrating, it’s about those who do.

The fact is “America” is over. The tyrants who own us now are far worse than King George, and it gets worse everyday.

Taxation without representation: We pay 50X the taxes the colonialists did.

The Bill of Rights: Dead.

The Constitution: Oh dear.

Future generations: Already bankrupt at birth.

Liberty & Freedom: Please do specify how free you believe you are. Please.

US Sovereignty: On the ropes.

Fireworks: Made in China.

You support the Constitution: You might be put on a terrorist list.

And then there’s the people who don’t even know the first things about the 4th of July:
26 percent of Americans have no clue what country US fought to gain its independence.

It’s still the 4th of July as I post this, and for those of you who are seeing it on this day, don’t feel bad, that you didn’t light some Chinese fireworks in an illegitimate celebration. A celebration as illegitimate as the government that enslaves us.