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Cancer is DEAD: Cancer cured from A to Z

2010 August 24
by wemustknow.koen

All credits go to IgnoranceIsntBliss a member of ATS forum.

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:

Cancer is DEAD: Cancer cured from A to Z
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.

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.

YouTube Link

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…

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.
Source: http://www.abovetopsecret.com/forum/cancerisdead.html

from → Cancer, Health, Truth

2 Responses leave one →
  1. Kristopher Thang (Imperium) permalink
    January 23, 2011

    Hi that’s a good post there. Just thought you might like to know that your page loads fine on my IPad 16GB running Wifi connection. Really Enjoy your site.

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