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The in vitro study, reported in the journal Carcinogenesis (Vol. 27, pp. 32-42), showed that vitamin D, in the form of the highly active 1alpha, 25-dihydroxyvitamin D3 (1,25-VD), inhibited the function of protease enzymes that are involved in tumour invasion. "We found that 1,25-VD decreased matric metalloproteinases (MMP-9) and cathepsins (CPs), while it [also] increased the activity of their counterparts, tissue inhibitors of metalloproteinase-1 (TIMP-1) and cathepsin inhibitors," wrote lead author Bo-Ying Bao from the University of Rochester and Taipei Medical University. "Mechanistic studies showed that 1,25-VD did not suppress MMP-9 expression at the transcriptional level, but reduced its mRNA stability," said Bao.

"Cancer lies dormant in all of us," he wrote in his new book, "Anticancer: A New Way of Life" (Viking, $25.95). "But our bodies are also equipped with a number of mechanisms that detect and keep such (defective) cells in check." Cancer rears its ugly head when things get out of balance, Servan-Schreiber said in an interview. And that can happen if the bad guys that promote the growth of cancer cells (tobacco, excessive alcohol, excessive sugar, hydrogenated fats, environmental pollutants) outnumber the good guys that support our natural defenses (cancer-fighting phytochemicals found in fruits, vegetables, herbs and teas; physical activity; and stress management techniques). But conventional treatment, while indispensable, focuses on a single target: destroying cancer cells. Doctors rarely address the other side: teaching patients how to fortify themselves using nutrition, exercise and stress-management techniques to create an inhospitable environment for cancer.

Blueberry Punch is an Australian product but is available for sale on the internet at £16 a bottle.\n\nIt also includes a host of other natural ingredients thought to boost health, including green tea, olive leaves, the herb tarragon and the spices turmeric and ginger.\n\nIt is thought the ingredients act together to cut inflammation and block a cancer gene.\n\nDr Jas Singh, who conducted the research on mice at Sydney University, said: "We have undertaken efficacy studies on individual components of Blueberry Punch in the same laboratory setting and found these effective in suppressing cell growth in culture.\n\n"We reasoned that synergistic or additive effects are likely to be achieved when they are combined."\n\nThe researchers looked at the effect of Blueberry Punch on both cancer cell cultures in the laboratory and genetically engineered mice with human prostate tumours. After only two weeks of having the syrupy solution added to their drinking water, their tumours had shrunk by

DCA is an organic compound, and a byproduct of TCE (trichloroethylene), a chemical that has been a concern in the development of cancer. In January 2007, researchers at the University of Alberta published a study in the journal Cancer Cell suggesting that DCA showed promise in shrinking tumors in lab rats as well as inhibiting growth of cultured human cancer cells. They hypothesized that DCA may be able to change cancer cells back to normal ones by switching them from the aberrant energy pathways they rely on to those used by normal cells.

Research just published in the American Association for Cancer Research's Cancer Prevention Research identifies a class of flavonoids called anthocyanins in black raspberries that's been shown to inhibit cancer cell growth and stimulate apoptosis (the death of cancer cells) in the esophagus of rats treated with an esophageal carcinogen

Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer. Michelakis ED, Webster L, Mackey JR. Br J Cancer. 2008 Oct 7;99(7):989-94. Epub 2008 Sep 2. Review. PMID: 18766181 doi:10.1038/sj.bjc.6604554 The unique metabolism of most solid tumours (aerobic glycolysis, i.e., Warburg effect) is not only the basis of diagnosing cancer with metabolic imaging but might also be associated with the resistance to apoptosis that characterises cancer. The glycolytic phenotype in cancer appears to be the common denominator of diverse molecular abnormalities in cancer and may be associated with a (potentially reversible) suppression of mitochondrial function. The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis. This reverses the suppressed mitochondrial apoptosis in cancer and results in suppression of tumour growth in vitro and in vivo. Here, we review the scientific and clinical rationale supporting the rapid translation of this promising metabolic modulator in early-phase cancer clinical trials More than 40 nonrandomised trials of DCA in small cohorts of patients have been reported, but the first two randomised control trials of chronic oral therapy with DCA in congenital mitochondrial diseases were reported in 2006. In the first, a blinded placebo-controlled study was performed with oral DCA administered at 25 mg kg-1 day-1 in 30 patients with MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) (Kaufmann et al, 2006). Most patients enrolled in the DCA arm developed symptomatic peripheral neuropathy, compared with 4 out of 15 in the placebo arm, leading to the termination of the study. Seventeen out of 19 patients had at least partial resolution of peripheral neurological symptoms by 9 months after discontinuation of DCA. This neurotoxicity res

"COLLEGE STATION - Mango. If you know little about this fruit, understand this: It's been found to prevent or stop certain colon and breast cancer cells in the lab. That's according to a new study by Texas AgriLife Research food scientists, who examined the five varieties most common in the U.S.: Kent, Francine, Ataulfo, Tommy/Atkins and Haden. Though the mango is an ancient fruit heavily consumed in many parts of the world, little has been known about its health aspects. The National Mango Board commissioned a variety of studies with several U.S. researchers to help determine its nutritional value. "If you look at what people currently perceive as a superfood, people think of high antioxidant capacity, and mango is not quite there," said Dr. Susanne Talcott, who with her husband, Dr. Steve Talcott, conducted the study on cancer cells. "In comparison with antioxidants in blueberry, acai and pomegranate, it's not even close." But the team checked mango against cancer cells anyway, and found it prevented or stopped cancer growth in certain breast and colon cell lines, Susanne Talcott noted. "It has about four to five times less antioxidant capacity than an average wine grape, and it still holds up fairly well in anticancer activity. If you look at it from the physiological and nutritional standpoint, taking everything together, it would be a high-ranking super food," she said. "It would be good to include mangoes as part of the regular diet." The Talcotts tested mango polyphenol extracts in vitro on colon, breast, lung, leukemia and prostate cancers. Polyphenols are natural substances in plants and are associated with a variety of compounds known to promote good health."

"Compounds similar to those found in cannabis have been shown to stop prostate cancer cells from multiplying. Two cannabinoid compounds, JWH-015 and MET, stopped prostate tumour growth in human prostate cells in Petri dishes and also in mice with the disease. They halted the cell-division cycle and killed the cancer cells, and had the greatest effect on aggressive prostate cancer cell types, which do not respond to hormone treatments. Some 192,000 men in the US alone are diagnosed with prostate cancer each year, and researchers Inés Díaz-Laviada Marturet at the University of Alcalá, Spain, and her colleagues say the results could offer hope to those affected. But before you go looking for a dealer, New Scientist answers a few questions"

Anticancer properties of Ganoderma lucidum methanol extracts in vitro and in vivo. Harhaji Trajković LM, Mijatović SA, Maksimović-Ivanić DD, Stojanović ID, Momcilović MB, Tufegdzić SJ, Maksimović VM, Marjanović ZS, Stosić-Grujicić SD. Nutr Cancer. 2009;61(5):696-707. PMID: 19838944 DOI: 10.1080/01635580902898743 Anticancer activities of various extracts of the medicinal mushroom, Ganoderma lucidum, have been widely demonstrated and are mainly associated with the presence of different bioactive polysaccharides and triterpenoids. We have evaluated and compared in vitro and in vivo the antitumor effects of two preparations from Ganoderma lucidum: a methanol extract containing total terpenoids (GLme) and a purified methanol extract containing mainly acidic terpenoids (GLpme). Both extracts inhibited tumor growth of B16 mouse melanoma cells inoculated subcutaneously into syngeneic C57BL/6 mice and reduced viability of B16 cells in vitro, whereby GLme exhibited stronger effect. Furthermore, anticancer activity of GLme was demonstrated for the first time against two other rodent tumor cell lines, L929-mouse fibrosarcoma and C6-rat astrocytoma. The mechanism of antitumor activity of GLme comprised inhibition of cell proliferation and induction of caspase-dependent apoptotic cell death mediated by upregulated p53 and inhibited Bcl-2 expression. Moreover, the antitumor effect of the GLme was associated with intensified production of reactive oxygen species, whereas their neutralization by the antioxidant, N-acetyl cysteine, resulted in partial recovery of cell viability. Thus, our results suggest that GLme might be a good candidate for treatment of diverse forms of cancers.

...has been the number one Google search term leading people to the blog this week - and that worries me. As I wrote about a week ago, dichloroacetate, or DCA, is the molecule tested recently by a team at University of Alberta for its ability to slow the growth of human lung cancer in immunocompromised rats. Among DCA's action is the ability to prevent cancer cells from producing lactic acid via aerobic glycolysis, a process used by more than half (but not all) tumors. Scientists continue to debate whether this process is a cause of cancer, or just a byproduct of malignant cell transformation. I am deeply concerned that desperate cancer patients may be trying to purchase dichloroacetate (DCA) and self-treat for cancer based on this highly-hyped single paper. To the credit of the researchers and their institution, who have set up a website to address the intense interest, they discourage such practice:

What if we didn't try to cure cancer, but simply kept tumors from growing too big? That's what radiologist Robert Gatenby of the Moffitt Cancer Center proposes this week in the journal Nature. Gatenby argues that high doses of powerful chemotherapies wreak havoc on a patient's immune system and foster the rapid regrowth of chemoresistant cancers that doctors have no hope of fighting.  So instead of curing cancer, he suggests doctors aim to stabilize the tumor at a tolerable size. In practice, this would mean that doctors identify a target size for an individual tumor that gives the patient the best quality of life.  Then, they will regularly monitor the tumor's growth with medical imaging equipment like a PET/CT scanner (see photo), and regulate doses of anticancer drugs to maintain it at a precise volume.

A collaborative study led by UCL (University College London) shows that the compound - inositol pentakisphosphate - found in beans, nuts and cereals inhibits a key enzyme (phosphoinositide 3-kinase) involved in tumour growth. The findings, published in the latest issue of Cancer Research, suggest that a diet enriched in such foods could help prevent cancer, while the inhibitor offers a new tool for anti-cancer therapy.

Dr Marco Falasca and colleagues have discovered that a natural compound, called inositol pentakisphosphate, which is found in most legumes as well as in wheat bran and nuts, blocks the activity of the enzyme. When they tested its action in mice with ovarian and lung cancer they found it not only blocked tumour growth but also enhanced the effect of other cancer-killing drug

Artemisinin (pronounced /ɑːtə'misinən/) is a drug used to treat multi-drug resistant strains of falciparum malaria. The compound (a sesquiterpene lactone) is isolated from the plant Artemisia annua. Not all plants of this species contain artemisinin. Apparently it is only produced when the plant is subjected to certain conditions, most likely biotic or abiotic stress. It can be synthesized from artemisinic acid.[1] The drug is derived from a herb used in Chinese traditional medicine, though it is usually chemically modified and combined with other medications. Artemisinin is under early research and testing for treatment of cancer, primarily by researchers at the University of Washington.[7][8] Artemisinin has a peroxide lactone group in its structure. It is thought that when the peroxide comes into contact with high iron concentrations (common in cancerous cells), the molecule becomes unstable and releases reactive oxygen species. It has been shown to reduce angiogenesis and the expression of vascular endothelial growth factor in some tissue cultures.

Docosahexaenoic acid suppresses arachidonic acid-induced proliferation of LS-174T human colon carcinoma cells. Habbel P, Weylandt KH, Lichopoj K, Nowak J, Purschke M, Wang JD, He CW, Baumgart DC, Kang JX. World J Gastroenterol. 2009 Mar 7;15(9):1079-84. PMID: 19266600

A multicountry ecologic study of risk and risk reduction factors for prostate cancer mortality. Grant WB. Eur Urol. 2004 Mar;45(3):271-9. PMID: 15036670 CONCLUSIONS: These results are consistent with insulin-like growth factor-I (IGF-I), being an important risk factor for prostate cancer, with alcohol and calcium being less important risk factors, and with allium family vegetables, and, to a lesser extent, vitamin D being important risk reduction factors. These results should provide guidance for additional studies on dietary and environmental links to prostate cancer.

Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase. Jiang F, Bao J, Li P, Nicosia SV, Bai W. J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12. PMID: 15485861 doi: 10.1074/jbc.M410395200 Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression. Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene. It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro

"Berberine is a quaternary ammonium salt from the group of isoquinoline alkaloids. It is found in such plants as Berberis, goldenseal (Hydrastis canadensis), and Coptis chinensis, usually in the roots, rhizomes, stems, and bark. Berberine is strongly yellow colored, which is why in earlier times berberis species were used to dye wool, leather and wood. Wool is still today dyed with berberine in Northern India Berberine (BBR) is a natural compound with up-regulating activity on both low-density-lipoprotein receptor (LDLR) and insulin receptor (InsR). This one-drug-multiple-target characteristic might be suitable for the treatment of metabolic syndrome.[12] Berberine has been tested and used successfully in experimental[13] and human diabetes mellitus.[14][15][16] Berberine has been shown to lower elevated blood glucose as effectively as metformin.[17] The mechanisms include inhibition of aldose reductase,[18] inducing glycolysis,[19] preventing insulin resistance[20] through increasing insulin receptor expression[14] and acting like incretins. Berberine has drawn extensive attention towards its antineoplastic effects.[43][44] It seems to suppress the growth of a wide variety of tumor cells including breast cancer,[45] leukemia, melanoma,[46] epidermoid carcinoma, hepatoma, oral carcinoma, tongue carcinoma,[47] glioblastoma, prostate carcinoma, gastric carcinoma.[48][49] Animal studies have shown that berberine can suppress chemical-induced carcinogenesis, tumor promotion, tumor invasion,[50][51][52][53][54] prostate cancer,[55][56][57][58] neuroblastoma,[59][60] and leukemia.[34][61] It is a radiosensitzer of tumor cells but not of normal cells