Cancer

Cancer Incidence and Mortality After Treatment With Folic Acid and Vitamin B12. Ebbing M, Bønaa KH, Nygård O, Arnesen E, Ueland PM, Nordrehaug JE, Rasmussen K, Njølstad I, Refsum H, Nilsen DW, Tverdal A, Meyer K, Vollset SE. JAMA. 2009 Nov 18;302(19):2119-2126. v PMID: 19920236 Conclusion Treatment with folic acid plus vitamin B12 was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease in Norway, where there is no folic acid fortification of foods.

ScienceDaily (Dec. 5, 2009) - A new study has found that the amount of vitamin D in patients being treated for diffuse large B-cell lymphoma was strongly associated with cancer progression and overall survival. The results will be presented at the annual meeting of the American Society of Hematology in New Orleans. Also, several recent reports have concluded that vitamin D deficiency is associated with poor outcomes in other cancers, including breast, colon and head and neck cancer. This is the first study to look at lymphoma outcome.

Vitamin D for cancer prevention: global perspective. Garland CF, Gorham ED, Mohr SB, Garland FC. Ann Epidemiol. 2009 Jul;19(7):468-83. Review. PMID: 19523595

A systematic review of the anticancer properties of berberine, a natural product from Chinese herbs. Sun Y, Xun K, Wang Y, Chen X. Anticancer Drugs. 2009 Oct;20(9):757-69. PMID: 19704371

Benefits of Vitamin D Supplementation Joel M. Kauffman, Ph.D. Journal of American Physicians and Surgeons Volume 14 Number 2 - Summer 2009 Clinical trials show that vitamin D supplementation at higher levels than previously recommended is beneficial for many conditions. It decreases the frequency of falls and fractures, helps prevent cardiovascular disease, and reduces symptoms of colds or influenza. Benefits are also seen in diabetes mellitus, multiple sclerosis, Crohn disease, pain, depression, and possibly autism. Sunlight does not cause an overdose of vitamin D production, and toxicity from supplementation is rare. Dose recommendations are increasing, but appear to be lagging the favorable trial results. A number of common drugs deplete vitamin D levels, and others may limit its biosynthesis from sunlight. People with adequate levels from sun exposure will not benefit from supplementation. While dietary intake is helpful, supplementation is better able to raise serum 25-hydroxyvitamin D , the major circulating metabolite, to the level now thought adequate, 30-50 ng/mL. Where there is inadequate daily sun exposure, oral doses of 1,000-2,000 IU/d are now considered routine, with much higher doses (up to 50,000 IU) for rapid repletion now considered safe.

"NOTTINGHAM, England, Dec. 29 (UPI) -- A drug derived from a mushroom -- cordycepin -- may be used to treat some cancers, British researchers say. Dr. Cornelia de Moor of The University of Nottingham in England and colleagues are investigating the drug originally extracted from a rare parasitic mushroom called cordyceps that grows on caterpillars. The researchers say low-dose cordycepin seems to inhibit the uncontrolled growth and division of cells and at high doses it also inhibits growth by stopping cells from sticking together. Both of these effects, they say, probably have the same underlying mechanism -- interfering with the production of cell proteins.

"(CBS) Your daily cup of java may deliver some unexpected health benefits. Studies have shown it may lower your risk for Type II diabetes and certain types of cancer (colon, mouth and throat), and protect against heart disease and cavities. Dr. Alanna Levine, a primary care physician, said on "The Early Show" researchers aren't sure exactly why coffee has these benefits, but speculated that perhaps the coffee has antioxidant properties. "

The Author The author of this site is the British writer, John Davidson. Please note that the author is neither a doctor, nor a qualified health practitioner. Every cancer patient should always consult his or her medical practitioner with regard to the use of complementary remedies or treatments, and nothing on this site should be construed in any way as medical or therapeutic advice. It is simply the result of one person's search for solutions. Please read our disclaimer. About This Site Internet searches trawl up vast amounts of information about cancer, from a broad spectrum of viewpoints. The information and internet links on this site are for those seeking to augment the treatment offered by their hospital oncology (cancer) unit. Of course, a great many other internet sites concerning cancer can be found by keying the requisite search words into any of the major search engines. The content of this site was initially prepared, at the request of medical and nursing staff and others, some weeks after I had had an emergency operation for the removal of a colon cancer, and while undergoing chemotherapy in case any cancer cells had gone AWOL. There had been some escape of cancer cells into associated lymph nodes (3 out of 17, including the most distal), but no other tumours had been picked up by a CT scan. When I returned home from hospital in September 2005, with the help of friends, I started doing some research on cancer. I was amazed to discover that despite the billions of pounds/euros/dollars etc. spent on cancer research, and the many advances in understanding the numerous variants of the disease, the standard treatment for my stage of colon cancer is still a drug (fluorouracil, also called 5FU) that has been in use for more than forty years, has uncomfortable side effects, and which only increases the chances of survival after five years by 5 to 10%.

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Anti-angiogenic foodstuffs. Fascinating! Combine that with low glycemic index/load diet to minimise your chances for getting cancer (and many other diseases). More and more evidence indicate that we could probably cure cancer with proper diet and other lifestyle changes.

By Randy Dotinga HealthDay Reporter MONDAY, Jan. 11 (HealthDay News) -- Preliminary research suggests that a combination of compounds in marijuana could help fight off a particularly deadly form of brain cancer. But the findings shouldn't send patients rushing to buy pot: the levels used in the research appear to be too high to obtain through smoking. And there's no sign yet that the approach works in laboratory animals, let alone people.

"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."

"Worcester, MA - Current research suggests that TNF-receptor associated protein-1 (TRAP-1) may prevent cancer cell death. The related report by Leav et al, "Cytoprotective Mitochondrial Chaperone TRAP-1 as a Novel Molecular Target in Localized and Metastatic Prostate Cancer," appears in the January 2010 issue of the American Journal of Pathology. Prostate cancer cells are often resistant to cell death. Researchers led by Dr. Dario C. Altieri of the University of Massachusetts Medical School, therefore, explored the role of TRAP-1, a protein thought to regulate cell death, in prostate cancer survival. TRAP-1 was highly expressed in both high-grade human prostate cancer lesions and mouse models of prostate cancer, but not in benign or normal prostate tissue. In addition, TRAP-1 overexpression in non-cancer prostate cells inhibited cell death, whereas TRAP-1-deficient prostate cancer cells had enhanced levels of cell death. Moreover, treatment with Gamitrinib, which inhibits TRAP-1, resulted in prostate cancer cell death, but not death of non-cancerous prostate cells. Therefore, targeting TRAP-1 via Gamitrinib treatment may be a viable therapeutic strategy for patients with advanced prostate cancer."

"For years, it's been the perfect excuse for secret admirers to steal a kiss with the object of their desire. But research suggests mistletoe could do much more than just ignite Christmas passions. Scientists have found an extract of the plant could help to fight bowel cancer, which affects 37,500 a year in the UK. Patients who had the mistletoe treatment regularly injected into their blood had fewer side-effects from toxic chemotherapy and radiotherapy and survived longer than those who did not. The extract is thought to help the body's immune system fight tumours and speed up the disposal of toxic 'debris' left by chemotherapy. Researchers led by Professor Kurt Zanker from the German Institute of Immunology and Experimental Oncology, concluded: 'The results suggest convincing evidence that there is a significant benefit from treatment with mistletoe extract.' The scientists treated 429 cancer patients with the mistletoe jab and compared them with 375 receiving conventional care. The results, published in the journal of The Society For Integrative Oncology, showed only 19 per cent of those in the mistletoe group suffered side-effects from toxic treatments, compared to 48 per cent in the other group. They were also 32 per cent more likely to still be alive five years after starting therapy."

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.

"Língzhī (traditional Chinese: 靈芝; simplified Chinese: 灵芝; Japanese: reishi; Korean: yeongji, hangul: 영지) is the name for one form of the mushroom Ganoderma lucidum, and its close relative Ganoderma tsugae. Ganoderma lucidum enjoys special veneration in Asia, where it has been used as a medicinal mushroom in traditional Chinese medicine for more than 4,000 years, making it one of the oldest mushrooms known to have been used in medicine. Lingzhi may possess anti-tumor, immunomodulatory and immunotherapeutic activities, supported by studies on polysaccharides, terpenes, and other bioactive compounds isolated from fruiting bodies and mycelia of this fungus (reviewed by R. R. Paterson[4] and Lindequist et al.[7]). It has also been found to inhibit platelet aggregation, and to lower blood pressure (via inhibition of angiotensin-converting enzyme[8]), cholesterol and blood sugar.[9] Laboratory studies have shown anti-neoplastic effects of fungal extracts or isolated compounds against some types of cancer. In an animal model, Ganoderma has been reported to prevent cancer metastasis,[10] with potency comparable to Lentinan from Shiitake mushrooms.[11] The mechanisms by which G. lucidum may affect cancer are unknown and they may target different stages of cancer development: inhibition of angiogenesis (formation of new, tumor-induced blood vessels, created to supply nutrients to the tumor) mediated by cytokines, cytoxicity, inhibiting migration of the cancer cells and metastasis, and inducing and enhancing apoptosis of tumor cells

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

"December 17, 2009 (San Antonio) - A new targeted cancer drug has been shown to shrink tumors in women with metastatic breast cancer after an average of seven other drugs, including Herceptin, failed. The new drug, called T-DM1, combines Herceptin with a potent chemotherapy drug. It's a Trojan horse approach, where Herceptin homes in on cancer cells and delivers the cancer-killing agent directly to its target. Tumors shrank in one-third of women with metastatic breast cancer given T-DM1, says Ian Krop, MD, of the Dana-Farber Cancer Institute in Boston. In another 12%, tumors stopped growing for at least six months. The women remained cancer-free for an average of seven months -- results unheard of in patients this sick, he says. All the women, who had breast tumors for an average of three years, had cancer that had metastasized, or spread to other parts of the body. They had been treated with an average of seven different therapies, including Herceptin, Tykerb, and Xeloda, and each had failed."

"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"

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

"This is a study to see whether radiotherapy plus chemotherapy (Temozolomide) plus Dichloracetate (DCA) improves overall survival and offers better control of the disease in patients with newly diagnosed Glioblastoma Multiforme Tumours"