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"Cigarette smoking and alcohol consumption before head and neck cancer diagnosis strongly predicts the patient's future risk of death, according to published studies. Now, results of a new study show a similar effect among those who continued these habits after cancer diagnosis. "Most cancer survivors are counseled to quit smoking; despite this, many still smoke. In our study, 21 percent continued to smoke even after their cancer diagnosis, increasing their risk of death," said researcher Susan T. Mayne, Ph.D. "Similarly, we found that continued drinking increases the risk of death.""

Simultaneously Blocking Glycolysis and Fat Metabolism Can the use of DCA and a fatty acid metabolism blocker together force more cancer cells into using aerobic metabolism? Tim McGough used green tea extract, which contains EGCG, in his fantastic response. DCA works by reactivating mitochondria and shifts metabolism from glycolysis to glucose oxidation. Hopefully the cancer cell will then undergo apoptosis. However, cancer cells have an alternate energy source: fat metabolism. This page explores to possibility of blocking fat metabolism to help force the cell into apoptosis. Oral squamous cell carcinoma is a cancer that does not respond well to DCA. This study, Head and Neck Cancer Cell Lines Are Resistant to Mitochondrial-Depolarization-Induced Apoptosis states: "Results: ΔΨm in head and neck cell lines started to show slight loss of ΔΨm, while HL-60 showed significant loss of ΔΨm after 30 min of treatment. All cell lines demonstrated complete mitochondrial depolarization within 24 h, however, only the control cell line HL-60 underwent apoptosis. In addition, HNSCC cell lines did not demonstrate cytoplasmic cytochrome c release despite significant mitochondrial membrane depolarization, while HL-60 cell initiated apoptosis and cytochcrome c release after 24 h of treatment. Conclusions: Head and neck cancer cell lines exhibit defects in mitochondrial-membrane-depolarization-induced apoptosis as well as impaired release of cytochrome c despite significant mitochondrial membrane depolarization. Proximal defects in the mitochondrial apoptosis pathway are a feature of HNSCC.(head and neck squamous cell carcinoma)" Note that although the cell lines were depolarized, apoptosis did not occur. So I checked to see if fatty acid metabolism is used by squamous cell carcinoma.

Changes of terminal cancer patients' health-related quality of life after high dose vitamin C administration.\nYeom CH, Jung GC, Song KJ.\nJ Korean Med Sci. 2007 Feb;22(1):7-11.\nPMID: 17297243

Cells from a suspicious purplish spot on her cervix were analyzed and identified as cancerous. They multiplied so quickly that, despite treatment, Mrs. Lacks died eight months later, at the age of 31…Today, however, her cells are still alive and are being used to help combat a wide variety of diseases all over the world.

Bioavailability and Kinetics of Sulforaphane in Humans after Consumption of Cooked versus Raw Broccoli Martijn Vermeulen*, Ineke W. A. A. Klpping-Ketelaars†, Robin van den Berg‡ and Wouter H. J. Vaes J. Agric. Food Chem., 2008, 56 (22), pp 10505-10509 Publication Date (Web): October 24, 2008 (Article) DOI: 10.1021/jf801989e

You-Lin Qiao, Sanford M. Dawsey, Farin Kamangar, Jin-Hu Fan, Christian C. Abnet, Xiu-Di Sun, Laura Lee Johnson, Mitchell H. Gail, Zhi-Wei Dong, Binbing Yu, Steven D. Mark, and Philip R. Taylor. Total and Cancer Mortality After Supplementation With Vitamins and Minerals: Follow-up of the Linxian General Population Nutrition Intervention Trial. Journal of the National Cancer Institute, 2009 March 24; DOI: 10.1093/jnci/djp037

ScienceDaily (Mar. 24, 2009) - Individuals who took a dietary supplement called "factor D", which included selenium, vitamin E, and beta-carotene, continued to have lower gastric cancer and overall mortality 10 years after supplementation ceased compared with individuals who did not take the supplements, according to long-term follow-up data from the randomized, double-blind General Population Nutrition Intervention Trial in Linxian, China.

Pilot study: potential role of vitamin D (Cholecalciferol) in patients with PSA relapse after definitive therapy. Woo TC, Choo R, Jamieson M, Chander S, Vieth R. Nutr Cancer. 2005;51(1):32-6. PMID: 15749627

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.

Second Expert Report\n\nFood, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective\n\nIt began in 2001 with AICR and its international affiliate, WCRF-UK committing themselves to systematically review and analyze the total body of scientific evidence on the relationship of diet, physical activity and weight management to cancer risk. After a rigorous five-year process, Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective does just that.

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

Complementary and alternative medicine (CAM) and complementary and integrative medicine (CIM) are therapies of proven or unproven efficacy that have been used to promote wellness, to manage symptoms associated with cancer and its treatment or to treat cancer. When properly combined with standard cancer treatments, some complementary therapies can enhance wellness and quality of life, but others may be harmful during or after treatment for cancer. Most, but not all, are natural products.

Most head-and-neck cancers that recur locally after prior full-dose conventional radiation therapy respond to Boron Neutron Capture Therapy (BNCT). These results were obtained in a Phase I/II study at the Helsinki University Hospital, Finland. The scienti

A new approach to cancer treatment called immunotherapy could spare patients at least some of the grueling battery of chemotherapy treatments by retraining the body's own defenders--the cells of the immune system--to recognize and destroy tumors. Now researchers at Harvard University have developed a simple way to do this inside the body: a polymer implant attracts and trains immune-system cells to go after cancer. The experimental approach has shown great success in animal studies, increasing the survival rate of mice with a deadly melanoma from 0 to 90 percent. The implant could also be used to treat diseases of the immune system such as arthritis and diabetes, and, potentially, to train other kinds of cells, including stem cells used to repair damage to the body.

For several types of cancer, persistently high levels of the soluble factor TGF-beta in the blood after surgery, chemotherapy, or radiation therapy correlate with increased risk of early metastasis and a poor prognosis. Using a mouse model of breast cance

After the news story in the Belgium press of two terminally ill cancer patients who used DCA and are now on the road to recovery, the Belgium people are asking questions. "It has brought a lot commotion in Belgium. All the people are wondering why they haven't heard from DCA any sooner! And they wonder why it isn't recognized yet as an official medicine for cancer!

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

Combination of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates cumulative recurrence of hepatocellular carcinoma. Yoshiji H, Noguchi R, Toyohara M, Ikenaka Y, Kitade M, Kaji K, Yamazaki M, Yamao J, Mitoro A, Sawai M, Yoshida M, Fujimoto M, Tsujimoto T, Kawaratani H, Uemura M, Fukui H. J Hepatol. 2009 Aug;51(2):315-21. Epub 2009 May 15. PMID: 19501932 CONCLUSIONS: The combination treatment of VK and ACE-I may suppress the cumulative recurrence of HCC after the curative therapy, at least partly through suppression of the VEGF-mediated neovascularization.

"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."