Cancer

A large number of new vitamin D studies have appeared in the scientific literature since I wrote my plea to the federal government. These studies don't just confirm what we knew 16 months ago-they show that optimizing vitamin D intake will save even more lives than what we projected. Vitamin D More Effective Than Previously Known For instance, a study published in June 2008 showed that men with low vitamin D levels suffer 2.42 times more heart attacks. Now look what this means in actual body counts.

High prevalence of vitamin D deficiency despite supplementation in premenopausal women with breast cancer undergoing adjuvant chemotherapy. Crew KD, Shane E, Cremers S, McMahon DJ, Irani D, Hershman DL. J Clin Oncol. 2009 May 1;27(13):2151-6. Epub 2009 Apr 6. PMID: 19349547 DOI: 10.1200/JCO.2008.19.6162 Conclusion Vitamin D deficiency is highly prevalent in women with breast cancer. The current recommended dietary allowance of vitamin D is too low to increase serum 25-OHD greater than 30 ng/mL. Optimal dosing for bone health and, possibly, improved survival has yet to be determined.

Evidence from clinical trials shows, with a wide margin of confidence, that a prolonged intake of 10,000IU/d of vitamin D3 poses no risk of adverse effects for adults, even if this is added to a rather high physiologic background level of vitamin D. Vitamin D and cancer mini-symposium: the risk of additional vitamin D. Vieth R.\nAnn Epidemiol. 2009 Jul;19(7):441-5. Epub 2009 Apr 11. PMID: 19364661 doi:10.1016/j.annepidem.2009.01.009

What is VITAL? The VITamin D and OmegA-3 TriaL (VITAL) is a research study in 20,000 U.S. men and women investigating whether taking daily dietary supplements of vitamin D (about 2000 IU) or fish oil (about 1 gram of omega-3 fatty acids) reduces the risk of developing cancer, heart disease, and stroke in people who do not have a prior history of these illnesses. Recruitment for the study will begin in January 2010.

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.

Development of HPV vaccines for HPV-associated head and neck squamous cell carcinoma. Devaraj K, Gillison ML, Wu TC. Crit Rev Oral Biol Med. 2003;14(5):345-62. Review. PMID: 14530303

Antitumor activity of human papillomavirus type 16 E7-specific T cells against virally infected squamous cell carcinoma of the head and neck. Albers A, Abe K, Hunt J, Wang J, Lopez-Albaitero A, Schaefer C, Gooding W, Whiteside TL, Ferrone S, DeLeo A, Ferris RL. Cancer Res. 2005 Dec 1;65(23):11146-55. PMID: 16322265

ScienceDaily (June 15, 2009) - Using a highly sensitive new test, scientists in Europe are reporting "convincing evidence" that marijuana smoke damages the genetic material DNA in ways that could increase the risk of cancer.

ROCHESTER, Minn. -- Two Mayo Clinic patients whose prostate cancer had been considered inoperable are now cancer free thanks in part to an experimental drug therapy that was used in combination with standardized hormone treatment and radiation therapy. The men were participating in a clinical trial of an immunotherapeutic agent called MDX-010 or ipilimumab. In these two cases, physicians say the approach initiated the death of a majority of cancer cells and caused the tumors to shrink dramatically, allowing surgery. In both cases, the aggressive tumors had grown well beyond the prostate into the

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Below is a list of publications covering the research being done by UW and other institutions on artemisinin and cancer. The list is organized into two categories: publications related to the effects of artemisinin and its analogs on cancer and artemisinin pharmacology and pharmacokinetics. You may find them useful when consulting with your personal physician. We have also compiled a comprehensive list of artemisinin-related articles (more than 350 publications) that you may also find useful.

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.

Artemisia Annua (Sweet Wormwood) is a shrubby perennial native to China. The leaf of the plant contains up to 0.04 percent Artemisinin. This herb has been used over the centuries by Chinese medical practitioners. Artemisinin came to the attention of the World Health Organization in the 1970s when Quinine lost efficacy against malaria. Artemisinin is the only drug effective against malaria and hundreds of millions of doses are prescribed for that purpose every year. The artemisinin molecule has an affinity for iron, which the malarial parasite sequesters internally. Artemisinin enters the malarial parasite and combines with sequestered iron to create Reactive Oxygen Species, rupturing the parasite. Like malarial parasites, cancer cells concentrate and sequester high levels of iron. Moreover cancer cells overexpress cell surface receptors for iron-containing compounds like ferritin and holotransferrin. Therefore, Artemisinin has a high affinity for cancer cells, and upon entering the cell combines with intercellular iron creating ROS-mediated apoptosis. Artemisinin is the only chemotherapeutic agent that lacks the tertiary amine necessary to usher the drug back out of the cell. This document is based on the research of Dr. Henry Lai and Dr. Narenda Singh at the University of Washington,and the medical practice of Dr. Ba Hoang of Vietnam and San Jose, California. There are a few points of divergence among experts studying Artemisinin, therefore more than one protocol is outlined below.

Nutritional intervention with omega-3 Fatty acids in a case of\nmalignant fibrous histiocytoma of the lungs. Pardini RS, Wilson D, Schiff S, Bajo SA, Pierce R. Nutr Cancer. 2005;52(2):121-9. PMID: 16201843

Other compounds to consider

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