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Mortality and cancer incidence in cohorts of Swedish fishermen and fishermen's wives: updated findings.\nMikoczy Z, Rylander L.\nChemosphere. 2009 Feb;74(7):938-43. Epub 2008 Nov 28.\nPMID: 19041115

Dichloroacetate (DCA) Promising for Endometrial Cancer DCA virtually disappeared from the news about a year ago when it was forced off the open market by the FDA and all research into its efficacy as a cancer therapeutic had to go through officially sanctioned channels. I've kept track of it all this time through Google Email Alerts. This is the first bit of news on it in relation to cancer in a long time.

BioVex Inc, a company developing new generation biologics for the treatment and prevention of cancer and infectious disease, announced that updated survival data from its Phase II study in metastatic melanoma will be presented at the 2009 American Society of Clinical Oncology (ASCO) Annual Meeting, taking place from May 29, 2009 - June 2, 2009 in Orlando, F

OncoLink was founded in 1994 by Penn cancer specialists with a mission to help cancer patients, families, health care professionals and the general public get accurate cancer-related information at no charge. Recent changes have been made to OncoLink to update the look and feel of our site. OncoLink is designed to make it easy for the general public to navigate through the pages to obtain the information that they want. The home page has buttons and hypertext links. If you click on the buttons or the underlined text with your mouse, you will go directly to your area of interest.

For the first time in the world, on December 7, 2007 we publicly shared our observational data from the treatment of 118 cancer patients with DCA. In March 2008 we updated our data from treating over 175 patients. As of August 2008, we have treated over 265 cancer patients with DCA. Results of the analysis of our latest data are very similar to our two earlier reports.

The April issue of the journal Cancer Prevention Research published the results of a trial conducted by scientists at Tokyo University of Science, the University of Tsukuba in Japan, and Johns Hopkins University which determined that the isothiocyanate sulforaphane, a compound that occurs in high amounts in broccoli and its sprouts, helps suppress infection by Helicobacter pylori (H. pylori), the bacteria responsible for stomach ulcers and many cases of stomach cancer. The trial is the first to demonstrate an effect for broccoli against H. pylori in humans.

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!

www.freeDCA.com is a scam A new scam site has popped up. www.freeDCA.com. This site has all the hallmarks of the previous scammer, who remains at large. Whether it is him or another person, this one is a fake.

This month, the authoritative International Agency for Research into Cancer (IARC) have weighed in on the issue. By gathering a group of expert scientists, they have looked at all the available evidence and published a detailed report on vitamin D and cancer. The massive tome weighs in at 465 pages, but we'll take a look at the key points in the first of two posts looking at the vitamin D debate. It is impossible for us to get more than about five percent of the vitamin D we need from our diet - unless, like Eskimos, we eat oily fish three times a day.

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.

Mice injected with cancer cells experienced significantly elevated levels of C-reactive protein, white blood cells, and lipid peroxidation compared with control mice. These levels were reduced in animals that received cisplatin and/or DHA. While treatment with 125 mg/kg DHA inhibited tumor growth by 38 percent compared to untreated animals, 250 mg/kg suppressed tumor growth by 79 percent, which was a greater effect than that of cisplatin alone (which was associated with a 55 percent reduction). The combination of DHA and cisplatin resulted in an 81 percent inhibition of growth, while reducing elevated white blood cell levels (leukocytosis) to normal levels. Treatment with the higher dose of DHA alone was associated with a similar reduction in white blood cells, which, when elevated, are associated with tumor growth. A strong relationship was observed between tumor growth and white blood cell levels as well as C-reactive protein levels. In another experiment with rats treated with cisplatin, the addition of 250 mg/kg DHA prevented lethal kidney toxicity in 88 percent of the animals that received it, while none of the rats that received cisplatin alone survived.