When we think of genetic factors which predispose people to developing cancer, we usually think of mutations in selective growth control genes. These mutations are irreversible. But what most people do not realize is that there is another group of genetic alterations which influence the development of cancer that are not mutations and ARE reversible. These genetic factors are considered epigenetic modifications of gene functioning.
Many genes, especially tumor suppressor genes, are inactivated when certain DNA sequences in these genes are hypermethylated. Gene methylation is a normal method by which gene activity is modulated. Unfortunately, DNA methyltransferases, the enzymes which transfer the methyl group to the gene sequences, are over expressed in almost all cancers. Prostate cancer harbors a very large number of methylated, therefore inactive, genes.
The reactivation of these genes by DNA methyltransferase inhibitors is a major area of scientific research.
The oncogene RAS, which exists in mutated form in 30-50% of ALL cancers and leukemias, is responsible for the over activation of the DNA methyltransferase genes, thereby stimulating the production of a large number of gene silencing methyltransferase enzymes. Those cancers that do not harbor mutations in the RAS gene have mutations in downstream RAS signaling pathways that also can contribute to DNA methyltransferase activity.
When DNA methyltransferase genes are introduced into normal cells, these cells become transformed or cancerous. If DNA methyltransferase genes are "turned off" by chemical means, the DNA in these cancer cells becomes demethylated and the cells die of apoptosis. DNA methyltransferase enzymes are clearly fundamental for the cancer transformation process.
A number of DNA methyltransferase inhibitors are in development. Unfortunately, some of these inhibitors have proven toxic to normal cells. Sodium selenite is a powerful inhibitor of DNA methyltransferases. The selenite molecule directly binds the methyltransferase enzyme and inhibits its activity. This inhibition has NOTHING to do with selenite's ability to induce oxidative stress. This means that selenite can induce apoptosis in cancer and leukemia cells regardless of their p53 status. This is very good news.
Sodium selenite remains a critical component of our cancer and leukemia treatment protocols. The dose is one milligram per day, or five 200 microgram pills over the course of a day. This dose of selenite is not toxic in humans.
Stay tuned...
Grouppe Kurosawa, Medicine in the Public Interest
http://www.grouppekurosawa.com
Because several reports said selenium as L-selenomethionine was more bio-available than sodium selenite and local-shop-available, I've been taking that. Has that been useless as source of selenium?
I've got a large supply of sodium selinite on order. It's not in my local shops.
Posted by: satx2 | November 28, 2008 at 12:22 PM
Yes it is useless for our purposes.
Posted by: Dr. Steve | November 28, 2008 at 01:40 PM