DCA and Vidaza and Colon Cancer
by Robert Miller
(Hollywood Beach Fl USA)
I may have told my story here before but it has changed so here goes.
DXed colon cancer 10/1/2006
Stage 2A no chemo for first two years thought I was cured by resection in 12/12/2006.
DXed with Metastatic Colon cancer 4/10 2009.
Started using DCA, Sodium Dichloroacetate, that is self medicating due to a strange set of circumstances 5/21/2009.
Tumor shrinkage reported in CT scan in July of 30%.
Tumor shrinkage reported in CT scan in Sept of and additional 25%.
Kept taking DCA for 14 more months and having no more shrinkage but stable desease.
Stopped taking DCA 11/3/2010 because of worries about peripheral neuropathy that DCA caused.
5 months later went on regular first line chemo, Folfiri and Avastin, still on them with 13 weeks to go.
What is new? I think I may have a cure for my colon cancer and other cancers. Why did DCA stop shrinking my tumor but keep it stable? This has been the question.
A researcher at The Georgia Medical Center asked a different question. Why did it take such a high dose of DCA to have an anti cancer affect and why did you have to take that high dose for three months before you saw any affect.
Good question except that in my case I had the most affect in the first four months at high dose. Why? I called him. It seems that in most cancer cells a gene, SLC5A8, is turned off. It is a very good sodium transporter, that is it transports molecules like Sodium Dichloroacetate, DCA, into normal cells. If DCA can get into a cancer cell it will die.
DCA can still get into a cancer cell even if the SLC5A8 gene is turned off but it is much harder and happens less often.
Viola, this fits my experience with Colon cancer and DCA. It seems that in Colon cancer as much as 48% of cells do NOT have the SLC5A8 gene turned off and DCA should have no problem getting into the cell and facilitating its death. And since I have KRAS Wild Type colon cancer even more of my cancer cells may have the SLC5A8 gene active.
So DCA was able to facilitate the death of a lot of my cancer cells at first, the easy ones with SLC5A8 turned on and later was able to kill enough of the cancer cells with SLC5A8 turned off to maintain a stable tumor size.
If this theory is correct then if you could turn back on the SLC5A8 gene in the remaining cancer cells where it is turned off you could eliminate all cancer cells easily.
The researcher at Georgia Medical Center says that using a DNA Methylation Inhibitor should do the trick and also allow the use of DCA at much reduced dosage which should keep the peripheral neuropathy at bay.
There is a drug he thinks would work, Vidaza from Celgene. It is a chemo itself but in our plan it would be used at 1/3 dosage to cause the SLC5A8 gene to be healed.
The neat thing about this to me is that in both cases, DCA and Vidaza, we are talking about correcting, healing, the cancer cell, bringing it back to a more normal function so that the cancer cell can kill itself thru the normal process of apoptosis.
There may be no getting around this process unlike with most chemo where the cancer finds a way to survive the chemo and come back. If you are just returning a cancer cell to a more normal existence wherein it decides thru a normal process to die what would cause it to defend against this action?
We may see Phase II trials of this soon. I hope so. In the meantime I am looking for a doctor to help me use DCA and Vidaza in an off label trial with me as the subject. Anyone know of someone?
robmxa@gmail.com
