Bob Miller asked me to post the following message. I suggest to anyone that has problems posting, to create a new account and try again.
There is a new theory on why DCA stops working after awhile. If true it would be possible to keep DCA working to kill cancer where it does now and make it work in other cancers.
A Dr. Ganapathy from the Georgia Medical Center has a paper out in which he explores why it takes a large dose of DCA to incur an anti cancer affect and why such a dose has to be taken over at least three months. I believe this was the same position taken by Dr. Evangelos Michelakis of the University of Alberta.
I called Dr. Ganapathy because my experience with DCA was the exact opposite of his thinking. I had a major reduction in Metastatic Colon Cancer tumor size in the first three months.
His theory is that a gene, SLC5A8, is not working in most cancer cells. SLC5A8 is a very efficient sodium transporter into all cells. It transports Sodium Dichloroacetate, DCA, into all cells where it is functioning.
In researching SLC5A8 and Colon Cancer cells I found that in 48% of colon cancer cells the SLC5A8 gene is NOT turned off. This might explain why DCA was able to kill off as much as 70% of my MCC tumor before it stopped. Even after DCA stopped shrinking my tumor it maintained the tumor in a stable condition for 14 months.
Why? Dr. Ganapathy says that DCA can still get into cancer cells where the SLC5A8 gene is not working but it has a much harder time doing so.
That would suggest that during the entire 18 months I took DCA it was able to easily kill off any cancer cell where the SLC5A8 gene was working. After DCA killed off all or most of the cells with a functioning SLC5A8 gene it was left with ONLY those cells where the SLC5A8 gene was NOT functioning and was only able to maintain a stable situation. Only kill cells at a rate that they were being replaced.
If so Dr. Ganapathy says that there is a fix for the SLC5A8 gene. A DNA Methylation Inhibitor like Vidaza could turn back on the SLC5A8 gene and allow the transport of DCA easily into the remaining cancer cells. If it could do so this could be a cure.
Dr. Ganapathy also says that if this is true you could take DCA at a much lower dose, say 25% of what people like me currently use, have used. If so the problem of Peripheral Neuropathy would be substantially reduced if not eliminated. PN has been the reason I and many had to stop using DCA.
Also Vidaza is a chemo itself but in this instance would not be used as such and could be used at only 1/3rd of the dose it is currently used at as a chemo.
The neat thing to me is that both DCA and Vidaza would be used not to directly kill cancer cells but to cure cancer cells, to correct functions of cancer cells so that they are more normal and can then kill themselves. This suggest to me at least that the cancer cell would not be able to or induced to try to find a way around this therapy like so many cancers do with current chemotherapies.
Anyway others are interested in this theory and a Phase II trial may be in the works.
I have found a doctor who is willing to work with me off label to try DCA with Vidaza though I will not be doing so immediately. At the moment I am on Folfiri and Avastin which are working very well to at least reduce my tumor load as they say.
But I plan on then going with DCA and Vidaza to deliver what I think could be a knock out punch for my MCC and many other cancers.
It has been almost five years since my initial Colon Cancer diagnosis and I credit being here to DCA. It may now be that DCA will get credit for my being here a while longer.