As I approach completing three years in this trial I am developing wild type melanoma on my chest and face. I have had six knife fights since Ausust getting rid of it while it is still in situ. The speculation is that the BRAF at V600 E has been acting as a governor of a cassette of downstream genes that keep them in check, but once the drugs took over the BRAF, and inhibited it, it caused the downstream grouping to fire up wild type melanoma. This is not happening with my non-redhead cohorts. There is a hypothesis that since my red haired genes are not recessive, but active, it only affects red heads.
The rest are not developing this wild type melanoma. I would like to know if this is happening to other red heads in the trial. The question to be answered is whether or not the BRAF has returned to normal, and if so, by stopping the inhibitors, would it again start to govern the downstream gene grouping that is causing the wild type melanoma, and shut it down. Isn't it a grand thing to be part of this cutting edge of knowledge? I feel so fortunate to still be here and have my primary BRAF positive cancer to remain in check so long, but maybe it is time for an experiment within the experiment and see what happens if I stop the meds. I might run out of skin to stretch if this goes on too long!
