50-60% of melanomas carry a BRAF gene V600E or V600K mutation. A less common, but still frequent mutation, is in the NRAS gene, where about 15-20% of melnaomas carry a mutation. BRAF and NRAS mutations are almost always mutually exclusive.
I don't have the BRAF V600E or K mutation (I do have a G466E BRAF mutation). However, I do have one of the common NRAS gene mutations, at codon (location) 12.
Mine is called a G12A NRAS mutation because what should be a glycerine acid (G) is an alanine acid (A) at position 12. This mutation does not currently have a directly targeted therapy. However, some current and upcoming MEK inhibitor and MEK combination trials (with PI3K inhibitors) are specifically targeting NRAS-mutant melanomas. My doctors think there may be some combination trials perhaps 6 months or so out from now that maybe it might be possible for me to be a candidate for.
I might have mixed up MEK combo trials in my previous post (conversation w/dermatologist), which would explain why my oncologist told me it would be ill advised for me to be on any combination trial where one agent was a BRAF inhibitor. Whereas a combination with a PI3K inhibitor could be of interest, he said.
I don't have the BRAF V600E or K mutation (I do have a G466E BRAF mutation). However, I do have one of the common NRAS gene mutations, at codon (location) 12.
Mine is called a G12A NRAS mutation because what should be a glycerine acid (G) is an alanine acid (A) at position 12. This mutation does not currently have a directly targeted therapy. However, some current and upcoming MEK inhibitor and MEK combination trials (with PI3K inhibitors) are specifically targeting NRAS-mutant melanomas. My doctors think there may be some combination trials perhaps 6 months or so out from now that maybe it might be possible for me to be a candidate for.
I might have mixed up MEK combo trials in my previous post (conversation w/dermatologist), which would explain why my oncologist told me it would be ill advised for me to be on any combination trial where one agent was a BRAF inhibitor. Whereas a combination with a PI3K inhibitor could be of interest, he said.
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