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Wednesday, May 27, 2015 9:36:43 AM
OK humor me. I will try to restate, based on looking at the papers recently cited and your post, and then if you wish you may correct.
There are many ways that p53, a critical gene for tumor suppression, may be disabled. It is possible that these different mechanisms of disabling the gene will lend themselves to different approaches to regulating cancer cell growth with p53 targets. More specifically, a missense mutation in one area of the gene may well do better with one small molecule than another, in terms of downgrading or restoring function.
Two drugs, APR246 and A190,appear to work by helping mutant p53 bind and function again.(Although A190 works not via p21 but through NEDD9 in this lung ca model)
K works to 1)degrade mutant mutant p53 and 2)directly induce apoptosis by reactions of this degraded p53 with cell cytoplasm/mitochondrial proteins.
It is not yet clear which approach will work best and if in fact many different approaches are needed.
Does that sound right to you?
On another note: remember when triple therapy for HIV was started, and how revolutionary it was at the time? Are we headed for triple p53 therapy?
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