Discovery of KRAS G12C mutation was important, and Inhibitors or "blockers" of this
protein have shown promise. However, with the rapid regeneration of the G12C
proteins, inhibition is no longer present. Rapid KRASD PCR could be helpful at initial
diagnosis/request, but wouldn't help as the G12C proteins regenerate. We need a
drug that turns off the production of G12C or one that has longer bioavailability so
the regenerated proteins are constant being inactivated. Gene modification seems
like the ideal target, unless the inhibitors have no significant side effects and can be
administered every day or every other day. Turning off/inactivating G12C alone
could be adequate in this setting, but direct gene suppression/modification would
seem more ideal.
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