I think subgroup analyses in some of the anti-EGFR antibody trials have shown that KRAS mutant patients actually did worse in terms of PFS than the control group. I can't recall any specific trials though.
Correct. Although of all the examples I cited it has the weakest dichotomy it nonetheless repeats across many different trials and combos in CRC. Each individual p value nothing definitive (except combo with FOLFOX) but in aggregate very definitive.
I think part of this may be due to do compensatory mechanisms, i.e. when you inhibit one pathway, you activate another one.
Agreed - but it is an interesting and non-intuitive effect. Damaging the OS I can understand (via toxicity to patient), but accelerated tumor growth commonly occurring across the meta-class is just very counter intuitive to me.
Or it could just be statistical noise.
No, I was moderately careful to pick only fairly definitive examples. That said, it is may be a little bit hyperbolic to say that more typical than atypical since even in these drugs I didn't check to see how many indications it happened in. E.g. Does Erbitux have similar characteristics in Head and Neck cancers?