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Biotech / Medical : ARIAD Pharmaceuticals -- Ignore unavailable to you. Want to Upgrade?

To: Biomaven who wrote (3258)	3/1/2014 10:35:15 AM
From: jaybe	Respond to of 4474

I see that MET inhibitors have a ways to go but dual-acting mechanisms against key cross-talk pathways could be what's needed. Why not inhibit both EMT and MET, isn't this desirable for advanced stages? I keep going back to receptors purely based on TC's "kinase that is well validated as driver of a set of oncogenes". It seems to me, admitted with limited knowledge in this area, that although fusion genes are drivers the target is typically a specific oncogene, not a "set". Regarding TMPRSS2/ERG, shouldn't we be looking for fusion proteins where one of the partners has a tyrosine domain?