Sunday, January 26, 2014

Puzzling c-KIT

C-kit presence has been used in the definition of GIST and its presence has been used for the sensitivity to TKI (Gleevec).  But this is proven when C-kit is a driver Mutation (driven by localized or in-situ) autoregulation), in other disease C-kit could be present as a secondary event (mitigated response in response to upstream gene overexpression-this conditioned by normal suppressive downregulation), in those cases, TKI will have a minimal effect....
Can Monteluskast or Zafirlukast improve outcome
or does blocking IL3 receptor change outcome
or should we introduce a JAK-STAT inhibitor to affect outcome since the SOCS genes seems to be involved?  SOCS1 is described as a negative inhibitor of JAK/STAT pathway!  Activators of SOCS1 are being looked at in Hepatoma, How frequently is c-Kit positivity in this disease?  What is the meaning of c-Kit in Adenoid Carcinoma (driver Vs secondary)?  Interesting questions indeed!
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