KIT and BRAF heterogeneous mutations in gastrointestinal stromal tumors after secondary imatinib resistance

Conclusions This finding, in combination with the loss of KIT expression, suggests the possibility of activation of RAS-RAF-MEK-ERK pathways driven by a KIT-independent oncogenic mechanism. Understanding the genetic aberrations beyond KIT and PDGFRA may lead to the identification of additional therapeutic targets for GISTs.

http://link.springer.com/10.1007/s10120-014-0414-7

Source: Gastric Cancer - September 18, 2015 Category: Gastroenterology Source Type: research