Gastrointestinal stromal tumors (GISTs) owe their development to the activating mutations in mast/stem cell
growth factor receptor (KIT) or platelet-derived growth factor receptor A (PDGFRA) oncogenes. Both these KIT and
PDGFRA oncogenes are members of the type III transmembrane receptor tyrosine kinase family that stimulates intracellular
signaling pathways controlling cell proliferation, adhesion, apoptosis, survival, and differentiation. The presence and
type of KIT/PDGFRA mutations help to predict the imatinib mesylate therapy, a selective tyrosine kinase inhibitor.
Moreover, there is reported a small proportion of wild-type GISTs for both KIT and PDGFRA genes, and tumors more often
acquire secondary mutations on KIT, that results into imatinib resistance. New patents to the GISTs imatinib resistant
have recently been introduced. At present, sunitinib, is prescribed as second line therapy for patients with imatinibresistant
or imatinib-intolerant GIST, and a number of other drugs, such as masitinib and valatinib, are in the pipeline. The
present research focuses on GISTs diagnostic, prognostic and therapeutic biomarkers and addresses the development of
novel patents for the treatment of these patients.