Open AccessMolecular basis and management of gastrointestinal stromal tumors
Author(s) -
Ulas D. Bayraktar,
Soley Bayraktar,
Caio Rocha-Lima
Publication year - 2010
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v16.i22.2726
Subject(s) - sunitinib , imatinib , stromal cell , gist , tyrosine kinase inhibitor , cancer research , tyrosine kinase , receptor tyrosine kinase , proto oncogene proteins c kit , imatinib mesylate , sunitinib malate , medicine , stem cell factor , oncology , biology , receptor , stem cell , cancer , progenitor cell , microbiology and biotechnology , myeloid leukemia
Molecularly targeted agents have dramatically impacted the management of several cancers. Targeting KIT has led to a new treatment paradigm in gastrointestinal stromal tumors (GISTs). KIT is a cell surface receptor with tyrosine kinases that, upon binding of its ligand, stem cell factor, activates various signaling pathways. Imatinib and sunitinib, both tyrosine kinase inhibitors directed to KIT, were approved for first- and second-line treatment of metastatic and unresectable GISTs. In this article, we will review the molecular pathogenesis of GISTs followed by a discussion of imatinib and sunitinib's role in the treatment of GISTs. Finally, we will introduce novel therapeutic options for imatinib- and sunitinib-resistant GISTs.