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World J Gastroenterol. Jun 14, 2010; 16(22): 2726-2734
Published online Jun 14, 2010. doi: 10.3748/wjg.v16.i22.2726
Published online Jun 14, 2010. doi: 10.3748/wjg.v16.i22.2726
Molecular basis and management of gastrointestinal stromal tumors
Ulas D Bayraktar, Soley Bayraktar, Caio M Rocha-Lima, Division of Hematology and Oncology, Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL 33136, United States
Author contributions: Bayraktar UD, Bayraktar S and Rocha-Lima CM performed the literature search; Bayraktar UD, Bayraktar S wrote the paper; Bayraktar UD, Rocha-Lima CM critically revised the paper.
Correspondence to: Ulas D Bayraktar, MD, Division of Hematology and Oncology, Sylvester Comprehensive Cancer Center, University of Miami, 1475 NW 12th Ave, St 3300, Miami, FL 33136, United States. ubayraktar@med.miami.edu
Telephone: +1-305-4580998 Fax: +1-305-5850037
Received: January 13, 2010
Revised: February 7, 2010
Accepted: February 14, 2010
Published online: June 14, 2010
Revised: February 7, 2010
Accepted: February 14, 2010
Published online: June 14, 2010
Abstract
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.
Keywords: Gastrointestinal stromal tumor, KIT, Imatinib, Sunitinib, Nilotinib