Letters To The Editor
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World J Gastroenterol. Jan 7, 2013; 19(1): 144-146
Published online Jan 7, 2013. doi: 10.3748/wjg.v19.i1.144
Is exon mutation analysis needed for adjuvant treatment of gastrointestinal stromal tumor?
Mehmet Ali Nahit Şendur, Nuriye Yıldırım Özdemir, Muhammed Bülent Akıncı, Dogan Uncu, Nurullah Zengin, Sercan Aksoy
Mehmet Ali Nahit Şendur, Nuriye Yıldırım Özdemir, Muhammed Bülent Akıncı, Dogan Uncu, Nurullah Zengin, Department of Medical Oncology, Ankara Numune Education and Research Hospital, Ankara 06100, Turkey
Sercan Aksoy, Department of Medical Oncology, Hacettepe University Instıtute of Oncology, Ankara 06100, Turkey
Author contributions: Şendur MAN, Aksoy S and Özdemir NY wrote the paper; Akıncı MB, Uncu D and Zengin N designed the paper.
Correspondence to: Mehmet Ali Nahit Şendur, MD, Department of Medical Oncology, Ankara Numune Education and Research Hospital, Sihhiye, Ankara 06100, Turkey. masendur@yahoo.com.tr
Telephone: +90-312-5084600 Fax: +90-312-3112778
Received: June 22, 2012
Revised: September 25, 2012
Accepted: November 11, 2012
Published online: January 7, 2013
Abstract

Gastrointestinal stromal tumors (GISTs) are the most common soft tissue sarcoma of the gastrointestinal tract, resulting from an activating mutation of stem cell factor receptor (KIT), and an activating mutation of the homologous platelet-derived growth factor receptor alpha (PDGFRA) kinase. Most GISTs (90%-95%) are KIT-positive. About 5% of GISTs are truly negative for KIT expression. GISTs have been documented to resistant conventional chemotherapeutics. Due to the KIT activation that occurs in the majority of the cases, KIT inhibition is the primary treatment approach in the adjuvant treatment of metastatic GISTs. Imatinib mesylate is an oral agent that is a selective protein tyrosine kinase inhibitor of the KIT protein tyrosine kinase, and it has demonstrated clinical benefit and objective tumor responses in most GIST patients in phase II and III trials. The presence and the type of KIT or PDGFRA mutation are predictive of response to imatinib therapy in patients with advanced and metastatic disease. Molecular analysis in phase I-II trials revealed significant differences in objective response, progression-free survival, and overall survival between GISTs with different kinase mutations. The aim of this letter is to touch on the need for exon mutation analysis for adjuvant treatment with imatinib in GIST patients.

Keywords: Imatinib; Gastrointestinal stromal tumor; Activating mutation; Stem cell factor receptor; Platelet-derived growth factor receptor alpha; Mutation analysis