Imatinib resistance in gastrointestinal stromal tumors.

Lei L Chen, Mahyar Sabripour, Robert H I Andtbacka, Shreyaskumar R Patel, Barry W Feig, Homer A Macapinlac, Haesun Choi, Elsie F Wu, Marsha L Frazier, Robert S Benjamin

Department of Sarcoma, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA. llchen@mdanderson.org

Current oncology reports 2005 Jul

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Conventional chemotherapeutic drugs are ineffective in treatment of gastrointestinal stromal tumors (GISTs). Imatinib (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs. Unfortunately, imatinib resistance has emerged. The reported mechanism of imatinib resistance in GISTs involves missense mutation in the kinase domain of KIT, including Thr670Ile, Tyr823Asp, and Val654Ala. The established mechanisms and potential mechanisms of imatinib resistance in GISTs, the imaging studies indicative of early development of imatinib resistance, and the management of imatinib-resistant GISTs are discussed.

Citation

Lei L Chen, Mahyar Sabripour, Robert H I Andtbacka, Shreyaskumar R Patel, Barry W Feig, Homer A Macapinlac, Haesun Choi, Elsie F Wu, Marsha L Frazier, Robert S Benjamin. Imatinib resistance in gastrointestinal stromal tumors. Current oncology reports. 2005 Jul;7(4):293-9