Chen Lei L, Sabripour Mahyar, Andtbacka Robert H I, Patel Shreyaskumar R, Feig Barry W, Macapinlac Homer A, Choi Haesun, Wu Elsie F, Frazier Marsha L, Benjamin Robert S
Department of Sarcoma, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
Curr Oncol Rep. 2005 Jul;7(4):293-9. doi: 10.1007/s11912-005-0053-6.
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.
传统化疗药物对胃肠道间质瘤（GISTs）治疗无效。伊马替尼（STI571、格列卫、甲磺酸伊马替尼；诺华制药公司，新泽西州东哈嫩）是一种KIT、ABL、BCR-ABL、PDGFRA和PDGFRB的选择性抑制剂，代表了靶向癌症治疗的新范例，并彻底改变了慢性粒细胞白血病和GISTs患者的治疗方式。不幸的是，伊马替尼耐药性已经出现。报道的GISTs中伊马替尼耐药机制涉及KIT激酶结构域的错义突变，包括Thr670Ile、Tyr823Asp和Val654Ala。本文讨论了GISTs中伊马替尼耐药的既定机制和潜在机制、提示伊马替尼耐药早期发展的影像学研究以及伊马替尼耐药GISTs的管理。
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