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胃肠道间质瘤发生的分子机制以及伊马替尼治疗研究进展
引用本文:龙庆林,房殿春. 胃肠道间质瘤发生的分子机制以及伊马替尼治疗研究进展[J]. 胃肠病学, 2008, 13(8): 452-455
作者姓名:龙庆林  房殿春
作者单位:第三军医大学西南医院消化科,400038
摘    要:
胃肠道间质瘤(GISTs)是胃肠道最常见的间叶肿瘤,其发生主要与Kit基因和血小板衍生生长因子受体(PDGFR)α基因突变有关。伊马替尼对GISTs有显著疗效,但也存在耐药问题。GISTs对伊马替尼的耐药分为原发性和继发性,原发性耐药与Kit外显子9和PDGFRα外显子18突变有关,继发性耐药与Kit基因继发性突变有关。本文就GISTs发生的分子机制以及伊马替尼治疗的进展作一概述。

关 键 词:胃肠道间质肿瘤  伊马替尼  分子机制  治疗

Molecular Pathogenesis of Gastrointestinal Stromal Tumors and Targeting Drug Therapy with Imatinib
LONG Qinglin,FANG Dianchun. Molecular Pathogenesis of Gastrointestinal Stromal Tumors and Targeting Drug Therapy with Imatinib[J]. Chinese Journal of Gastroenterology, 2008, 13(8): 452-455
Authors:LONG Qinglin  FANG Dianchun
Affiliation:. (Department of Gastroenterology, Southwest Hospital, The Third Military Medical University, Chongqing (400038))
Abstract:
Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. Mutations in Kit gene and platelet-derived growth factor receptor alpha (PDGFRα) gene are strongly correlated with the molecular pathogenesis of GISTs. Imatinib has dramatic antitumor effect on GISTs,however,many patients eventually develop resistance to imatinib. Primary imatinib resistance is related to mutations at exon 9 of Kit and exon 18 of PDGFRα. Secondary imatinib resistance is associated with secondary Kit mutation. In this article,we review the recent advances on the study of molecular pathogenesis of GISTs and treatment of GISTs with imatinib.
Keywords:Gastrointestinal Stromal Tumors  Imatinib  Molecular Mechanisms of Action  Therapy
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