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首页> 外文期刊>European Journal of Cancer Supplements >Molecular basis for treatment of gastrointestinal stromal tumours
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Molecular basis for treatment of gastrointestinal stromal tumours

机译：胃肠道间质瘤治疗的分子基础

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Gastrointestinal stromal tumour (GIST) is a rare tumour of the gastrointestinal tract that arises from activating mutations in KIT or platelet-derived growth factor receptor alpha (PDGFRalpha). Imatinib, a molecularly targeted therapy that inhibits the kinase activity of KIT, PDGFRs, ABL, and BCR-ABL, has been shown to be highly efficacious in patients with advanced GIST. Most patients with advanced GIST treated with imatinib achieve either a partial response or experience stable disease, and median survival is longer than 3 years in either case. There is a strong correlation between the type of KIT or PDGFRA mutation and the clinical response to imatinib in patients with advanced GIST. In a phase II trial, significantly higher partial response rates were achieved in patients with GISTs harbouring KIT exon 11 mutations than in patients with GISTs harbouring KIT exon 9 mutations or in patients with GISTs exhibiting no detectable KIT or PDGFRA mutations. Resistance to imatinib treatment is a clinical challenge in the management of patients with advanced GIST. Many imatinib-resistant GISTs have an associated secondary kinase mutation of KIT or PDGFRA. Continuing research efforts are directed at optimising the use of imatinib in patients with advanced GIST as well as the development of novel treatment approaches to prevent and/or treat imatinib-resistant clones of GIST.
机译：胃肠道间质瘤（GIST）是胃肠道的一种罕见肿瘤，由KIT或血小板源性生长因子受体α（PDGFRalpha）的激活突变引起。伊马替尼是一种分子靶向疗法，可抑制KIT，PDGFRs，ABL和BCR-ABL的激酶活性，在晚期GIST患者中非常有效。接受伊马替尼治疗的大多数晚期GIST患者可达到部分缓解或经历稳定的疾病，两种情况下中位生存期均超过3年。晚期GIST患者的KIT或PDGFRA突变类型与对伊马替尼的临床反应之间存在很强的相关性。在一项II期试验中，具有KIT外显子11突变的GIST患者比具有KIT外显子9突变的GIST患者或未表现出可检测到的KIT或PDGFRA突变的GIST患者获得了更高的部分缓解率。对伊马替尼治疗的耐药性是晚期GIST患者治疗中的临床挑战。许多抗伊马替尼的GIST具有相关的KIT或PDGFRA继发激酶突变。持续的研究工作旨在优化伊马替尼在晚期GIST患者中的使用，以及开发预防和/或治疗伊马替尼耐药性GIST克隆的新型治疗方法。

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