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胃肠道间质瘤的分子基础与治疗。

Molecular basis and management of gastrointestinal stromal tumors.

机构信息

Division of Hematology and Oncology, Sylvester Comprehensive Cancer Center, University of Miami, 1475 NW 12th Ave, St 3300, Miami, FL 33136, USA.

出版信息

World J Gastroenterol. 2010 Jun 14;16(22):2726-34. doi: 10.3748/wjg.v16.i22.2726.

Abstract

Molecularly targeted agents have dramatically impacted the management of several cancers. Targeting KIT has led to a new treatment paradigm in gastrointestinal stromal tumors (GISTs). KIT is a cell surface receptor with tyrosine kinases that, upon binding of its ligand, stem cell factor, activates various signaling pathways. Imatinib and sunitinib, both tyrosine kinase inhibitors directed to KIT, were approved for first- and second-line treatment of metastatic and unresectable GISTs. In this article, we will review the molecular pathogenesis of GISTs followed by a discussion of imatinib and sunitinib's role in the treatment of GISTs. Finally, we will introduce novel therapeutic options for imatinib- and sunitinib-resistant GISTs.

摘要

分子靶向药物极大地改变了多种癌症的治疗方式。针对 KIT 的治疗已经为胃肠道间质瘤(GISTs)带来了新的治疗范例。KIT 是一种细胞表面受体,具有酪氨酸激酶,当它的配体干细胞因子结合时,会激活各种信号通路。伊马替尼和舒尼替尼,这两种针对 KIT 的酪氨酸激酶抑制剂,被批准用于转移性和不可切除的 GISTs 的一线和二线治疗。在本文中,我们将回顾 GISTs 的分子发病机制,然后讨论伊马替尼和舒尼替尼在 GISTs 治疗中的作用。最后,我们将介绍针对伊马替尼和舒尼替尼耐药的 GISTs 的新的治疗选择。

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Molecular basis and management of gastrointestinal stromal tumors.胃肠道间质瘤的分子基础与治疗。
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KIT mutations in GIST.胃肠道间质瘤中的KIT基因突变
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