Systemic Therapy for Advanced Gastrointestinal Stromal Tumors: Beyond Imatinib

被引：15

作者：

Kim, Edward J. ^{[1
]}

Zalupski, Mark M. ^{[1
]}

机构：

[1] Univ Michigan, Dept Internal Med, Div Hematol & Oncol, Ann Arbor, MI 48109 USA

来源：

JOURNAL OF SURGICAL ONCOLOGY | 2011年 / 104卷 / 08期

关键词：

GIST; tyrosine kinase inhibitors; KIT PDGFR; ENDOTHELIAL GROWTH-FACTOR; TYROSINE KINASE INHIBITORS; DASATINIB BMS-354825; KIT MUTATIONS; PHASE-II; RESISTANT; ANGIOGENESIS; MECHANISMS; MASITINIB; MOTESANIB;

D O I：

10.1002/jso.21872

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Progression on first-line therapy with imatinib in gastrointestinal stromal tumors (GIST) is caused by either initial resistance or more often a secondary mutation in tyrosine kinases KIT or PDGFR. Therapies in development for imatinib-resistant GIST include agents that target KIT/PDGFR with greater potency or possess broader kinase inhibition profiles including VEGFR. To circumvent secondary mutations in KIT/PDGFR, inhibition of the downstream signaling in PI3K/Akt/mTOR pathway and enhanced degradation of KIT/PDGFR are also under investigation. J. Surg. Oncol. 2011;104:901-906. (C) 2011 Wiley Periodicals, Inc.

引用

页码：901 / 906

页数：6

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