期刊
CELL CYCLE
卷 7, 期 19, 页码 2949-2955出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.7.19.6760
关键词
GISTs; insulin growth factor; imatinib mesylate; tyrosine kinase inhibitors; NYP-AEW541
类别
资金
- NIH [CA106588, U10 CA21661, CA009035-31]
- FCCC Translational Research Committee [P30 CA006927]
- GIST Cancer Research Fund
- NATIONAL CANCER INSTITUTE [P30CA006927, T32CA009035, R01CA106588, U10CA021661] Funding Source: NIH RePORTER
The majority of gastrointestinal stromal tumors (GISTs) are characterized by oncogenic gain-of-function mutations in the receptor tyrosine kinase (RTK) c-KIT with a minority in PDGFR alpha. Therapy for GISTs has been revolutionized by the use of the selective tyrosine kinase inhibitor imatinib mesylate (IM). For the subset (similar to 10-15%) of GISTs that lack oncogenic mutations in these receptors, the genetic changes driving tumorigenesis are unknown. We recently reported that the gene encoding the insulin-like growth factor 1 receptor (IGF-1R) is amplified in a subset of GISTs, and the IGF-1R protein is overexpressed in wild-type and pediatric GISTs. In this report we present a more complete picture of the involvement of components of the insulin-like growth factor-signaling pathway in the pathogenesis of GISTs. We also discuss how the IGF pathway may provide additional molecular targets for the treatment of GISTs that respond poorly to IM therapy.
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