The insulin-like growth factor system as a potential therapeutic target in gastrointestinal stromal tumors

Martin G. Belinsky, Lori Rink, Kathy Q. Cai, Michael F. Ochs, Burton Eisenberg, Min Huang, Margaret Von Mehren, Andrew K. Godwin

Research output: Contribution to journalArticlepeer-review

Abstract

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 PDGFRα. Therapy for GISTs has been revolutionized by the use of the selective tyrosine kinase inhibitor imatinib mesylate (IM). For the subset (∼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.

Original languageEnglish (US)
Pages (from-to)2949-2955
Number of pages7
JournalCell cycle (Georgetown, Tex.)
Volume7
Issue number19
StatePublished - Oct 1 2008

Keywords

  • GISTs
  • Imatinib mesylate
  • Insulin growth factor
  • NYP-AEW541
  • Tyrosine kinase inhibitors

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

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