Targeting ETV1 in gastrointestinal stromal tumors: tripping the circuit breaker in GIST?
Activating mutations in the KIT or PDGFRA receptor tyrosine kinase genes are the key oncogenic drivers in the majority of gastrointestinal stromal tumors (GIST), but novel results now show that aberrant kinase signaling is potentiated by a positive feedback circuit that involves the ETS transcription factor ETV1. Targeting ETV1 can disrupt this circuit and represents a promising new therapeutic approach for the treatment of GISTs.
Cancer Therapeutics Program, University of Pittsburgh Cancer Institute, Hillman Cancer Center, Pittsburgh, Pennsylvania. Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. aduensin@pitt.edu.
Anette
A
Duensing
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D046152:Gastrointestinal Stromal Tumors / Q000378:metabolism*; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D014157:Transcription Factors / Q000378:metabolism*
D000970:Antineoplastic Agents; D004268:DNA-Binding Proteins; C095239:ETV1 protein, human; D047428:Protein Kinase Inhibitors; D014157:Transcription Factors; D019009:Proto-Oncogene Proteins c-kit; D020928:Mitogen-Activated Protein Kinases