Understanding the MIG6-EGFR Signaling Axis in Lung Tumorigenesis.
With multiple clinical trials under way targeting mutant EGFR in patients with lung cancer, Maity and colleagues address important aspects of a MIG6-EGFR signaling axis using genetically engineered mouse models expressing mutated EGFRs on the MIG6-deficient background. This study extends our understanding of EGFR regulation by MIG6 and reveals that MIG6 antagonizes tumor formation in mutant EGFR-driven lung adenocarcinoma.
Division of Head and Neck Cancer Research, Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University, Baltimore, Maryland.
Evgeny
E
Izumchenko
Division of Head and Neck Cancer Research, Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University, Baltimore, Maryland. dsidrans@jhmi.edu.
David
D
Sidransky
D048868:Adaptor Proteins, Signal Transducing / Q000172:deficiency*; D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology*; D000077192:Adenocarcinoma of Lung; D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D066246:ErbB Receptors / Q000235:genetics*; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics* / Q000473:pathology*; D009154:Mutation; D025521:Tumor Suppressor Proteins / Q000172:deficiency*
D048868:Adaptor Proteins, Signal Transducing; C484017:ERRFI1 protein, human; D025521:Tumor Suppressor Proteins; D066246:ErbB Receptors