Erbb3 is Not Required for Tumorigenesis by Mutant EGFR
Xiaoling Song1, Pang-Dian Fan2, Udayan Guha3, David Threadgill4, Harold Varmus5 and Katerina Politi1
1Department of Pathology and Yale Cancer Center, Yale School of Medicine, New Haven, CT; 2Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY; 3Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD; 4Department of Genetics, North Carolina State University, Raleigh, NC; 5National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA
BACKGROUND
Lung cancer is the leading cause of cancer-related death in the USA and worldwide. Mutations in the Epidermal Growth Factor Receptor (EGFR) are found in 15% of lung adenocarcinomas. Tumors bearing EGFR mutations are sensitive to treatment with specific tyrosine kinase inhibitors (TKIs) and show radiographic responses in about 70% of cases. However, it is not known why the remaining 30% of the tumors do not respond to these drugs, and patients who initially respond to TKI treatment eventually develop drug resistance on average within a year. Mutant EGFR-induced signaling is initiated by the formation of EGFR homodimers or heterodimers with other members of the EGFR family (ERBB2, ERBB3 or ERBB4). Here the role of EGFR family members in the tumorigenic process driven by mutant EGFR was studied using genetically engineered mouse models.
©2012 Yale Department of Pathology. All rights reserved.
Any redistribution or reproduction of part or all of the contents in any form is prohibited. You may not, except with express written permission of the author or the Department of Pathology, distribute or commercially exploit the content, nor may you transmit it or store it in any other website or other form of electronic retrieval system, including use for educational purposes.