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[Cancer Research 65, 11478-11485, December 15, 2005]
© 2005 American Association for Cancer Research

Cell and Tumor Biology

High Expression of ErbB Family Members and Their Ligands in Lung Adenocarcinomas That Are Sensitive to Inhibition of Epidermal Growth Factor Receptor

Nobukazu Fujimoto1, Marie Wislez1,4, Jie Zhang1, Kentaro Iwanaga1, Jennifer Dackor5, Amy E. Hanna1, Shailaja Kalyankrishna1, Dianna D. Cody2, Roger E. Price2, Mitsuo Sato6, Jerry W. Shay6, John D. Minna6, Michael Peyton6, Ximing Tang1, Erminia Massarelli1, Roy Herbst1, David W. Threadgill5, Ignacio I. Wistuba1,3 and Jonathan M. Kurie1

Departments of 1 Thoracic/Head and Neck Medical Oncology, 2 Imaging Physics, and 3 Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas; 4 UPRESEA 3493, CHU Saint-Antoine, Universite Paris VI, Paris, France; 5 Department of Genetics, Curriculum in Genetics and Molecular Biology, Lineberger Cancer Center, University of North Carolina, Chapel Hill, North Carolina; and 6 Harold Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas

Requests for reprints: Jonathan M. Kurie, The University of Texas M.D. Anderson Cancer Center, Box 432, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: 713-792-6363; Fax: 713-796-8655; E-mail: jkurie{at}mdanderson.org.

Recent findings in tumor biopsies from lung adenocarcinoma patients suggest that somatic mutations in the genes encoding epidermal growth factor receptor (EGFR) and Kirsten ras (KRAS) confer sensitivity and resistance, respectively, to EGFR inhibition. Here, we provide evidence that these genetic mutations are not sufficient to modulate the biological response of lung adenocarcinoma cells to EGFR inhibition. We found high expression of ErbB family members, ErbB ligands, or both in three models that were sensitive to EGFR inhibition, including alveolar epithelial neoplastic lesions in mice that develop lung adenocarcinoma by oncogenic KRAS, human lung adenocarcinoma cell lines, and tumor biopsies from lung adenocarcinoma patients. Thus, lung adenocarcinoma cells that depend on EGFR for survival constitutively activate the receptor through a combination of genetic mutations and overexpression of EGFR dimeric partners and their ligands. (Cancer Res 2005; 65(24): 11478-85)




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