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The Role of the ErbB Family Members in Non–Small Cell Lung Cancers Sensitive to Epidermal Growth Factor Receptor Kinase Inhibitors

Authors' Affiliations: ¹ Massachusetts General Hospital Cancer Center; ² Department of Systems Biology, Harvard Medical School; and ³ Department of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, Massachusetts

Requests for reprints: Jeffrey A. Engelman, Department of Systems Biology, Harvard Medical School, New Research Building, 77 Avenue Louis Pasteur, Room 1052, Boston, MA 02115. Phone: 617-667-0934; Fax: 617-667-0957; E-mail: jengelman{at}partners.org.

Inhibitors targeting the epidermal growth factor receptor (EGFR) are effective in a subset of non–small cell lung cancers. Such cancers often harbor EGFR mutations and/or amplification. These cancers require EGFR activity for the maintenance of critical intracellular survival and growth signaling pathways. Evidence is now accruing that EGFR works in concert with other ErbB family members, particularly HER2 and ErbB3, to activate these signaling pathways in lung cancers. These findings have important implications regarding the biology of these cancers and may lead to improved methods for identifying tumors that are responsive to EGFR kinase inhibitors and alternative therapies to treat cancers driven by ErbB signaling.

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