© 2005 Oxford University Press
EDITORIAL |
Gefitinib Versus Cetuximab in Lung Cancer: Round One
Affiliation of authors: Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX
Correspondence to: John D. Minna, MD, Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd., Dallas, TX 75309-8593 (e-mail: john.minna@utsouthwestern.edu).
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Despite clinically significant advances in conventional forms of chemotherapy (1), the prospects for long-term control of lung cancer reside in therapies targeted to specific molecular changes that are characteristic of the tumor and whose function the tumor must maintain to survive (oncogenic changes to which the tumor is "addicted"). Just over a year ago, intense excitement was generated by the finding that mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene are highly predictive (in general) of clinical responses to EGFR TK inhibitors (TKIs) (2,3). In this issue of the Journal, Mukohara et al.
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