Role of Epidermal Growth Factor Receptor Inhibitors in Epidermal Growth Factor Receptor Wild-Type Non–Small-Cell Lung Cancer

• Published in: Journal of clinical oncology Vol. 31; no. 8; pp. 1061 - 1069
• Main Authors: Laurie, Scott A., Goss, Glenwood D.
• Format: Journal Article
• Language: English
• Published: United States American Society of Clinical Oncology 10.03.2013
• Subjects: Antineoplastic Agents - therapeutic use; Biomarkers, Tumor - genetics; Carcinoma, Non-Small-Cell Lung - drug therapy; Carcinoma, Non-Small-Cell Lung - genetics; Clinical Trials as Topic; Disease-Free Survival; Humans; Lung Neoplasms - drug therapy; Lung Neoplasms - genetics; Mutation; Platinum Compounds - therapeutic use; Predictive Value of Tests; Prognosis; Receptor, Epidermal Growth Factor - antagonists & inhibitors; Receptor, Epidermal Growth Factor - genetics
• ISSN: 0732-183X; 1527-7755; 1527-7755
• DOI: 10.1200/JCO.2012.43.4522

Worldwide, the majority of patients with advanced non–small-cell lung cancer (NSCLC) do not have activating mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR). These wild-type patients comprise a significant proportion of those treated with inhibitors of this pathway, and data from randomized trials suggest that some of these wild-type patients will derive a modest benefit from these agents. Although the detection of an activating mutation predicts for a greater likelihood of response and longer progression-free survival from an EGFR tyrosine kinase inhibitor, currently there are no biomarkers that consistently and reproducibly predict for lack of benefit in wild-type patients. Several strategies to increase the efficacy of these inhibitors in wild-type NSCLC are the subject of ongoing investigations.