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Epidermal growth factor receptor‐tyrosine kinase inhibitors in advanced squamous cell carcinoma of the lung: A meta‐analysis
Author(s) -
Ameratunga Malaka,
Pavlakis Nick,
Gebski Val,
Broad Adam,
Khasraw Mustafa
Publication year - 2014
Publication title -
asia‐pacific journal of clinical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 29
eISSN - 1743-7563
pISSN - 1743-7555
DOI - 10.1111/ajco.12231
Subject(s) - tyrosine kinase , cancer research , squamous cell carcinoma of the lung , epidermal growth factor receptor , lung , epidermal growth factor , basal cell , platelet derived growth factor receptor , receptor tyrosine kinase , carcinoma , receptor , medicine , oncology , chemistry , growth factor
Abstract Aim Tyrosine kinase inhibitors ( TKI s) targeting the epidermal growth factor receptor ( EGFR ) are well established in treating metastatic pulmonary adenocarcinoma, especially patients with activating EGFR mutations. EGFR mutations are rare in pulmonary squamous cell carcinomas ( SCC s). There are conflicting data supporting the efficacy of EGFR ‐ TKI s in advanced lung SCC . We analyzed the impact of EGFR ‐ TKI s on progression‐free survival ( PFS ) and overall survival ( OS ) in unselected patients with lung SCC . Methods We searched for randomized controlled trials ( RCT s) comparing EGFR ‐ TKI s alone with placebo in patients with metastatic non‐small cell lung cancer. RCT s in all settings (front line/maintenance/subsequent) were included. The primary outcome was OS in the SCC population. We used published hazard ratios ( HR s), and when unavailable, unpublished data were sought. Pooled estimates of treatment effect on OS and PFS were calculated using the fixed‐effects inverse variance weighted method. Results Eight eligible RCT s were included: 2 first‐line, 6 second‐line or beyond, evaluating 1781 patients. Data were available for OS in four studies (second‐line; N = 1420) and for PFS in four studies (3 second‐line, 1 first‐line; N = 788). EGFR ‐ TKI s significantly prolonged OS with a HR of 0.88 (95% confidence interval [ CI ] 0.78–1.00, P = 0.04), and significantly prolonged PFS with a HR of 0.77 (95% CI 0.65–0.92, P = 0.004). Conclusion EGFR mutations are rare in lung SCC . However, EGFR ‐ TKI s have a modest therapeutic effect compared to placebo in unselected patients with advanced pulmonary SCC , and can be considered in these patients. EGFR ‐mutation‐independent mechanisms may explain efficacy of EGFR inhibitors in this setting.