期刊
AMERICAN JOURNAL OF CLINICAL PATHOLOGY
卷 133, 期 6, 页码 922-934出版社
OXFORD UNIV PRESS INC
DOI: 10.1309/AJCPST1CTHZS3PSZ
关键词
EGFR; Non-small cell lung carcinoma; Mutation; Fluorescence in situ hybridization; Chromogenic in situ hybridization; Immunohistochemistry; Erlotinib
类别
资金
- National Institutes of Health, Bethesda, MD [R01 CA114465]
- Pfizer, New York, NY
- NATIONAL CANCER INSTITUTE [R01CA114465] Funding Source: NIH RePORTER
About 10% of patients with non small cell lung carcinoma (NSCLC) respond to epidermal growth factor receptor (EGFR)-targeted tyrosine kinase inhibitors (TKIs). More than 75% of responders have activating mutations in EGFR. However, mutation analysis is not widely available, and proposed alternatives (in situ hybridization and immunohistochemical analysis) have shown inconsistent associations with outcome. Fluorescence in situ hybridization (FISH), chromogenic in situ hybridization (CISH), immunohistochemical analysis, and DNA sequencing were compared in this study of 40 NSCLC samples from TKI-treated patients. Response rates were 12 of 19 in EGFR-mutant vs I of 20 EGFR wild-type tumors (P = .0001), 7 of 19 FISH+ vs 4 of 17 FISH- tumors (not significant [NS]), 5 of 16 CISH+ vs 6 of 21 CISH- tumors (NS), and 3 of 9 immunohistochemically positive vs 7 of 22 immunohistochemically negative tumors (NS). EGFR mutation was associated with improved progression-free survival (P = .0004). Increased copy number (FISH or CISH) and protein expression (immunohistochemical) did not independently predict outcome. Thus, EGFR sequence analysis was the only method useful for predicting response and progression-free survival following TKI therapy in NSCLC.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据