作者: Liza C. Villaruz , Mark A. Socinski , Shira Abberbock , Lynne D. Berry , Bruce E. Johnson
DOI: 10.1002/CNCR.29042
关键词:
摘要: BACKGROUND The advent of effective targeted therapy for BRAFV600E-mutant lung adenocarcinomas necessitates further exploration the unique clinical features and behavior advanced-stage BRAF-mutant adenocarcinomas. METHODS Data were reviewed patients with advanced enrolled in Lung Cancer Mutation Consortium whose tumors underwent testing mutations epidermal growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), human 2 (HER2), AKT1, BRAF, dual-specificity mitogen-activated protein kinase 1 (MEK1), neuroblastoma RAS (v-ras) (NRAS), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (PIK3CA); anaplastic lymphoma (ALK) translocations; MET amplification. RESULTS Twenty-one BRAF identified 951 (2.2%; 95% confidence interval [CI], 1.4%-3.4%): 17 (81%; CI, 60%-92%) BRAFV600E mutations, 4 non-BRAFV600E mutations. Among 733 cases tested all 10 genes, more likely to occur than most other genotypic abnormalities current or former smokers (BRAF vs sensitizing EGFR, 82% 36%, mid-P .20). CONCLUSIONS BRAF occurred 2.2% adenocarcinomas, commonly V600E, associated distinct clinicopathologic comparison genomic subtypes a high mutation rate gene. These findings underscore importance comprehensive profiling assessing adenocarcinomas. 2015;121:448–456. © 2014 American Society.