作者: Ralph H. Hruban , William H. Westra , G. Johan A. Offerhaus , Kiersten Wilson , Inge O. Baas
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摘要: Atypical alveolar hyperplasia (AAH) is a potential precursor lesion from which lung adenocarcinomas arise and may be good target for studying the early events of tumorigenesis. A common genetic alteration in mutational activation K- ras . To determine timing activation, we evaluated formalin-fixed paraffin-embedded tissue samples 41 AAHs their paired neoplasms 28 patients codon 12 point mutations oncogene. were detected using PCR followed by allele-specific oligonucleotide hybridization. Mutations found 16 (39%) AAHs, 8 (42%) 18 adenocarcinomas, none (0%) 5 that not adenocarcinomas. Of with both an AAH synchronous adenocarcinoma, 6 had adenocarcinoma but AAH, 4 did harbor either or 2 adenocarcinoma. In just 1 was same mutation present patient. The detection independent activating cancer-causing gene points to neoplastic nature suggests glandular background field cancerization.