Disproportionate representation of KRAS gene mutation in atypical adenomatous hyperplasia, but even distribution of EGFR gene mutation from preinvasive to invasive adenocarcinomas

• DOI: 10.1002/path.2165
• Publication Date: 2007-05-29T13:11:07Z
• Authors: H Sakamoto; J Shimizu; Y Horio; R Ueda; T Takahashi; T Mitsudomi; Y Yatabe
• Keywords: Atypical adenomatous hyperplasia

In the resected lung, additional small lesions are occasionally found incidentally, and include full spectrum of preinvasive to invasive under current putative schema sequential development lung cancer. this study, we examined EGFR KRAS gene mutations in 119 synchronous pulmonary lesions, including 40 precursor (atypical adenomatous hyperplasia, AAH), 26 carcinomas situ (non-mucinous bronchioloalveolar carcinoma, BAC), 14 minimally adenocarcinomas, 34 overt five other subtypes Although mutually exclusive nature was maintained even incidences along progression were quite different. The mutated 33% AAH, 12% situ, 8% adenocarcinomas 0% well-differentiated whereas frequencies mutation did not fluctuate greatly, at 25%, 51%, 36%, 86% 67%, respectively. These results consistent with findings a published gene-targeted mouse model; mice expressing oncogenic developed AAH but adenocarcinoma, observed mutant EGFR. Taking these factors together, it is suggested that could develop by either or mutation, harbouring might progress further an