作者: Seol Bong Yoo , Jin-Haeng Chung , Hyun Ju Lee , Choon-Taek Lee , Sanghoon Jheon
DOI: 10.1097/JTO.0B013E3181DD15C0
关键词: Molecular biology 、 Adenocarcinoma of the lung 、 Biology 、 Atypical adenomatous hyperplasia 、 Adenocarcinoma 、 Cancer research 、 Point mutation 、 Epidermal growth factor receptor 、 EGFR Gene Mutation 、 Carcinogenesis 、 Exon
摘要: Introduction A progression model of atypical adenomatous hyperplasia (AAH) to bronchioloalveolar carcinoma (BAC) invasive adenocarcinoma (ADC) has been proposed. However, the genetic alterations AAH-BAC-ADC sequence are not clearly established. We examined mutation epidermal growth factor receptor ( EGFR ) gene and p53 protein overexpression in AAH, BAC, small ADC understand their role pulmonary pathogenesis. Methods Twenty 43 BAC (21 Noguchi type 22 B), 47 (Noguchi C) were enrolled this study. mutations at exons 18–21 by polymerase chain reaction-direct sequencing immunohistochemistry, respectively. Results Mutations noted 45 (40.9%) lesions, which included 7 (35.0%) 15 (34.9%) 23 (48.9%) ADC. Twenty-six (23.6%) detected as exon 19 deletion, 18 (16.4%) 21 point mutation, 1 (0.9%) mutation. Overexpression was found (17.2%) none 4 (9.8%) (31.9%) Multivariate analysis showed that associated with P = 0.003). Conclusions High frequency similar incidence support occurs early stage development tumor initiation from preneoplastic lung parenchyma neoplastic conditions. On contrary, is a late event during plays peripheral