作者: Shinsuke Aida , Junko Aida , Kayo Hasegawa , Toshio Kumasaka , Hideyuki Shimazaki
DOI: 10.1159/000437357
关键词: Basal (phylogenetics) 、 Carcinogenesis 、 Genome instability 、 Telomere 、 Cancer 、 Lung cancer 、 Biology 、 Pathology 、 In situ hybridization 、 Telomere Homeostasis
摘要: Background: Telomeres are repetitive DNA sequences located at the ends of chromosomes. Chromosomal and genomic instability due to telomere dysfunction has been known play an important role in carcinogenesis some organs. Objectives: The aim this study was examine correlation between smoking length human bronchial epithelial cells individuals with without lung cancer. Patients Methods: We examined 68 non-lung cancer adult autopsy cases 24 surgically resected squamous cell carcinoma. Telomere lengths basal epithelium were measured using tissue quantitative fluorescence situ hybridization method expressed normalized telomere-to-centromere ratios (NTCRs). Results: autopsied included 27 current smokers (CuS), 33 never-smokers (NeS), 8 ex-smokers (ExS). NTCRs central bronchi CuS, NeS, ExS 1.515, 1.372, 1.204, respectively. telomeres CuS significantly longer than those non-CuS (NeS + ExS). When analysis conducted separately for females males, a significant difference NeS recognized only males. 1.514 1.385, Conclusions: Our findings suggest that causes telomeric elongation epithelium. Therefore, it appears mechanism smoking-related carcinomas may differ from many other which genetic aging-related shortening is assumed role.