Telomere length and carcinogenesis of human bronchial epithelium, study using tissue quantitative fluorescence in situ hybridization

应用Q-FISH方法对72例成人非肺癌尸检标本和24例手术切除的肺鳞癌标本进行了端粒长度测量，并以端粒/着丝粒比值(NTCRS)表示。尸检对象包括27名吸烟者(CU)、33名从不吸烟者(NES)、8名戒烟者(EXS)和4例不明原因病例。CU、NES和EXS的NTCR分别为1.515、1.372和1.204。CUS组的支气管上皮端粒长度明显长于非吸烟组(NES EXS)。肺癌患者和肺癌组织中支气管上皮细胞的NTCR分别为1.514和1.385。我们的发现表明，吸烟会导致支气管上皮细胞端粒延长。吸烟相关癌症的致癌机制被认为与许多其他癌症不同，在这些癌症中，衰老相关的端粒缩短所致的遗传不稳定性被认为起了作用。

Telomere lengths of the bronchial epithelium of 72 non-lung cancer adult autopsy cases and 24 surgically resected cases of lung squamous cell carcinoma were measured using Q-FISH method, and were expressed in normalized telomere:centromere ratios (NTCRs). The autopsied individuals included 27 current smokers (CuS), 33 never-smokers (NeS), 8 ex-smokers (ExS), and 4 unknown cases. The NTCRs of CuS, NeS and ExS were 1.515, 1.372 and 1.204, respectively. The bronchial epithelial telomeres of CuS were significantly longer than those of non-current smokers (NeS+ExS). The NTCRs of the bronchial epithelium of lung cancer cases and lung cancer tissue are 1.514 and 1.385, respectively. Our findings suggest that smoking causes telomeric elongation in the bronchial epithelium. The mechanism of carcinogenesis in smoking-related carcinomas is suggested to differ from that of many other carcinomas in which genetic instability due to aging-related telomeric shortening is considered to play a role.