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

采用Q-FISH法测定了72例成人非肺癌尸检病例和24例手术切除的肺鳞状细胞癌支气管上皮端粒长度，并以标准化端粒：着丝粒比（ntcr）表达。尸检个体包括27例当前吸烟者（CuS）， 33例从不吸烟者（NeS）， 8例戒烟者（ExS）和4例未知病例。cu、NeS和ExS的ntcr分别为1.515、1.372和1.204。吸烟组的支气管上皮端粒明显长于非吸烟组（NeS+ExS）。肺癌病例支气管上皮和肺癌组织的ntcr分别为1.514和1.385。我们的研究结果表明吸烟导致支气管上皮端粒伸长。吸烟相关癌的致癌机制与许多其他癌症不同，在这些癌症中，由于衰老相关的端粒缩短而导致的遗传不稳定被认为起作用。

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.