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使用组织定量荧光原位杂交技术测量人类成人支气管上皮和支气管源性鳞状细胞癌的端粒长度。

Telomere Length of Human Adult Bronchial Epithelium and Bronchogenic Squamous Cell Carcinoma Measured Using Tissue Quantitative Fluorescence in situ Hybridization.

作者信息

Aida Shinsuke, Aida Junko, Hasegawa Kayo, Kumasaka Toshio, Shimazaki Hideyuki, Tamai Seiichi, Takubo Kaiyo

机构信息

Department of Pathology, Mita Hospital, International University of Health and Welfare, Tokyo, Japan.

出版信息

Respiration. 2015;90(4):321-6. doi: 10.1159/000437357. Epub 2015 Sep 4.

Abstract

BACKGROUND

Telomeres are repetitive DNA sequences located at the ends of chromosomes. Chromosomal and genomic instability due to telomere dysfunction has been known to play an important role in the carcinogenesis of some organs.

OBJECTIVES

The aim of this study was to examine the correlation between smoking and the telomere length of human bronchial epithelial cells in individuals with and without lung cancer.

PATIENTS AND METHODS

We examined 68 non-lung cancer adult autopsy cases and 24 surgically resected cases of lung squamous cell carcinoma. Telomere lengths of the basal cells of bronchial epithelium were measured using the tissue quantitative fluorescence in situ hybridization method and were expressed in normalized telomere-to-centromere ratios (NTCRs).

RESULTS

The autopsied individuals included 27 current smokers (CuS), 33 never-smokers (NeS), and 8 ex-smokers (ExS). The NTCRs in the central bronchi 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-CuS (NeS + ExS). When the analysis was conducted separately for females and males, a significant difference between CuS and NeS + ExS was recognized only for males. The NTCRs of the bronchial epithelium of lung cancer cases and lung cancer tissue are 1.514 and 1.385, respectively.

CONCLUSIONS

Our findings suggest that smoking causes telomeric elongation in the bronchial epithelium. Therefore, it appears that the mechanism of carcinogenesis in smoking-related carcinomas may differ from that of many other carcinomas in which genetic instability due to aging-related telomeric shortening is assumed to play a role.

摘要

背景

端粒是位于染色体末端的重复DNA序列。已知端粒功能障碍导致的染色体和基因组不稳定在某些器官的致癌过程中起重要作用。

目的

本研究旨在探讨吸烟与有无肺癌个体的人支气管上皮细胞端粒长度之间的相关性。

患者与方法

我们检查了68例非肺癌成人尸检病例和24例手术切除的肺鳞状细胞癌病例。使用组织定量荧光原位杂交方法测量支气管上皮基底细胞的端粒长度,并以标准化的端粒与着丝粒比率(NTCRs)表示。

结果

尸检个体包括27名当前吸烟者(CuS)、33名从不吸烟者(NeS)和8名既往吸烟者(ExS)。CuS、NeS和ExS中央支气管的NTCRs分别为1.515、1.372和1.204。CuS的支气管上皮端粒明显长于非CuS者(NeS + ExS)。当分别对女性和男性进行分析时,仅在男性中发现CuS与NeS + ExS之间存在显著差异。肺癌病例和肺癌组织的支气管上皮NTCRs分别为1.514和1.385。

结论

我们的研究结果表明,吸烟导致支气管上皮端粒延长。因此,吸烟相关癌症的致癌机制似乎可能不同于许多其他癌症,在这些癌症中,与衰老相关的端粒缩短导致的基因不稳定被认为起作用。

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