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背景与目的:染色体不平衡在肺癌发生中具有重要作用,并可能受不同致癌物的影响。本研究旨在探讨原发性肺鳞状细胞癌(squamous cell carcinoma,SCC)染色体不平衡特征及吸烟对其的影响。方法:采用比较基因组杂交(comparative genomic hybridization,CGH)技术对39例原发性肺SCC的染色体扩增和缺失进行检测,并分析吸烟与肺SCC染色体不平衡之间的关系。结果:肺SCC染色体扩增常见于3q(74.4%,29/39),5p(66.7%,26/39),1q(43.6%,17/39),8q(41%,16/39),12p(42.6%,18/39),2p(38.5%,15/39)、18p(33.3%,13/39)等;最小扩增区位于3q26.2鄄29、5p14.3鄄15.3、1q41鄄44、8q23和12p13;38.5%和15.4%的病例发生3q和5p高拷贝扩增。染色体缺失主要见于3p(56.4%,22/39),5q(53.8%,21/39),13q(51.3%,20/39),8p(46.1%,18/39),4p(43.6%,17/39)、4q(43.6%,17/39)、1p(41%,16/39)、2q(38.5%,15/39),9q(35.9%,14/39)、13p(35.9%,14/39)、16p(35.9%,14/39),6p(33%,13/39)、6q(30.7%,12/39)等;最小缺失区位于3p14.2鄄21.2(51.3%,20/39)、5q15鄄22(51.3%,20/39)、13q14.2鄄21.2(48.7%,19/39)、8p21.1鄄22(44%,17/39)、2q32(36%,14/39)和16p12鄄13.1(33%,13/39)。与非吸烟患者相比,吸烟患者3q和8q扩增率显著增加(P<0.05);两者共同的染色体?
Background and purpose: Chromosomal imbalance plays an important role in the development of lung cancer and may be affected by different carcinogens. This study aimed to investigate the chromosomal imbalance characteristics of primary squamous cell carcinoma (SCC) and the effect of smoking on it. METHODS: Combinative genomic hybridization (CGH) technique was used to detect chromosome amplification and deletion in 39 cases of primary lung SCC, and the relationship between smoking and lung SCC chromosome imbalance was analyzed. Results: The chromosome amplification of lung SCC was commonly found in 3q (74.4%, 29/39), 5p (66.7%, 26/39), 1q (43.6%, 17/39), 8q (41%, 16/39), 12p (42.6%, 18/39), 2p (38.5%, 15/39), 18p (33.3%, 13/39), etc.; the smallest amplification region is located at 3q26.2鄄29, 5p14.3鄄15.3, 1q41鄄44. 3q and 5p high copy amplifications occurred in 38.5 and 15.4% of cases, 8q23 and 12p13; The chromosome deletions were mainly found in 3p (56.4%, 22/39), 5q (53.8%, 21/39), 13q (51.3%, 20/39), 8p (46.1%, 18/39), 4p (43.6%, 17). /39), 4q (43.6%, 17/39), 1p (41%, 16/39), 2q (38.5%, 15/39), 9q (35.9%, 14/39), 13p (35.9%, 14 /39), 16p (35.9%, 14/39), 6p (33%, 13/39), 6q (30.7%, 12/39), etc.; the smallest missing region is located at 3p14.2鄄21.2 (51.3%, 20/ 39), 5q15鄄22 (51.3%, 20/39), 13q14.2鄄21.2 (48.7%, 19/39), 8p21.1鄄22 (44%, 17/39), 2q32 (36%, 14/ 39) and 16p12鄄13.1 (33%, 13/39). Compared with non-smokers, the 3q and 8q amplification rates were significantly increased in smoking patients (P<0.05);