原发性肺鳞状细胞癌染色体不平衡及其与吸烟的关系

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

Chromosomal imbalance in primary lung squamous cell carcinoma and their relationship with smoking

BACKGROUND & OBJECTIVE: Chromosomal imbalance plays an important role in tumorigenesis of lung cancer, and may be influenced by different carcinogens. This study was to examine chromosomal imbalance in primary lung squamous cell carcinoma (LSCC), and their association with smoking. METHODS: Chromosomal gains and losses in 39 specimens of LSCC were identified by comparative genomic hybridization (CGH), the association between chromosomal imbalances in LSCC and smoking was analyzed. RESULTS: The most frequent chromosomal gains of LSCC were detected on chromosomal arms 3q (74.4%, 29/39), 5p (66.7%, 26/39), 1q (43.6%, 17/39), 8q (41.0%, 16/39), 12p (42.6%, 18/39), 2p (38.5%, 15/39), and 18p (33.3%, 13/39), with minimal amplified regions (MAR) at 3q26.2-29 (74.4%, 29/39), 5p14.3-15.3 (66.7%, 26/39), 1q41-44(41.0%, 16/39), 8q23 (41.0%, 16/39), 12p13 (41.0%, 16/39), and 18p11.2 (33.3%, 13/39)u high-copy-number amplification at chromosomal arms 3q, and 5p were found in 15 (38.5%), and 6 (15.4%) patients. Chromosomal losses mainly involved chromosomal arms 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 (41.0%, 16/39), 2q (38.5%, 15/39), 9q (35.9%, 14/39), 13p (35.9%, 14/39), 16p (35.9%, 14/39) ,6p (33.3%, 13/39), and 6q (30.7%, 12/39), with minimal deleted regions (MDR) at 3p14.2-21.2 (51.3%, 20/39), 5q15-22 (51.3%, 20/39), 13q14.2-21.2 (48.7%, 19/39), 8p21.1-22 (43.6%, 17/39), 2q32 (35.9%, 14/39), and 16p12-13.1 (33.3%, 13/39). Amplification rates of chromosomal arms 3q, and 8q in smoking LSCC patients were significantly higher than those in non-smoking LSCC patients (P=0.002,P=0.031). While high incidences of gains at chromosomal arms 5p and 12p, and of losses at chromosomal arms 3p, 4q, and 5q were the common feature of chromosomal changes of smoking and non-smoking LSCC patients. CONCLUSION: 3q, 5p, 1q, 8q, 12p, 2p, 18p gains and 3p, 5q, 13q, 8p, 4p, 4q, 1p, 2q, 9q, 13p,16p, 6p, 6q loses might be involved in tumorigenesis and/or progression of LSCC, smoking-induced lung cancer may be associated with 3q, 8q gains.