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Smoking, chromosomal aberrations, and cancer incidence in healthy subjects
Mutation Research/Genetic Toxicology and Environmental Mutagenesis ( IF 2.3 ) Pub Date : 2021-06-18 , DOI: 10.1016/j.mrgentox.2021.503373
Gyöngyi Farkas 1 , Zsuzsa S Kocsis 1 , Gábor Székely 1 , Mária Dobozi 2 , István Kenessey 2 , Csaba Polgár 3 , Zsolt Jurányi 1
Affiliation  

Chromosomal aberrations (CAs) in peripheral blood lymphocytes can be used as biomarkers of cancer risk. Cytogenetic tests were conducted on 2396 healthy Hungarian individuals and cancer incidence was followed up from 1989 to 2018. Venous blood samples were obtained from the subjects and metaphases from lymphocyte cultures were prepared. We compared the CA frequencies of the various smoking (1−5; 6−10; 11−19; or 20−40 cigarettes/day) and exposure (irradiation; chemical industry; chemical research laboratory) groups. Chromatid break (p = 0.0002), total aberration (p = 0.002), and aberrant cell (p = 0.001) frequencies were higher in smokers than in non-smokers. For very heavy smokers, total CAs were significantly higher than for non-smokers (<0.001) or less intensive smokers (p = 0.003−0.0006). Intensity of smoking was a predictor of chromosomal aberrations, while duration was not. During follow-up, 177 (7.3 %) cancer cases were found. A Cox-regression model showed that subjects with cell values ≥2 CAs developed cancer more frequently (hazard ratio = 1.39; 95 % CI, 1.02–1.90). The relative risks of cancer were 1.06 (95 % CI 0.53−2.06) for light smokers and 1.74 (95 % CI 1.08−2.77) for very heavy smokers. The distributions of cancer sites showed differences between smoker and non-smoker groups: in male smokers, lung cancer, in non-smokers, prostate, and in females (both groups) breast cancer were most common. Cancer incidence correlated with chromosome aberrations; smoking was not a confounder in this relationship.



中文翻译:

健康受试者的吸烟、染色体畸变和癌症发病率

外周血淋巴细胞中的染色体畸变 (CA) 可用作癌症风险的生物标志物。对 2396 名健康的匈牙利人进行了细胞遗传学测试,并跟踪了 1989 年至 2018 年的癌症发病率。从受试者身上获取了静脉血样本,并准备了淋巴细胞培养的中期。我们比较了各种吸烟(1-5;6-10;11-19;或 20-40 支香烟/天)和暴露(辐射;化学工业;化学研究实验室)组的 CA 频率。吸烟者的染色单体断裂 (p = 0.0002)、总畸变 (p = 0.002) 和异常细胞 (p = 0.001) 频率高于非吸烟者。对于非常重度吸烟者,总 CA 显着高于非吸烟者 (<0.001) 或强度较低的吸烟者 (p = 0.003−0.0006)。吸烟强度是染色体畸变的预测因子,而持续时间则不是。在随访期间,发现了 177 (7.3%) 例癌症病例。Cox 回归模型显示,细胞值 ≥ 2 CA 的受试者患癌症的频率更高(风险比 = 1.39;95 % CI,1.02–1.90)。轻度吸烟者患癌症的相对风险为 1.06 (95 % CI 0.53-2.06),重度吸烟者为 1.74 (95 % CI 1.08-2.77)。癌症部位的分布显示吸烟者和非吸烟者之间的差异:男性吸烟者肺癌,非吸烟者前列腺癌和女性(两组)乳腺癌最常见。癌症发病率与染色体畸变相关;吸烟不是这种关系的混杂因素。Cox 回归模型显示,细胞值 ≥ 2 CA 的受试者患癌症的频率更高(风险比 = 1.39;95 % CI,1.02–1.90)。轻度吸烟者患癌症的相对风险为 1.06 (95 % CI 0.53-2.06),重度吸烟者为 1.74 (95 % CI 1.08-2.77)。癌症部位的分布显示吸烟者和非吸烟者之间的差异:男性吸烟者肺癌,非吸烟者前列腺癌和女性(两组)乳腺癌最常见。癌症发病率与染色体畸变相关;吸烟不是这种关系的混杂因素。Cox 回归模型显示,细胞值 ≥ 2 CA 的受试者患癌症的频率更高(风险比 = 1.39;95 % CI,1.02–1.90)。轻度吸烟者患癌症的相对风险为 1.06 (95 % CI 0.53-2.06),重度吸烟者为 1.74 (95 % CI 1.08-2.77)。癌症部位的分布显示吸烟者和非吸烟者之间的差异:男性吸烟者肺癌,非吸烟者前列腺癌和女性(两组)乳腺癌最常见。癌症发病率与染色体畸变相关;吸烟不是这种关系的混杂因素。癌症部位的分布显示吸烟者和非吸烟者之间的差异:男性吸烟者肺癌,非吸烟者前列腺癌和女性(两组)乳腺癌最常见。癌症发病率与染色体畸变相关;吸烟不是这种关系的混杂因素。癌症部位的分布显示吸烟者和非吸烟者之间的差异:男性吸烟者肺癌,非吸烟者前列腺癌和女性(两组)乳腺癌最常见。癌症发病率与染色体畸变相关;吸烟不是这种关系的混杂因素。

更新日期:2021-06-23
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