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作 者:沈月平[1] 武俊青[2] 张子豹[2] De-Kun Li 高尔生[2]
机构地区:[1]苏州大学放射医学与公共卫生学院流行病与卫生统计教研室,苏州215123 [2]上海市计划生育科学研究所 [3]美国Kaiser研究所
出 处:《中国公共卫生》2007年第8期897-899,共3页Chinese Journal of Public Health
基 金:国家自然科学基金项目(39770659);美国国立卫生研究所基金项目(RO1-CA71777)
摘 要:目的研究CYP1A1 MspⅠ,ERα PvuⅡ,ERα XbaⅠ基因多态性与生殖、生育因素在乳腺癌发生中的协同作用。方法本研究样本来自1999年1月-2001年4月,在上海市进行的以人群为基础的乳腺癌病例对照研究。采用PCR-限制性酶切长度多态性法(PIER—RFLP)对282例乳腺癌病例和298例口腔黏膜细胞对照标本进行3个候选基因位点的检测,拟合Logistic回归模型,估计基因多态与生殖、生育因素对乳腺癌协同作用OR值和95%CI,并采用Rothman方法对基因一环境的协同作用进行估计。结果良性乳腺疾病史与CYPIA1 MspⅠ多态存在正相加协同作用。与基准组比较,OR为5.66(95%CI=3.28-9.76),协同作用指数S=2.05,协同作用归因比AP=0.42,经检验差异有统计学意义(P〈0.05)。未发现其他生殖、生育因素与3个基因位点有显著的协同作用。结论良性乳腺疾病史与CYP1A1 MspⅠ基因之间存在增加乳腺危险的协同作用。Objective To determine whether there were synergic effects of increasing risk of breast cancer in Chinese women between the genetic polymorphisms of CYP1A1 MspⅠ,ERα PvuⅡ,ERα XbaⅠ and reproductive factors or not. Methods The study subjects were a subset of a population - based case - control study conducted in Shanghai between Jan 1,1999 and Apr 30, 2001. PCR restrictive length fragment polymorphism (PCR- RFLP) method was used to examine the 3 candidate polymorphisms in DNA extracted from buccal cell in 282 breast cancer cases and 298 age frequency- matched controis. Multivariate Logistic model was used to estimate the OR and 9596 CI for the group who were both with reproductive factors and with change of one of the candidate genetic polymorphisms. The synergic effects (additive model) between the reproductive factors and one of 3 candidate genetic polymorphisms were estimated by Rothman's method. Results There was a statistically significant positive additive synergic effect of increasing the breast cancer risk (OR = 5.66, 9596 CI:3.28- 9.76, S = 2.05, AP = 0.42, u = 1.982, P 〈 0.05) between the benign breast disease history and CYP/A/ MspⅠ polymorphism. No significant additive synergic effects were observed between the 3 candidate polymorphisms and other reproductive factors. Conclusion Probably, there were additive synergic effects of increasing breast cancer risk between the benign breast disease history and CYP1A1 MspⅠ polymorphism
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