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目的:探讨内源性雌激素及雌激素α受体(ERα)XbaⅠ和PvuⅡ基因多态性与宫颈癌发生的关系,以及两者在宫颈癌发生中的交互效应。方法:采用频数匹配的病例对照研究方法,选择在山西省肿瘤医院经病理学确诊的102例宫颈癌新发患者为病例组,以同期在同一医院确诊、相同数量的子宫肌瘤患者为对照组,采集其月经周期第8~10天空腹静脉血,应用ELISA法测定血清雌二醇(E2)水平,利用PCR-RFLP技术检测ERαXbaⅠ和PvuⅡ基因多态性。结果:病例组E2水平(47.57±14.27)ρg/mL,显著高于对照组(26.10±12.34)ρg/mL,差异有统计学意义,t=6.85,P<0.001。XbaⅠXX/Xx基因型频率病例组(42.2%)低于对照组(56.9%),差异有统计学意义,χ2=4.41,P=0.052;调整aOR=0.57(95%CI:0.33~0.97),而PvuⅡ基因(PP/Pp)频率在病例组和对照组间差异无统计学意义。交互作用分析显示,XbaI XX/Xx基因型频率与E2水平在宫颈癌发生中存在拮抗作用。结论:内源性雌激素水平异常增高可增加宫颈癌发生的危险性,而ERαXbaI XX/Xx基因型可降低罹患宫颈癌的风险,两者之间可能存在拮抗效应。
Objective: To investigate the relationship between endogenous estrogen, estrogen receptor α (ERα) Xba Ⅰ and Pvu Ⅱ gene polymorphisms and the occurrence of cervical cancer and their interaction in cervical carcinogenesis. Methods: A frequency-matched case-control study was conducted in 102 cancer patients newly diagnosed by pathology in Shanxi Tumor Hospital. The patients were diagnosed in the same hospital in the same period and the same number of patients with uterine fibroids as control group The fasting venous blood was collected on the 8th to 10th days of the menstrual cycle. Serum estradiol (E2) level was measured by ELISA. The polymorphisms of ERαXbaⅠ and PvuⅡ were detected by PCR-RFLP. Results: E2 level in case group (47.57 ± 14.27) ρg / mL was significantly higher than that in control group (26.10 ± 12.34) ρg / mL, the difference was statistically significant, t = 6.85, P <0.001. The frequency of genotype XbaⅠXX / Xx was lower than that of the control group (42.2%, χ2 = 4.41, P = 0.052), and the adjusted aOR was 0.57 (95% CI: 0.33-0.97) The frequency of Pvu Ⅱ gene (PP / Pp) was not significantly different between the case group and the control group. Interaction analysis showed that XbaI XX / Xx genotype frequency and E2 levels in the occurrence of cervical cancer antagonism. Conclusion: The abnormal increase of endogenous estrogen may increase the risk of cervical cancer. The ERαXbaI XX / Xx genotype may reduce the risk of cervical cancer, and there may be antagonism between the two.