PDF(Pubmed)
Abstract：
Testicular cancer is believed to originate from disruptions of normal androgen-estrogen balance in-utero. α-fetoprotein (AFP) may modify fetal response to estrogens via estrogen interaction. In a cohort study, we investigated the association between circulating maternal pregnancy AFP and testicular cancer risk in offspring. Of the 56,709 live-born males from a pregnancy screening registry in 1980-1995, our study included 50,519 singleton males with available second trimester blood samples from their mothers and complete covariate ascertainment. Testicular cancer diagnoses and covariate data were obtained from nationwide Danish health registries. Cox regression and Kaplan-Meier analyses estimated the prospective risk of testicular cancer (all, seminoma, nonseminoma) by AFP multiples of the median. During follow-up, 163 (0.3%) of the included males developed testicular cancer, of which 89 (54.6%) were nonseminomas. Maternal serum AFP levels greater than/equal to the median were associated with a relative risk of testicular cancer close to unity (RR 1.04, 95% CI 0.76; 1.41) compared to AFP below the median. Associations differed by type of testicular cancer (RRseminoma 0.81, 95% CI 0.51; 1.29, RRnonseminoma 1.31, 95% CI 0.85; 2.02). On balance, our findings do not support that serum AFP in pregnancy can be used as a predictor of testicular cancer in offspring.
摘要：
人们认为睾丸癌起源于子宫内正常雄激素-雌激素平衡的破坏。甲胎蛋白（AFP）可能通过雌激素相互作用改变胎儿对雌激素的反应。在一项队列研究中，我们调查了循环母体妊娠AFP与后代睾丸癌风险之间的关系.在1980-1995年怀孕筛查登记处的56,709名活产男性中，我们的研究包括50,519名单胎男性，其母亲的孕中期血液样本和完整的协变量确定。睾丸癌诊断和协变量数据来自丹麦全国卫生登记处。Cox回归和Kaplan-Meier分析估计了睾丸癌的前瞻性风险(所有，精原细胞瘤,非精原细胞瘤）按AFP中位数倍数计算。随访期间,纳入的男性中有163人（0.3％）患有睾丸癌，其中89例（54.6%）为非精原细胞瘤。与AFP低于中位数相比，母亲血清AFP水平高于/等于中位数与睾丸癌的相对风险接近一致（RR1.04，95％CI0.76；1.41）。根据睾丸癌的类型，关联存在差异（RR精原细胞瘤0.81，95％CI0.51；1.29，RRnon精原细胞瘤1.31，95％CI0.85；2.02）。在平衡，我们的研究结果不支持妊娠期血清AFP可作为后代睾丸癌的预测因子.
