Department of Obstetrics and Gynaecology, Faculty of Medical and Health Science, The University of Auckland, Auckland 1141, New Zealand.
Department of Gynecological Cancer, Wuxi Maternity and Child Health Hospital Affiliated to Nanjing Medical University, Nanjing 214002, China.
Endocrinology. 2022 Oct 11;163(11). doi: 10.1210/endocr/bqac141.
It is well known that many factors, including infertility, obesity, type 2 diabetes, and family history of cancer, increase the risk of developing endometrial and ovarian cancer. However, multiparous women are known to have a lower risk of developing either ovarian or endometrial cancer than nonparous women. The lack of ovulation and shifting of sex hormonal balance, with decreased estrogen levels and increased progesterone levels during pregnancy, has traditionally been thought to be the major contributor to this decreased risk. However, in reality, the mechanisms underlying this phenomenon are relatively unknown. Increasing evidence suggests that endocrine factors are unlikely to completely explain the protective effect of pregnancies, and that multiple other nonendocrine mechanisms including fetal antigens and the newly proposed dormant cells hypothesis may also be involved. In this review, we summarize recent evidence and describe the potential underlying mechanisms that may explain how pregnancy protects against the development of ovarian and endometrial cancers in women's later life.
众所周知，许多因素会增加子宫内膜癌和卵巢癌的发病风险，包括不孕、肥胖、2 型糖尿病和癌症家族史。然而，多产妇发生卵巢癌和子宫内膜癌的风险低于未产妇。传统观点认为，妊娠期间排卵停止和性激素平衡转移，雌激素水平降低、孕激素水平升高是导致这种风险降低的主要原因。然而，实际上，这种现象的潜在机制尚不清楚。越来越多的证据表明，内分泌因素不太可能完全解释妊娠的保护作用，可能还涉及多种其他非内分泌机制，包括胎儿抗原和新提出的休眠细胞假说。在这篇综述中，我们总结了最近的证据，并描述了可能的潜在机制，这些机制可以解释妊娠如何预防女性晚年卵巢癌和子宫内膜癌的发生。
