Division of Cancer Epidemiology and Biostatistics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway.
J Intern Med. 2018 May;283(5):430-445. doi: 10.1111/joim.12747. Epub 2018 Mar 25.
An understanding of the origin of cancer is critical for cancer prevention and treatment. Complex biological mechanisms promote carcinogenesis, and there is increasing evidence that pregnancy-related exposures influence foetal growth cell division and organ functioning and may have a long-lasting impact on health and disease susceptibility in the mothers and offspring. Nulliparity is an established risk factor for breast, ovarian, endometrial and possibly pancreatic cancer, whilst the risk of kidney cancer is elevated in parous compared with nulliparous women. For breast, endometrial and ovarian cancer, each pregnancy provides an additional risk reduction. The associations of parity with thyroid and colorectal cancers are uncertain. The timing of reproductive events is also recognized to be important. Older age at first birth is associated with an increased risk of breast cancer, and older age at last birth is associated with a reduced risk of endometrial cancer. The risks of breast and endometrial cancers increase with younger age at menarche and older age at menopause. The mechanisms, and hormone profiles, that underlie alterations in maternal cancer risk are not fully understood and may differ by malignancy. Linking health registries and pooling of data in the Nordic countries have provided opportunities to conduct epidemiologic research of pregnancy exposures and subsequent cancer. We review the maternal risk of several malignancies, including those with a well-known hormonal aetiology and those with less established relationships. The tendency for women to have fewer pregnancies and at later ages, together with the age-dependent increase in the incidence of most malignancies, is expected to affect the incidence of pregnancy-associated cancer.
了解癌症的起源对于癌症的预防和治疗至关重要。复杂的生物学机制促进了癌症的发生，越来越多的证据表明，与妊娠相关的暴露会影响胎儿的生长、细胞分裂和器官功能，并可能对母亲和后代的健康和疾病易感性产生持久影响。未生育是乳腺癌、卵巢癌、子宫内膜癌和可能的胰腺癌的既定危险因素，而与未生育的女性相比，生育过的女性患肾癌的风险增加。对于乳腺癌、子宫内膜癌和卵巢癌，每次妊娠都会降低额外的风险。生育次数与甲状腺癌和结直肠癌的关联尚不确定。生殖事件的时间也被认为是重要的。初产年龄越大，患乳腺癌的风险就越高，而最后一次生育的年龄越大，患子宫内膜癌的风险就越低。初潮年龄越早，绝经年龄越晚，患乳腺癌和子宫内膜癌的风险就越高。导致母亲患癌症风险改变的机制和激素特征尚未完全了解，并且可能因恶性肿瘤而有所不同。将健康登记处联系起来并在北欧国家汇总数据，为进行妊娠暴露和随后癌症的流行病学研究提供了机会。我们回顾了几种恶性肿瘤的母亲风险，包括那些具有明确激素病因的恶性肿瘤和那些与癌症关系不太明确的恶性肿瘤。女性生育次数减少且年龄增大，以及大多数恶性肿瘤的发病率随年龄增长而增加，这预计会影响与妊娠相关的癌症的发病率。
