Characteristics relating to ovarian cancer risk: collaborative analysis of 12 US case-control studies. IV. The pathogenesis of epithelial ovarian cancer. Collaborative Ovarian Cancer Group.
Characteristics relating to ovarian cancer risk: collaborative analysis of 12 US case-control studies. IV. The pathogenesis of epithelial ovarian cancer. Collaborative Ovarian Cancer Group.
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与卵巢癌风险相关的特征：12 项美国病例对照研究的协作分析。
DOI：
10.1093/oxfordjournals.aje.a116429
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发表时间：
1992
影响因子：
5
通讯作者：
Itnyre,J
中科院分区：
文献类型：
--
作者：
Whittemore,AS;Harris,R;Itnyre,J
已经提出了两种假说来解释与妊娠和口服避孕药使用相关的上皮性卵巢癌风险降低。第一种说法是排卵的一些后遗症增加了恶性肿瘤的可能性，怀孕和口服避孕药通过抑制排卵来保护。第二种假说认为，循环中垂体促性腺激素水平增加了恶性肿瘤的风险，怀孕和口服避孕药通过抑制这些激素的分泌来保护。作者根据1956年至1986年进行的12项美国白色妇女上皮性卵巢癌病例-奥昔特罗研究的综合数据评估了这两种假设。虽然一些观察支持这两种假设，但也有例外。与妊娠和口服避孕药使用相关的差异性风险降低（妊娠对年轻女性更有效，对老年女性效果较差）与第一个“排卵”假设相冲突，而与母乳喂养相关的风险降低和与雌激素替代治疗相关的风险改变的缺乏与第二个“促性腺激素”假设相冲突。有几个发现是两种假设都无法预测的，例如，只有微弱的趋势表明癌症风险与初潮年龄有关，在老年妇女中，没有明确的趋势表明风险与绝经年龄有关。由于报告个人特征的错误而导致的比值比衰减可能是造成这些不一致的原因。需要多学科的研究来阐明排卵和促性腺激素刺激的作用，这两者都可能促进卵巢上皮的癌变。
Two hypotheses have been proposed to explain the reduced risk of epithelial ovarian cancer associated with pregnancy and oral contraceptive use. The first states that some sequelae of ovulation increase the likelihood of malignancy and that pregnancies and oral contraceptives protect by suppressing ovulation. The second hypothesis states that circulating levels of pituitary gonadotropins increase the risk of malignancy and that pregnancies and oral contraceptives protect by suppressing secretion of these hormones. The authors evaluate the two hypotheses in light of combined data from 12 United States case-oxitrol studies of epithelial ovarian cancer in white women conducted from 1956 to 1986. While a number of observations support both hypotheses, there are exceptions. Differential risk reduction associated with pregnancy and oral contraceptive use (pregnancy being the more effective in young women and the less effective in older women) conflicts with the first “ovulation” hypothesis, while reduced risk associated with breast feeding and absence of altered risk associated with estrogen replacement therapy conflicts with the second “gonadotropin” hypothesis. Several findings would not have been predicted by either hypothesis, e.g., only weak trends relate cancer risk to age at menarche, and, among older women, no clear trends relate risk to age at menopause. Odds ratio attenuation due to errors in reporting personal characteristics may be responsible for some of these inconsistencies. Multidisciplinary research is needed to clarify the etkrfogic roles of ovulation and gonadotropin stimulation, both of which may enhance carcinogenesis in the ovarian epithelium.Am J Epidemiol1992: 136: 1212–20