Reproductive characteristics in relation to ovarian cancer risk by histologic pathways
Reproductive characteristics in relation to ovarian cancer risk by histologic pathways
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DOI：
10.1093/humrep/des466
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发表时间：
2013-05-01
影响因子：
6.1
通讯作者：
Terry, K. L.
中科院分区：
文献类型：
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作者：
Merritt, M. A.;De Pari, M.;Terry, K. L.
在二元模型（I/II型）或基于组织学路径的分类定义的侵袭性上皮性卵巢癌（EOC）亚组之间，生殖风险因素相关性是否存在差异？与产次、子宫内膜异位症病史、输卵管结扎术和子宫切除术在I型和II型输卵管炎的情况下是不同的。II和卵巢癌的组织学途径分类。共有的分子改变和候选的前体病变表明，肿瘤组织学和分级可用于将卵巢肿瘤分类为可能的病因学途径。这项病例对照研究包括1571名诊断为浸润性EOC的妇女和2100名诊断为浸润性EOC的妇女。1992年至2008年登记的基于人群的对照。通过面对面访谈评估生殖风险因素以及其他可能的卵巢癌风险因素。符合条件的病例被诊断为偶发卵巢癌，年龄在18岁及以上，居住在美国东部马萨诸塞州或新罕布什尔州。通过随机数字拨号、驾驶执照和城镇居民名单确定对照组，并根据年龄和研究中心与病例频率匹配，我们使用多分类logistic回归估计I/II型EOC或使用基于路径的组织学亚型分组的优势比（OR）和95置信区间（CI）。在多变量分析中，我们观察到有子宫内膜异位症病史（OR 1.92，95 CI：1.362.71）增加了I型肿瘤的风险。与I型肿瘤风险呈强负相关的因素包括产次（3对0名儿童，OR 0.15，95 CI：0.110.21），既往输卵管结扎（OR 0.40，95 CI：0.260.60）和子宫切除术（OR 0.71，95 CI：0.451.13）。在组织学途径分析中，产次（3对0名儿童，OR 0.13，95 CI：0.100.18）和既往输卵管结扎术（OR 0.41，95 CI：0.280.60）或子宫切除术（OR 0.54，95 CI：0.340.86）与卵巢样/透明细胞肿瘤的风险呈负相关。有子宫内膜异位症病史的患者患子宫内膜样/透明细胞瘤的风险显著增加（OR 2.41，95 CI：1.783.26）。我们没有观察到这些肿瘤分类与初潮年龄、月经周期长度或不孕症的风险相关性有显著差异。本研究的一个潜在局限性是将病例分为亚组可能会限制这些分析的效力，特别是对于不太常见的肿瘤类型。由于病例是在诊断后入组的，这项研究提供了关于生殖因素在途径风险中的作用的见解，基于卵巢癌的亚组，进一步证实可能有助于开发预防这些不同肿瘤类型的改进策略。研究所，国防部卵巢癌研究计划和卵巢癌研究基金。作者没有竞争利益声明。不适用。
Do reproductive risk factor associations differ across subgroups of invasive epithelial ovarian cancer (EOC) defined by the dualistic model (type I/II) or a histologic pathway-based classification?Associations with parity, history of endometriosis, tubal ligation and hysterectomy were found to differ in the context of the type I/II and the histologic pathways classification of ovarian cancer.Shared molecular alterations and candidate precursor lesions suggest that tumor histology and grade may be used to classify ovarian tumors into likely etiologic pathways.This casecontrol study included 1571 women diagnosed with invasive EOC and 2100 population-based controls that were enrolled from 1992 to 2008. Reproductive risk factors as well as other putative risk factors for ovarian cancer were assessed through in-person interviews.Eligible cases were diagnosed with incident ovarian cancer, were aged 18 and above and resided in eastern Massachusetts or New Hampshire, USA. Controls were identified through random digit dialing, drivers license and town resident lists and were frequency matched with the cases based on age and study center.We used polytomous logistic regression to estimate odds ratios (ORs) and 95 confidence intervals (CIs) for type I/II EOC or using a pathway-based grouping of histologic subtypes. In multivariate analyses, we observed that having a history of endometriosis (OR 1.92, 95 CI: 1.362.71) increased the risk for a type I tumor. Factors that were strongly inversely associated with risk for a type I tumor included parity (3 versus 0 children, OR 0.15, 95 CI: 0.110.21), having a previous tubal ligation (OR 0.40, 95 CI: 0.260.60) and more weakly hysterectomy (OR 0.71, 95 CI: 0.451.13). In analyses of histologic pathways, parity (3 versus 0 children, OR 0.13, 95 CI: 0.100.18) and having a previous tubal ligation (OR 0.41, 95 CI: 0.280.60) or hysterectomy (OR 0.54, 95 CI: 0.340.86) were inversely associated with risk of endometrioid/clear cell tumors. Having a history of endometriosis strongly increased the risk for endometrioid/clear cell tumors (OR 2.41, 95 CI: 1.783.26). We did not observe significant differences in the risk associations across these tumor classifications for age at menarche, menstrual cycle length or infertility.A potential limitation of this study is that dividing the cases into subgroups may limit the power of these analyses, particularly for the less common tumor types. Since cases were enrolled after their diagnosis, it is possible that the most aggressive cases were not included in the study.This study provides insights about the role of reproductive factors in relation to risk of pathway-based subgroups of ovarian cancer that with further confirmation may assist with the development of improved strategies for the prevention of these different tumor types.This research is funded by grants from the National Cancer Institute, the Department of Defense Ovarian Cancer Research Program and the Ovarian Cancer Research Fund. The authors have no competing interests to declare.Not applicable.