Ovarian cancer and smoking: individual participant meta-analysis including 28,114 women with ovarian cancer from 51 epidemiological studies.
Ovarian cancer and smoking: individual participant meta-analysis including 28,114 women with ovarian cancer from 51 epidemiological studies.
复制标题
DOI：
10.1016/s1470-2045(12)70322-4
复制
发表时间：
2012-09
期刊：
影响因子：
--
通讯作者：
Peto R
中科院分区：
文献类型：
--
作者：
Collaborative Group on Epidemiological Studies of Ovarian Cancer;Beral V;Gaitskell K;Hermon C;Moser K;Reeves G;Peto R
吸烟与粘液性卵巢癌有关，但它对其他卵巢癌亚型和总体卵巢癌风险的影响尚不清楚，而且大多数有相关数据的研究结果都未发表。为了评估这些关联，我们回顾了已发表和未发表的证据。符合条件的流行病学研究通过电子搜索、综述文章和与同事的讨论来确定。对来自51项流行病学研究的28名患有卵巢癌的 114名女性和94名未患卵巢癌的 942的个人参与者数据进行了集中分析，得出了吸烟者与从不吸烟者患卵巢癌的调整后相对风险(RR)。在排除了吸烟可能影响招募的医院对照研究后，与从不吸烟的女性相比，现在吸烟者的总体卵巢癌发病率仅略有增加(RR 1·06，95%CI 1·01-1·11，p=0.01)。在17例特定组织学类型的 641上皮性癌中，粘液性癌2 314例(13%)，子宫内膜样癌2 36 0例(13%)，透明细胞癌96 9例(5%)，浆液性癌90 86例(52%)。与吸烟相关的风险在这些亚型中有很大的不同(肺炎性)。对于粘液性癌，现吸烟者的发病率高于从不吸烟者(1.79，95%CI 1·60~2·00，p<；0.0001)，但这种增加主要发生在交界性恶性肿瘤中，而不是完全恶性(2.25，95%CI 1.91~2.65 vs 1.49，1.28~1.73；肺炎性=0.01；几乎一半的粘液性肿瘤仅为交界性恶性肿瘤)。在现有吸烟者中，子宫内膜样变(0.81，95%CI为0.72~0.92，p=0.001)和透明细胞卵巢癌风险(0.80，95%CI为0.65~0.97，p=0.03)均降低，与浆液性卵巢癌无显著相关性(0.99，95%CI为0.93~1.06，p=0.8)。女性的13个社会人口学和个人特征，包括她们的体重指数、产次、酒精的使用、口服避孕药和更年期激素治疗，这些相关性没有显著差异。吸烟者中粘液性卵巢癌的过剩，主要是交界性恶性肿瘤，大致被子宫内膜样癌和透明细胞卵巢癌的缺陷所抵消。不同肿瘤亚型的吸烟相关风险的显著差异对于了解卵巢癌的发生很重要。英国癌症研究中心和MRC。
Smoking has been linked to mucinous ovarian cancer, but its effects on other ovarian cancer subtypes and on overall ovarian cancer risk are unclear, and the findings from most studies with relevant data are unpublished. To assess these associations, we review the published and unpublished evidence. Eligible epidemiological studies were identified by electronic searches, review articles, and discussions with colleagues. Individual participant data for 28 114 women with and 94 942 without ovarian cancer from 51 epidemiological studies were analysed centrally, yielding adjusted relative risks (RRs) of ovarian cancer in smokers compared with never smokers. After exclusion of studies with hospital controls, in which smoking could have affected recruitment, overall ovarian cancer incidence was only slightly increased in current smokers compared with women who had never smoked (RR 1·06, 95% CI 1·01–1·11, p=0·01). Of 17 641 epithelial cancers with specified histology, 2314 (13%) were mucinous, 2360 (13%) endometrioid, 969 (5%) clear-cell, and 9086 (52%) serous. Smoking-related risks varied substantially across these subtypes (pheterogeneity<0·0001). For mucinous cancers, incidence was increased in current versus never smokers (1·79, 95% CI 1·60–2·00, p<0·0001), but the increase was mainly in borderline malignant rather than in fully malignant tumours (2·25, 95% CI 1·91–2·65 vs 1·49, 1·28–1·73; pheterogeneity=0·01; almost half the mucinous tumours were only borderline malignant). Both endometrioid (0·81, 95% CI 0·72–0·92, p=0·001) and clear-cell ovarian cancer risks (0·80, 95% CI 0·65–0·97, p=0·03) were reduced in current smokers, and there was no significant association for serous ovarian cancers (0·99, 95% CI 0·93–1·06, p=0·8). These associations did not vary significantly by 13 sociodemographic and personal characteristics of women including their body-mass index, parity, and use of alcohol, oral contraceptives, and menopausal hormone therapy. The excess of mucinous ovarian cancers in smokers, which is mainly of tumours of borderline malignancy, is roughly counterbalanced by the deficit of endometrioid and clear-cell ovarian cancers. The substantial variation in smoking-related risks by tumour subtype is important for understanding ovarian carcinogenesis. Cancer Research UK and MRC.