Frances E M Albers, Makayla W C Lou, S Ghazaleh Dashti, Christopher T V Swain, Sabina Rinaldi, Vivian Viallon, Amalia Karahalios, Kristy A Brown, Marc J Gunter, Roger L Milne, Dallas R English, Brigid M Lynch
{"title":"Sex-steroid hormones and risk of postmenopausal estrogen receptor-positive breast cancer: a case-cohort analysis.","authors":"Frances E M Albers, Makayla W C Lou, S Ghazaleh Dashti, Christopher T V Swain, Sabina Rinaldi, Vivian Viallon, Amalia Karahalios, Kristy A Brown, Marc J Gunter, Roger L Milne, Dallas R English, Brigid M Lynch","doi":"10.1007/s10552-024-01856-6","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Sex-steroid hormones are associated with postmenopausal breast cancer but potential confounding from other biological pathways is rarely considered. We estimated risk ratios for sex-steroid hormone biomarkers in relation to postmenopausal estrogen receptor (ER)-positive breast cancer, while accounting for biomarkers from insulin/insulin-like growth factor-signaling and inflammatory pathways.</p><p><strong>Methods: </strong>This analysis included 1208 women from a case-cohort study of postmenopausal breast cancer within the Melbourne Collaborative Cohort Study. Weighted Poisson regression with a robust variance estimator was used to estimate risk ratios (RRs) and 95% confidence intervals (CIs) of postmenopausal ER-positive breast cancer, per doubling plasma concentration of progesterone, estrogens, androgens, and sex-hormone binding globulin (SHBG). Analyses included sociodemographic and lifestyle confounders, and other biomarkers identified as potential confounders.</p><p><strong>Results: </strong>Increased risks of postmenopausal ER-positive breast cancer were observed per doubling plasma concentration of progesterone (RR: 1.22, 95% CI 1.03 to 1.44), androstenedione (RR 1.20, 95% CI 0.99 to 1.45), dehydroepiandrosterone (RR: 1.15, 95% CI 1.00 to 1.34), total testosterone (RR: 1.11, 95% CI 0.96 to 1.29), free testosterone (RR: 1.12, 95% CI 0.98 to 1.28), estrone (RR 1.21, 95% CI 0.99 to 1.48), total estradiol (RR 1.19, 95% CI 1.02 to 1.39) and free estradiol (RR 1.22, 95% CI 1.05 to 1.41). A possible decreased risk was observed for SHBG (RR 0.83, 95% CI 0.66 to 1.05).</p><p><strong>Conclusion: </strong>Progesterone, estrogens and androgens likely increase postmenopausal ER-positive breast cancer risk, whereas SHBG may decrease risk. These findings strengthen the causal evidence surrounding the sex-hormone-driven nature of postmenopausal breast cancer.</p>","PeriodicalId":9432,"journal":{"name":"Cancer Causes & Control","volume":null,"pages":null},"PeriodicalIF":2.2000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11130059/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Causes & Control","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10552-024-01856-6","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/16 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose: Sex-steroid hormones are associated with postmenopausal breast cancer but potential confounding from other biological pathways is rarely considered. We estimated risk ratios for sex-steroid hormone biomarkers in relation to postmenopausal estrogen receptor (ER)-positive breast cancer, while accounting for biomarkers from insulin/insulin-like growth factor-signaling and inflammatory pathways.
Methods: This analysis included 1208 women from a case-cohort study of postmenopausal breast cancer within the Melbourne Collaborative Cohort Study. Weighted Poisson regression with a robust variance estimator was used to estimate risk ratios (RRs) and 95% confidence intervals (CIs) of postmenopausal ER-positive breast cancer, per doubling plasma concentration of progesterone, estrogens, androgens, and sex-hormone binding globulin (SHBG). Analyses included sociodemographic and lifestyle confounders, and other biomarkers identified as potential confounders.
Results: Increased risks of postmenopausal ER-positive breast cancer were observed per doubling plasma concentration of progesterone (RR: 1.22, 95% CI 1.03 to 1.44), androstenedione (RR 1.20, 95% CI 0.99 to 1.45), dehydroepiandrosterone (RR: 1.15, 95% CI 1.00 to 1.34), total testosterone (RR: 1.11, 95% CI 0.96 to 1.29), free testosterone (RR: 1.12, 95% CI 0.98 to 1.28), estrone (RR 1.21, 95% CI 0.99 to 1.48), total estradiol (RR 1.19, 95% CI 1.02 to 1.39) and free estradiol (RR 1.22, 95% CI 1.05 to 1.41). A possible decreased risk was observed for SHBG (RR 0.83, 95% CI 0.66 to 1.05).
Conclusion: Progesterone, estrogens and androgens likely increase postmenopausal ER-positive breast cancer risk, whereas SHBG may decrease risk. These findings strengthen the causal evidence surrounding the sex-hormone-driven nature of postmenopausal breast cancer.
目的:性类固醇激素与绝经后乳腺癌有关,但很少考虑其他生物途径可能造成的混淆。我们估算了性类固醇激素生物标志物与绝经后雌激素受体(ER)阳性乳腺癌的风险比,同时考虑了胰岛素/胰岛素样生长因子信号传导和炎症途径的生物标志物:这项分析包括墨尔本队列协作研究(Melbourne Collaborative Cohort Study)中绝经后乳腺癌病例队列研究的 1208 名妇女。使用加权泊松回归和稳健方差估计器估算了绝经后ER阳性乳腺癌的风险比(RRs)和95%置信区间(CIs),以及孕酮、雌激素、雄激素和性激素结合球蛋白(SHBG)血浆浓度每增加一倍的风险比。分析包括社会人口学和生活方式混杂因素,以及其他被确定为潜在混杂因素的生物标志物:结果:观察到绝经后ER阳性乳腺癌的风险随着孕酮(RR:1.22,95% CI 1.03 至 1.44)、雄二酮(RR:1.20,95% CI 0.99 至 1.45)、脱氢表雄酮(RR:1.15,95% CI 1.00至1.34)、总睾酮(RR:1.11,95% CI 0.96至1.29)、游离睾酮(RR:1.12,95% CI 0.98至1.28)、雌酮(RR 1.21,95% CI 0.99至1.48)、总雌二醇(RR 1.19,95% CI 1.02至1.39)和游离雌二醇(RR 1.22,95% CI 1.05至1.41)。SHBG的风险可能降低(RR 0.83,95% CI 0.66 至 1.05):结论:孕酮、雌激素和雄激素可能会增加绝经后ER阳性乳腺癌的风险,而SHBG可能会降低风险。这些发现加强了有关绝经后乳腺癌由性激素驱动的因果关系的证据。
期刊介绍:
Cancer Causes & Control is an international refereed journal that both reports and stimulates new avenues of investigation into the causes, control, and subsequent prevention of cancer. By drawing together related information published currently in a diverse range of biological and medical journals, it has a multidisciplinary and multinational approach.
The scope of the journal includes: variation in cancer distribution within and between populations; factors associated with cancer risk; preventive and therapeutic interventions on a population scale; economic, demographic, and health-policy implications of cancer; and related methodological issues.
The emphasis is on speed of publication. The journal will normally publish within 30 to 60 days of acceptance of manuscripts.
Cancer Causes & Control publishes Original Articles, Reviews, Commentaries, Opinions, Short Communications and Letters to the Editor which will have direct relevance to researchers and practitioners working in epidemiology, medical statistics, cancer biology, health education, medical economics and related fields. The journal also contains significant information for government agencies concerned with cancer research, control and policy.