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Sökning: WFRF:(Eliassen A Heather)

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  • Föregående 12[3]
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  • Gaudet, Mia M., et al. (författare)
  • Interactions between breast cancer susceptibility loci and menopausal hormone therapy in relationship to breast cancer in the Breast and Prostate Cancer Cohort Consortium
  • 2016
  • Ingår i: Breast Cancer Research and Treatment. - 0167-6806 .- 1573-7217. ; 155:3, s. 531-540
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Current use of menopausal hormone therapy (MHT) has important implications for postmenopausal breast cancer risk, and observed associations might be modified by known breast cancer susceptibility loci. To provide the most comprehensive assessment of interactions of prospectively collected data on MHT and 17 confirmed susceptibility loci with invasive breast cancer risk, a nested case-control design among eight cohorts within the NCI Breast and Prostate Cancer Cohort Consortium was used. Based on data from 13,304 cases and 15,622 controls, multivariable-adjusted logistic regression analyses were used to estimate odds ratios (OR) and 95 % confidence intervals (CI). Effect modification of current and past use was evaluated on the multiplicative scale. P values &lt; 1.5 x 10(-3) were considered statistically significant. The strongest evidence of effect modification was observed for current MHT by 9q31-rs865686. Compared to never users of MHT with the rs865686 GG genotype, the association between current MHT use and breast cancer risk for the TT genotype (OR 1.79, 95 % CI 1.43-2.24; P (interaction) = 1.2 x 10(-4)) was less than expected on the multiplicative scale. There are no biological implications of the sub-multiplicative interaction between MHT and rs865686. Menopausal hormone therapy is unlikely to have a strong interaction with the common genetic variants associated with invasive breast cancer.</p>
  • Gaudet, Mia M, et al. (författare)
  • Pooled Analysis of Nine Cohorts Reveals Breast Cancer Risk Factors by Tumor Molecular Subtype.
  • 2018
  • Ingår i: Cancer Research. - 0008-5472 .- 1538-7445. ; 78:20, s. 6011-6021
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Various subtypes of breast cancer defined by estrogen receptor (ER), progesterone receptor (PR), and HER2 exhibit etiologic differences in reproductive factors, but associations with other risk factors are inconsistent. To clarify etiologic heterogeneity, we pooled data from nine cohort studies. Multivariable, joint Cox proportional hazards regression models were used to estimate HRs and 95% confidence intervals (CI) for molecular subtypes. Of 606,025 women, 11,741 invasive breast cancers with complete tissue markers developed during follow-up: 8,700 luminal A–like (ER<sup>+</sup> or PR<sup>+</sup>/HER2<sup>−</sup>), 1,368 luminal B–like (ER<sup>+</sup> or PR<sup>+</sup>/HER2<sup>+</sup>), 521 HER2-enriched (ER<sup>−</sup>/PR<sup>−</sup>/HER2<sup>+</sup>), and 1,152 triple-negative (ER<sup>−</sup>/PR<sup>−</sup>/HER2<sup>−</sup>) disease. Ever parous compared with never was associated with lower risk of luminal A–like (HR, 0.78; 95% CI, 0.73–0.83) and luminal B–like (HR, 0.74; 95% CI, 0.64–0.87) as well as a higher risk of triple-negative disease (HR, 1.23; 95% CI, 1.02–1.50; <em>P</em> value for overall tumor heterogeneity &lt; 0.001). Direct associations with luminal-like, but not HER2-enriched or triple-negative, tumors were found for age at first birth, years between menarche and first birth, and age at menopause (<em>P</em> value for overall tumor heterogeneity &lt; 0.001). Age-specific associations with baseline body mass index differed for risk of luminal A–like and triple-negative breast cancer (<em>P</em> value for tumor heterogeneity = 0.02). These results provide the strongest evidence for etiologic heterogeneity of breast cancer to date from prospective studies.</p><p><strong>Significance:</strong> These findings comprise the largest study of prospective data to date and contribute to the accumulating evidence that etiological heterogeneity exists in breast carcinogenesis. <em>Cancer Res; 78(20); 6011–21. ©2018 AACR</em>.</p><p>.</p>
  • Ge, Wenzhen, et al. (författare)
  • Circulating anti-Müllerian hormone and breast cancer risk : a study in ten prospective cohorts
  • 2018
  • Ingår i: International Journal of Cancer. - Hoboken : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 142:11, s. 2215-2226
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>A strong positive association has been observed between circulating anti‐Müllerian hormone (AMH), a biomarker of ovarian reserve, and breast cancer risk in three prospective studies. Confirming this association is important because of the paucity of biomarkers of breast cancer risk in premenopausal women. We conducted a consortium study including ten prospective cohorts that had collected blood from premenopausal women. A nested case–control design was implemented within each cohort. A total of 2,835 invasive (80%) and <em>in situ</em> (20%) breast cancer cases were individually matched to controls (<em>n</em> = 3,122) on age at blood donation. AMH was measured using a high sensitivity enzyme‐linked immunoabsorbent assay. Conditional logistic regression was applied to the aggregated dataset. There was a statistically significant trend of increasing breast cancer risk with increasing AMH concentration (<em>p</em><sub>trend</sub> across quartiles &lt;0.0001) after adjusting for breast cancer risk factors. The odds ratio (OR) for breast cancer in the top <em>vs</em>. bottom quartile of AMH was 1.60 (95% CI = 1.31–1.94). Though the test for interaction was not statistically significant (<em>p</em><sub>interaction</sub> = 0.15), the trend was statistically significant only for tumors positive for both estrogen receptor (ER) and progesterone receptor (PR): ER+/PR+: OR<sub>Q4–Q1</sub> = 1.96, 95% CI = 1.46–2.64, <em>p</em><sub>trend</sub> &lt;0.0001; ER+/PR−: OR<sub>Q4–Q1</sub> = 0.82, 95% CI = 0.40–1.68, <em>p</em><sub>trend</sub> = 0.51; ER−/PR+: OR<sub>Q4–Q1</sub> = 3.23, 95% CI = 0.48–21.9, <em>p</em><sub>trend</sub> = 0.26; ER−/PR−: OR<sub>Q4–Q1</sub> = 1.15, 95% CI = 0.63–2.09, <em>p</em><sub>trend</sub> = 0.60. The association was observed for both pre‐ (OR<sub>Q4–Q1</sub>= 1.35, 95% CI = 1.05–1.73) and post‐menopausal (OR<sub>Q4–Q1</sub> = 1.61, 95% CI = 1.03–2.53) breast cancer (<em>p</em><sub>interaction</sub> = 0.34). In this large consortium study, we confirmed that AMH is associated with breast cancer risk, with a 60% increase in risk for women in the top <em>vs</em>. bottom quartile of AMH.</p><p>What's new? To make informed decisions about screening and prevention, women need tools to accurately assess their breast cancer risk. Young women have few predictive biomarkers to look to; estrogen and progesterone are only weakly predictive before menopause. Anti-Müllerian hormone (AMH), which strongly correlates with age at menopause, may also correlate with breast cancer risk, according to some previous data. Here, the authors test this correlation by conducting nested case-control studies within ten different cohorts. They found that breast cancer risk increased along with increasing AMH concentration, confirming this hormone as a possible biomarker for breast cancer.</p>
  • Playdon, Mary C., et al. (författare)
  • Metabolomics Analytics Workflow for Epidemiological Research : Perspectives from the Consortium of Metabolomics Studies (COMETS)
  • 2019
  • Ingår i: Metabolites. - MDPI. - 2218-1989 .- 2218-1989. ; 9:7
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The application of metabolomics technology to epidemiological studies is emerging as a new approach to elucidate disease etiology and for biomarker discovery. However, analysis of metabolomics data is complex and there is an urgent need for the standardization of analysis workflow and reporting of study findings. To inform the development of such guidelines, we conducted a survey of 47 cohort representatives from the Consortium of Metabolomics Studies (COMETS) to gain insights into the current strategies and procedures used for analyzing metabolomics data in epidemiological studies worldwide. The results indicated a variety of applied analytical strategies, from biospecimen and data pre-processing and quality control to statistical analysis and reporting of study findings. These strategies included methods commonly used within the metabolomics community and applied in epidemiological research, as well as novel approaches to pre-processing pipelines and data analysis. To help with these discrepancies, we propose use of open-source initiatives such as the online web-based tool COMETS Analytics, which includes helpful tools to guide analytical workflow and the standardized reporting of findings from metabolomics analyses within epidemiological studies. Ultimately, this will improve the quality of statistical analyses, research findings, and study reproducibility.</p>
  • Borgquist, Signe, et al. (författare)
  • Statin Use and Breast Cancer Risk in the Nurses' Health Study.
  • 2016
  • Ingår i: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. - American Association for Cancer Research. - 1538-7755. ; 25:1, s. 201-206
  • Tidskriftsartikel (refereegranskat)abstract
    • Preclinical studies support an anticancer effect of statin drugs, yet epidemiologic evidence remains inconsistent regarding their role in breast cancer primary prevention. Here, we report an updated analysis of the association between statin use and breast cancer incidence in the Nurses' Health Study (NHS) cohort. Postmenopausal NHS participants without a cancer history were followed from 2000 until 2012 (n = 79,518). Data on statin use were retrieved from biennial questionnaires. We fit Cox regression models to estimate associations between longitudinal statin use and breast cancer incidence. Over 823,086 person-years of follow-up, 3,055 cases of invasive breast cancer occurred. Compared with never users, both former and current statin users had similar rates of invasive breast cancer incidence [former users: HRadj, 0.96; 95% confidence interval (CI), 0.82-1.1; current users: HRadj, 1.1; 95% CI, 0.92-1.3]. Associations did not differ by estrogen receptor (ER) status or histology (ductal vs. lobular carcinoma). Statin use was not associated with risk of invasive breast cancer, irrespective of histologic subtype and ER status. Statin drugs do not appear to modify processes involved in breast cancer initiation. Cancer Epidemiol Biomarkers Prev; 25(1); 201-6. ©2016 AACR.
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