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      Smoking and breast cancer risk by race/ethnicity and oestrogen and progesterone receptor status: the Multiethnic Cohort (MEC) study

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          Abstract

          The purpose of this study was to examine if the smoking-related higher breast cancer risk was similar for the five race/ethnicity groups in the Multiethnic Cohort (MEC) study and by oestrogen (ER) and progesterone (PR) receptor status. From 1993 to 2013, we followed 67 313 women who were enrolled in the MEC study at 45–75 years of age. We identified breast cancer cases and tumour receptor status via linkage to the Hawaii and California Surveillance, Epidemiology and End Results Program cancer registries through December 2013. We used Cox proportional hazards regression to estimate multivariable-adjusted hazard ratios with 95% confidence intervals (CI). During a mean follow-up of 16.7 years, we identified 4230 incident, invasive breast cancer cases. Compared with parous never smokers, parous ever smokers who had smoked more than 5 years before their first live childbirth had a higher risk of breast cancer overall of 31% (95% CI: 1.14–1.51). This higher risk was 51% (95% CI: 1.05–2.16) for African Americans, 66% (95% CI: 1.10–2.50) for Native Hawaiians, 42% (95% CI: 1.13–1.78) for Whites, 37% (95% CI: 1.17–1.61) for ER-positive (ER+) tumours and 33% (95% CI: 1.11–1.59) for PR+ tumours. No difference was suggested by racial/ethnic groups ( P heterogeneity  = 0.15) or tumour receptor status ( P heterogeneity  = 0.60 by ER status and 0.95 by PR status). We find that the higher breast cancer risk related to smoking is similar across racial/ethnic groups and by ER and PR status, indicating that breast cancer should be considered as a smoking-related cancer.

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          A multiethnic cohort in Hawaii and Los Angeles: baseline characteristics.

          The authors describe the design and implementation of a large multiethnic cohort established to study diet and cancer in the United States. They detail the source of the subjects, sample size, questionnaire development, pilot work, and approaches to future analyses. The cohort consists of 215,251 adult men and women (age 45-75 years at baseline) living in Hawaii and in California (primarily Los Angeles County) with the following ethnic distribution: African-American (16.3%), Latino (22.0%), Japanese-American (26.4%), Native Hawaiian (6.5%), White (22.9%), and other ancestry (5.8%). From 1993 to 1996, participants entered the cohort by completing a 26-page, self-administered mail questionnaire that elicited a quantitative food frequency history, along with demographic and other information. Response rates ranged from 20% in Latinos to 49% in Japanese-Americans. As expected, both within and among ethnic groups, the questionnaire data show substantial variations in dietary intakes (nutrients as well as foods) and in the distributions of non-dietary risk factors (including smoking, alcohol consumption, obesity, and physical activity). When compared with corresponding ethnic-specific cancer incidence rates, the findings provide tentative support for several current dietary hypotheses. As sufficient numbers of cancer cases are identified through surveillance of the cohort, dietary and other hypotheses will be tested in prospective analyses.
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            Applying Cox regression to competing risks.

            Two methods are given for the joint estimation of parameters in models for competing risks in survival analysis. In both cases Cox's proportional hazards regression model is fitted using a data duplication method. In principle either method can be used for any number of different failure types, assuming independent risks. Advantages of the augmented data approach are that it limits over-parametrisation and it runs immediately on existing software. The methods are used to reanalyse data from two well-known published studies, providing new insights.
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              Active smoking and breast cancer risk: original cohort data and meta-analysis.

              The relationship between active cigarette smoking and breast cancer risk remains controversial because of unresolved issues of confounding and dose response. To investigate these issues further, we analyzed data from 73 388 women in the American Cancer Society's Cancer Prevention Study II (CPS-II) Nutrition Cohort. Analyses were based on 3721 invasive breast cancer case patients identified during a median follow-up of 13.8 years. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from multivariable-adjusted Cox proportional hazard regression models. P values were two-sided. We also conducted meta-analyses of our results with those published from 14 other cohort studies. In CPS-II, incidence was higher in current (HR = 1.24, 95% CI = 1.07 to 1.42) and former smokers (HR =1.13, 95% CI = 1.06 to 1.21) than in never smokers. Women who initiated smoking before menarche (HR = 1.61, 95% CI = 1.10 to 2.34) or after menarche but 11 or more years before first birth (HR = 1.45, 95% CI = 1.21 to 1.74) had higher risk (P trend = .03). No relationships were observed with other smoking parameters. Alcohol consumption did not confound associations with smoking status, although neither current nor former smoking were associated with risk among never drinkers (P interaction = .11). In meta-analyses, current (HR = 1.12, 95% CI = 1.08 to 1.16) and former smoking (HR = 1.09, 95% CI = 1.04 to 1.15) were weakly associated with risk; a stronger association (HR = 1.21, 95% CI = 1.14 to 1.28) was observed in women who initiated smoking before first birth. These results support the hypothesis that active smoking is associated with increased breast cancer risk for women who initiate smoking before first birth and suggest that smoking might play a role in breast cancer initiation.
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                Author and article information

                Journal
                International Journal of Epidemiology
                Oxford University Press (OUP)
                0300-5771
                1464-3685
                April 2019
                April 01 2019
                January 18 2019
                April 2019
                April 01 2019
                January 18 2019
                : 48
                : 2
                : 501-511
                Affiliations
                [1 ]Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway
                [2 ]Population Science in the Pacific, Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI, USA
                [3 ]Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
                Article
                10.1093/ije/dyy290
                6469313
                30668861
                de8795ca-a9ce-41fc-9669-fe8d6fe1e545
                © 2019

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model


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