#2 Interaction of adolescent anthropometric characteristics and family history on breast cancer risk in a cohort study of 426 families.

摘要

PURPOSE: To determine whether the association of adolescent anthropometric characteristics with breast cancer incidence is modified by a family history of the disease.METHODS: We used a historical cohort of 426 families of breast cancer probands diagnosed between 1944 and 1952 at the University of Minnesota. The incidence of cancer and the measurement of risk factors in sisters, daughters, granddaughters, nieces and marry-ins were determined through telephone interviews and mailed questionnaires conducted from 1991-1996. Cox proportional hazards regression, accounting for age, birth cohort, adult body mass index, and clustering within families, was used to estimate relative risks (RR) and 95% confidence intervals of breast cancer.RESULTS: Among 4,632 women available for analysis, 175 developed breast cancer. In the 426 families, sisters and daughters of the probands with above average weight at age 12, compared to those with below average weight at age 12, were at increased risk of breast cancer (RR = 2.75; 1.07-7.05), while the risk for above average weight at age 12 among grand-daughters and nieces was weaker (RR = 1.47; 0.54-4.02). In contrast, among marry-ins, women with above average weight at age 12 were at lower risk of breast cancer (RR = 0.47; 0.17-1.27), and the test for interaction between degree of relationship to proband and relative weight at age 12 on breast cancer risk was highly statistically significant (p = 0.002). The interaction was apparent for both premenopausal (p = 0.08) and postmenopausal (p = 0.02) breast cancer risk. There was no important interaction between degree of relationship to proband and height (p = 0.55), weight at age 18 (p = 0.22) or body mass index at age 18 (p = 0.63) on breast cancer risk.CONCLUSION: Family history appears to modify the effect of obesity in early adolescence on subsequent breast cancer risk, and may identify differing etiologic pathways.