• Breast Cancer Res. Treat. · Oct 2010

    Review Meta Analysis

    Adult weight gain in relation to breast cancer risk by estrogen and progesterone receptor status: a meta-analysis.

    • Alina Vrieling, Katharina Buck, Rudolf Kaaks, and Jenny Chang-Claude.
    • Division of Cancer Epidemiology, German Cancer Research Center DKFZ, Im Neuenheimer Feld 280, 69120, Heidelberg, Germany. a.vrieling@dkfz-heidelberg.de
    • Breast Cancer Res. Treat. 2010 Oct 1; 123 (3): 641-9.

    AbstractAdult weight gain is positively associated with postmenopausal breast cancer and inversely associated with premenopausal breast cancer risk. To date, no meta-analysis has been conducted to assess this association by estrogen receptor (ER) and progesterone receptor (PR) status. We searched PubMed for relevant studies published through March 2010. Summarized risk estimates (REs) with 95% confidence intervals (CIs) were calculated using random effects or fixed effects models. We retrieved nine articles on weight gain from adulthood to reference age and ER- and/or PR-defined breast cancer risk, reporting on three prospective cohort studies and eight case-control studies. Comparing the highest versus the lowest categories of adult weight gain, risk was increased for ER(+)PR(+) and ER(+) tumors combined (11 studies; RE = 2.03; 95% CI 1.62, 2.45). Statistically significant heterogeneity (p (heterogeneity) = 0.002) was shown between REs for a mixed population of pre- and postmenopausal women combined (4 studies; RE = 1.54; 95% CI 0.86, 2.22) and for postmenopausal women only (7 studies; RE = 2.33; 95% CI 2.05, 2.60). Risk for ER(-)PR(-) tumors among postmenopausal women was also slightly increased (7 studies; RE = 1.34; 95% CI 1.06, 1.63), but statistically significantly different from risk for ER(+)PR(+) tumors (p (heterogeneity) < 0.0001). No associations were observed for ER(+)PR(-) tumors whereas risk for ER(-)PR(+) tumors could not be assessed. In conclusion, the association between adult weight gain and postmenopausal breast cancer risk is heterogeneous according to ER/PR status and stronger for ER(+)PR(+) than for ER(-)PR(-) tumors.

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