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The greater impact of menopause on ER– than ER+ breast cancer incidence: a possible explanation (United States)

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Abstract

Objective: Analysis of 3359 Danish breast cancer cases indicated that menopause exerted a greater protective effect on estrogen- receptor negative (ER–) breast cancer than on estrogen- receptor positive (ER+) breast cancer. We examined US age-specific breast cancer rates by hormone receptor status in white and black women and men to investigate this unexpected result. Methods: Age-specific breast cancer incidence rates from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute were analyzed by joint estrogen receptor and progesterone receptor (ER/PR) status of 101,140 white female and 8870 black female cases and by ER status in 706 white male and black male cases diagnosed from 1992 to 1998. Changes in the rate of increase in rates with age were identified using Poisson regression analyses. Results: For both white women and black women the age-specific rates of ER– breast cancer cease increasing after 50 years of age, but age-specific rates of ER+ breast cancer continue to increase after 50 years of age. For men the incidence of ER– cancers may increase at a slower rate than incidence of ER+ cancers in older ages. In women the black rates of ER+ cancers are greater than white rates only until age 35, but black rates of ER– cancers are greater than white rates for all ages. Conclusions: Differences in age-specific breast cancer incidence patterns by hormone receptor status are similar for black women and white women. The incidence pattern for ER– cancers is consistent with a paracrine model for hormone-stimulated growth in normal breast tissue. The continued increase in ER+ cancers after menopause may be explained by both the paracrine growth model and an increase in the proliferation rate of ER+ cells with age.

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Tarone, R.E., Chu, K.C. The greater impact of menopause on ER– than ER+ breast cancer incidence: a possible explanation (United States). Cancer Causes Control 13, 7–14 (2002). https://doi.org/10.1023/A:1013960609008

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