Abstract

Abstract Purpose: To evaluate the extent to which the black-white disparity in mortality following breast cancer diagnosis is explained by the expression status of four biomarkers - estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and p53 protein. Methods: The four biomarkers were assessed in paraffin-embedded breast tumor tissue for 1204 (523 black, 681 white) women, ages 35-64 years at diagnosis, who participated in the Women's CARE Study, a population-based case-control study of newly incident breast cancer, and who accrued a median of 10 years follow-up. The impact of these biomarkers on black-white disparity in breast cancer-specific and all-cause mortality was determined by fitting multivariable Cox proportional hazards regression models. Results: The black-white disparity in breast cancer-specific mortality was 54% in an age- and study site-adjusted model (relative risk [RR], 1.54; 95% confidence interval [CI], 1.21 to 1.97); it declined to a 36% greater risk for black women than white women after additionally controlling the status of the four markers (RR, 1.36; 95% CI, 1.06 to 1.75). Similar results were observed for all cause-mortality. Separate analyses for triple negative (ER-/PR-/HER2-) and luminal A (ER+ and/or PR+ plus HER2-) tumors showed that the black-white differences in mortality were predominately observed for older (50-64 years) women with luminal A tumors (breast cancer-specific RR, 2.07; 95% CI, 1.16 to 3.70; all-cause RR, 2.21; 95% CI, 1.40 to 3.47). For luminal A tumors, the greater mortality risk for older black women was attenuated after adjustment for stage, comorbidities, and education, and was most evident for all-cause mortality. Conclusions: Black-white differences in mortality following breast cancer diagnosis vary by tumor biomarker subtypes. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3590. doi:1538-7445.AM2012-3590

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