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Brief Report
August 2017

Association Between Benign Breast Disease in African American and White American Women and Subsequent Triple-Negative Breast Cancer

Author Affiliations
  • 1Breast Oncology Program, Department of Surgery, International Center for the Study of Breast Cancer Subtypes, Henry Ford Health System, Detroit, Michigan
  • 2Breast Oncology Program, Department of Pathology, Henry Ford Health System, Detroit, Michigan
  • 3Department of Biostatistics and Biomathematics, Fred Hutchinson Comprehensive Cancer Center, Seattle, Washington
  • 4Breast Oncology Program, Department of Otolaryngology, Henry Ford Health System, Detroit, Michigan
  • 5Breast Oncology Program, Department of Radiology, Henry Ford Health System, Detroit, Michigan
  • 6Division of Cancer Prevention, National Cancer Institute, Rockville, Maryland
  • 7Fox Chase Cancer Center, Philadelphia, Pennsylvania
JAMA Oncol. 2017;3(8):1102-1106. doi:10.1001/jamaoncol.2016.5598
Key Points

Question  Does race/ethnicity affect breast cancer risk among women with benign breast disease?

Findings  A review of a cohort comprising 2588 African American (AA) women and 3566 white American (WA) women with biopsy-proven benign breast disease revealed subsequent ductal carcinoma in situ in 30 (1.18%) AA patients and 30 (0.85%) WA patients and subsequent invasive cancer in 73 (2.8%) AA patients and in 111 (3.1%) WA patients. Of the subsequent invasive cancers, triple-negative breast cancer was more common among AA members than among WA members of the cohort (16 [24.2%] vs 7 [7.4%], respectively).

Meaning  African American identity is a risk factor for triple-negative breast cancer among women with benign breast disease.


Importance  Compared with white American (WA) women, African American (AA) women have a 2-fold higher incidence of breast cancers that are negative for estrogen receptor, progesterone receptor, and ERBB2 (triple-negative breast cancer [TNBC]). Triple-negative breast cancer, compared with non-TNBC, likely arises from different pathogenetic pathways, and benign breast disease (BBD) predicts future non-TNBC.

Objective  To determine whether AA identity remains associated with TNBC for women with a prior diagnosis of BBD.

Design, Setting, and Participants  This study is a retrospective analysis of data of a cohort of 2588 AA and 3566 WA women aged between 40 and 70 years with a biopsy-proven BBD diagnosis. The data—obtained from the Pathology Information System of Henry Ford Health System (HFHS), an integrated multihospital and multispecialty health care system headquartered in Detroit, Michigan—include specimens of biopsies performed between January 1, 1994, and December 31, 2005. Data analysis was performed from November 1, 2015, to June 15, 2016.

Main Outcomes and Measures  Subsequent breast cancer was stratified on the basis of combinations of hormone receptor and ERBB2 expression.

Results  Case management, follow-up, and outcomes received or obtained by our cohort of 2588 AA and 3566 WA patients were similar, demonstrating that HFHS delivered care equitably. Subsequent breast cancers developed in 103 (4.1%) of AA patients (mean follow-up interval of 6.8 years) and 143 (4.0%) of WA patients (mean follow-up interval of 6.1 years). More than three-quarters of subsequent breast cancers in each subset were ductal carcinoma in situ or stage I. The 10-year probability estimate for developing TNBC was 0.56% (95% CI, 0.32%-1.0%) for AA patients and 0.25% (95% CI, 0.12%-0.53%) for WA patients. Among the 66 AA patients who developed subsequent invasive breast cancer, 16 (24.2%) developed TNBC compared with 7 (7.4%) of the 94 WA patients who developed subsequent invasive breast cancers and had complete biomarker data (P = .01).

Conclusions and Relevance  This study is the largest analysis to date of TNBC in the context of racial/ethnic identity and BBD as risk factors. The study found that AA identity persisted as a significant risk factor for TNBC. This finding suggests that AA identity is associated with inherent susceptibility for TNBC pathogenetic pathways.