title: Impact of race and tumor subtype on second malignancy risk in women with breast cancer.
abstract: OBJECTIVE
  Women with breast cancer are at increased risk of second malignancy (SM). However, the impact of race and the hormone receptor (HR) status of the primary breast tumor on risk of SM are not known. The purpose of this study is to analyze the incidence of SM in women with a history of breast cancer according to race and HR status.
  
  
  METHODS
  In the surveillance, epidemiology, and end results database, multiple primary standardized incidence ratio sessions were used to compare the incidence of SM in women with a history breast cancer to the cancer incidence in the general population. Analyses of SM by age, race, and hormone-receptor status were performed using the absolute excess risk (AER) and observed/expected (O/E) ratio.
  
  
  RESULTS
  Younger black women (under the age of 50) were at greater risk of SM with an AER = 76.03 (O/E = 2.3, 95 % CI = 12.19-2.4) compared to younger white women who had an AER = 38.59 (O/E = 1.55, 95 % CI = 1.53-1.58). Older black women (50 years and older) had at an increased risk of SM with an AER = 42.26 (O/E = 1.3, 95 % CI = 1.26-1.34) compared to older white women who had an AER = 11.56 (O/E = 1.07, 95 % CI = 1.06-1.08). Second breast malignancy is the predominant SM in both black and white women. Women with hormone-receptor (HR)-negative breast cancer had higher risk of SMs with an AER = 43.53 (O/E = 1.41, 95 % CI = 1.38- 0.145-3.31) compared to women with HR-positive disease with an AER = 21.43 (O/E = 1.17, 95 % CI = 1.16-0.1.18). In HR-negative women, younger black women had an AER = 96.46 (O/E = 2.99, 95 % CI = 2.70-3.31), younger white women had an AER = 66 (O/E = 2.25, 95 % CI = 2.13-2.36), older black women had an AER = 58.58 (O/E = 1.45, 95 % CI = 1.34-1.57), and older white women had an AER = 20.88 (O/E = 1.14, 95 % CI = 1.11-1.18).
  
  
  CONCLUSIONS
  Black breast cancer survivors and women with HR-negative breast cancer are at increased risk of SM, which deserves further evaluation to understand the biological and clinical basis for this increased risk.
authors.affiliation: Vanderbilt University, Nashville, TN USA.
authors.forename: Nicholas
authors.initials: N
authors.lastname: Diab
authors.affiliation: Array BioPharma, Inc., Boulder, CO USA.
authors.forename: Gary
authors.initials: G
authors.lastname: Clark
authors.affiliation: Genetic Risk Evaluation and Testing Program, Compass Oncology, Portland, OR USA.
authors.forename: Lucy
authors.initials: L
authors.lastname: Langer
authors.affiliation: Texas Children Hospital, Houston, TX USA.
authors.forename: Yunfei
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Genetic Risk Evaluation and Testing Program, Rocky Mountain Cancer Centers, Denver, CO USA.
authors.forename: Barbara
authors.initials: B
authors.lastname: Hamlington
authors.affiliation: Genetic Risk Evaluation and Testing Program, Rocky Mountain Cancer Centers, Denver, CO USA.
authors.forename: Laura
authors.initials: L
authors.lastname: Brzeskiewicz
authors.affiliation: Baylor Charles A. Sammons Cancer Center, Texas Oncology, US Oncology, Dallas, TX USA.
authors.forename: Joyce
authors.initials: J
authors.lastname: O'Shaughnessy
authors.affiliation: Genetic Risk Evaluation and Testing Program, Rocky Mountain Cancer Centers, Denver, CO USA.
authors.forename: Sami
authors.initials: S
authors.lastname: Diab
authors.affiliation: Rutgers Cancer Institute of New Jersey Rutgers, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ USA.
authors.forename: Salma K
authors.initials: SK
authors.lastname: Jabbour