Cancer Causes & Control

, Volume 23, Issue 5, pp 671–681

Estrogen-related genes and their contribution to racial differences in breast cancer risk

  • Kerryn W. Reding
  • Chu Chen
  • Kimberly Lowe
  • David R. Doody
  • Christopher S. Carlson
  • Christina T. Chen
  • John Houck
  • Linda K. Weiss
  • Polly A. Marchbanks
  • Leslie Bernstein
  • Robert Spirtas
  • Jill A. McDonald
  • Brian L. Strom
  • Ronald T. Burkman
  • Michael S. Simon
  • Jonathan M. Liff
  • Janet R. Daling
  • Kathleen E. Malone
Original paper

DOI: 10.1007/s10552-012-9925-x

Cite this article as:
Reding, K.W., Chen, C., Lowe, K. et al. Cancer Causes Control (2012) 23: 671. doi:10.1007/s10552-012-9925-x

Abstract

Racial differences in breast cancer risk, including the risks of hormone receptor subtypes of breast cancer, have been previously reported. We evaluated whether variation in genes related to estrogen metabolism (COMT, CYP1A1, CYP1B1, CYP17A1, CYP19A1, ESR1, GSTM1, GSTP1, GSTT1, HSD17B1, SULT1A1, and UGT1A1) contributes to breast cancer risk and/or racial differences in risk within the CARE study, a multi-centered, population-based case–control study of breast cancer. Genetic variation was assessed as single nucleotide polymorphisms (SNPs), haplotypes, and SNP–hormone therapy (HT) interactions within a subset of 1,644 cases and 1,451 controls, including 949 Black women (493 cases and 456 controls), sampled from the CARE study population. No appreciable associations with breast cancer risk were detected for single SNPs or haplotypes in women overall. We detected SNP–HT interactions in women overall within CYP1B1 (rs1800440; phet = 0.003) and within CYP17A1 (rs743572; phet = 0.009) in which never users of HT were at a decreased risk of breast cancer, while ever users were at a non-significant increased risk. When investigated among racial groups, we detected evidence of an SNP–HT interaction with CYP1B1 in White women (p value = 0.02) and with CYP17A1 in Black women (p value = 0.04). This analysis suggests that HT use may modify the effect of variation in estrogen-related genes on breast cancer risk, which may affect Black and White women to a different extent.

Keywords

Breast cancer Genetic variation Racial disparities Gene–environment interactions Hormone therapy 

Supplementary material

10552_2012_9925_MOESM1_ESM.pdf (66 kb)
Supplementary material 1 (PDF 67 kb)
10552_2012_9925_MOESM2_ESM.pdf (36 kb)
Supplementary material 2 (PDF 36 kb)
10552_2012_9925_MOESM3_ESM.pdf (40 kb)
Supplementary material 3 (PDF 41 kb)

Copyright information

© Springer Science+Business Media B.V. 2012

Authors and Affiliations

  • Kerryn W. Reding
    • 1
    • 2
  • Chu Chen
    • 1
    • 3
  • Kimberly Lowe
    • 4
  • David R. Doody
    • 1
  • Christopher S. Carlson
    • 1
    • 3
  • Christina T. Chen
    • 1
  • John Houck
    • 1
  • Linda K. Weiss
    • 5
  • Polly A. Marchbanks
    • 6
  • Leslie Bernstein
    • 7
  • Robert Spirtas
    • 8
  • Jill A. McDonald
    • 6
  • Brian L. Strom
    • 9
  • Ronald T. Burkman
    • 10
  • Michael S. Simon
    • 11
  • Jonathan M. Liff
    • 12
  • Janet R. Daling
    • 1
  • Kathleen E. Malone
    • 1
    • 3
  1. 1.Division of Public Health SciencesFred Hutchinson Cancer Research CenterSeattleUSA
  2. 2.Department of Biobehavioral Nursing and Health SystemsUniversity of WashingtonSeattleUSA
  3. 3.Department of EpidemiologyUniversity of WashingtonSeattleUSA
  4. 4.ExponentSeattleUSA
  5. 5.Cancer Centers ProgramNational Cancer InstituteRockvilleUSA
  6. 6.Division of Reproductive HealthCenters for Disease Control and PreventionAtlantaUSA
  7. 7.Beckman Research InstituteCity of HopeDuarteUSA
  8. 8.George Washington University School of Public Health and Health ServicesWashingtonUSA
  9. 9.Center for Clinical Epidemiology and Biostatistics and Department of Biostatistics and EpidemiologyUniversity of PennsylvaniaPhiladelphiaUSA
  10. 10.Department of Obstetrics and GynecologyBaystate HealthSpringfieldUSA
  11. 11.Department of Oncology, Karmanos Cancer InstituteWayne State UniversityDetroitUSA
  12. 12.Department of Epidemiology, Rollins School of Public HealthEmory UniversityAtlantaUSA