title: Mammographic density, response to hormones, and breast cancer risk.
abstract: BACKGROUND
  Percent mammographic density (PMD) is a strong risk factor for breast cancer that changes in response to changes in hormone exposure. We have examined the magnitude of the association of hormone exposure with PMD according to subsequent breast cancer risk.
  
  
  METHODS
  In three case-control studies, with 1,164 patient cases and 1,155 controls nested in cohorts of women screened with mammography, we examined the association of PMD measured in the baseline mammogram with risk of breast cancer in the following 1 to 8 years (mean, 3 years), according to use of oral contraceptives (OCs) in premenopausal women, menopause, and hormone therapy (HT) in postmenopausal women. All statistical comparisons are adjusted for age and other risk factors.
  
  
  RESULTS
  In premenopausal women who later developed breast cancer (patient cases), PMD was 5.3% greater in past users of OCs than in nonusers (P = .06). In controls, OC users had 2% less density than nonusers (P = .44; test for interaction P = .06). The difference in PMD between premenopausal and postmenopausal women for patient cases was 8.5% (P < .001) and for controls, 3.9% (P = .01; test for interaction P = .03). In postmenopausal women, PMD was 6% greater in patients who used HT than in never users (P < .001). Controls who used HT had 1.6% greater PMD (P = .26) than never users (test for interaction P = .001). Differences in PMD resulted mainly from differences in the dense area of the mammogram.
  
  
  CONCLUSIONS
  Differences in PMD associated with differences in hormone exposure were greater in women who later developed breast cancer than in controls in each of the hormone exposures examined.
authors.affiliation: DSc, Ontario Cancer Institute, 610 University Ave, Room 10-415, Toronto, Ontario, Canada. boyd@uhnres.utoronto.ca
authors.forename: Norman F
authors.initials: NF
authors.lastname: Boyd
authors.forename: Olga
authors.initials: O
authors.lastname: Melnichouk
authors.forename: Lisa J
authors.initials: LJ
authors.lastname: Martin
authors.forename: Greg
authors.initials: G
authors.lastname: Hislop
authors.forename: Anna M
authors.initials: AM
authors.lastname: Chiarelli
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Yaffe
authors.forename: Salomon
authors.initials: S
authors.lastname: Minkin
mesh_terms: D000328:Adult; D000368:Aged; D001940:Breast / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D001943:Breast Neoplasms / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000378:metabolism / Q000473:pathology*; D001955:British Columbia / Q000453:epidemiology; D018270:Carcinoma, Ductal, Breast / Q000378:metabolism / Q000473:pathology*; D016022:Case-Control Studies; D003278:Contraceptives, Oral, Hormonal / Q000008:administration & dosage; D015914:Estrogen Replacement Therapy; D005260:Female; D006801:Humans; D016014:Linear Models; D008327:Mammography; D008403:Mass Screening / Q000379:methods*; D008875:Middle Aged; D015999:Multivariate Analysis; D009376:Neoplasms, Hormone-Dependent / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000378:metabolism / Q000473:pathology*; D009864:Ontario / Q000453:epidemiology; D018579:Patient Selection; D017698:Postmenopause; D011237:Predictive Value of Tests; D017697:Premenopause; D011960:Receptors, Estrogen / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism*; D017584:Reproductive History; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors
chemical_list: D003278:Contraceptives, Oral, Hormonal; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone