A prospective study of estradiol and breast cancer in Japanese women

Citation
M. Kabuto et al., A prospective study of estradiol and breast cancer in Japanese women, CANC EPID B, 9(6), 2000, pp. 575-579
Citations number
22
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
ISSN journal
10559965 → ACNP
Volume
9
Issue
6
Year of publication
2000
Pages
575 - 579
Database
ISI
SICI code
1055-9965(200006)9:6<575:APSOEA>2.0.ZU;2-X
Abstract
Few studies have prospectively examined endogenous hormone levels as risk f actors for breast cancer, The present study compares prediagnostic hormone levels using stored serum from breast cancer cases and controls selected fr om the Life Span Study population of the Radiation Effects Research Foundat ion in Hiroshima and Nagasaki, Japan. Stored serum samples collected in 196 8-1970 were assayed for 72 women subsequently diagnosed with breast cancer and 150 control subjects in 72 case-control sets matched on age, date of bl ood collection, exposure, radiation dose, and city, Serum levels were deter mined for sex hormone binding globulin, total estradiol (E-2), bioavailable E-2, dehydroepiandrosterone sulfate, and prolactin, Matched case-control c omparisons of hormone levels were carried out by conditional logistic regre ssion and were adjusted for menopausal status at the time of blood drawing. The odds ratio per unit log change in bioavailable E-2 was 2.2 [95% confid ence interval (CI), 1.02-5.3] for all subjects, and 2.3 (95% CI, 0.55-6.8) and 2.1 (95% CI, 0.55-9.7), respectively, based only on premenopausal or po stmenopausal serum. The estimated odds ratios in each quintile of bioavaila ble E2 level, using the lowest quintile as referent, were 1.00, 1.89, 1.43, 3.45, and 3.37 (P for trend = 0.035), For sex hormone binding globulin, th e overall odds ratio was 0.58 (95% CI, 0.14-2.26), and 1.00 (95% CI, 0.19-5 .45) and 0.21 (95% CI, 0.02-1.88) based on premenopausal and postmenopausal serum, respectively, This study offers further prospective support for the hypothesis that a high level of biologically available E-2 is a risk facto r for the subsequent development of breast cancer.