caa a22 4500 397566042 CHVBK 20180308164828.0 cr unu---uuuuu 161202e19960821xx s 000 0 eng 10.1093/jnci/88.16.1127 doi (NATIONALLICENCE)oxford-10.1093/jnci/88.16.1127 Case—Control Study of Endogenous Steroid Hormones and Endometrial Cancer [Elektronische Daten] [Nancy Potischman, Robert N. Hoover, Louise A. Brinton, Pentti Siiteri, Joanne F. Dorgan, Christine A. Swanson, Michael L. Berman, Rodrigue Mortel, Leo B. Twiggs, Rolland J. Barrett, George D. Wilbanks, Victoria Persky, John R. Lurain] Background: It has been suggested that identified risk factors for endometrial cancer operate through a single etiologic pathway, i.e., exposure to relatively high levels of unopposed estrogen (estrogen in the absence of progestins). Only a few studies, however, have addressed this issue directly. Purpose: We assessed the risk of developing endometrial cancer among both premenopausal and postmenopausal women in relation to the circulating levels of steroid hormones and sex hormone-binding globulin (SHBG). The independent effect of hormones was assessed after adjustment for other known risk factors. Methods: The data used in the analysis are from a case—control study conducted in five geographic regions in the United States. Incident cases were newly diagnosed during the period from June 1, 1987, through May 15, 1990. The case patients, aged 20-74 years, were matched to control subjects by age, race, and geographic region. The community control subjects were obtained by random-digit-dialing procedures (for subjects 20-64 years old) and from files of the Health Care Financing Administration (for subjects ≥65 years old). Additional control subjects who were having a hysterectomy performed for benign conditions were obtained from the participating centers. Women reporting use of exogenous estrogens or oral contraceptives within 6 months of interview were excluded, resulting in 68 case patients and 107 control subjects among premenopausal women and 208 case patients and 209 control subjects among postmenopausal women. The hormone analyses were performed on blood samples obtained from case patients or from hysterectomy control subjects before surgery. The odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by use of an unconditional logistic regression analysis after we controlled for matching variables and potential confounders. All P values were two-sided. Results: High circulating levels of androstenedione were associated with 3.6-fold and 2.8-fold increased risks among premenopausal and postmenopausal women, respectively, after adjustment for other factors (P for trend =.01 and <.001, respectively). Risks related to other hormone fractions varied by menopausal status. Among postmenopausal women, a reduced risk was associated with high SHBG levels and persisted after adjustment was made for obesity and other factors (OR = 0.51; 95% CI = 0.27-0.95). High estrone levels were associated with increased risk (OR = 3.8; 95% CI = 2.2-6.6), although adjustment for other risk factors (particularly body mass index) diminished the effect (OR = 2.2; 95% CI = 1.2-4.4). Albumin-bound estradiol (E2), a marker of the bioavailable fraction, also remained an important risk factor after adjustment was made for other factors (OR = 2.0; 95% CI = 1.0-3.9). In contrast, high concentrations of total, free, and albumin-bound E2 were unrelated to increased risk in premenopausal women. In both premenopausal and postmenopausal groups, risks associated with obesity and fat distribution were not affected by adjustment for hormones. Conclusion: High endogenous levels of unopposed estrogen are related to increased risk of endometrial cancer, but their independence from other risk factors is inconsistent with being a common underlying biologic pathway through which all risk factors for endometrial cancer operate. Implications: Further research should focus on alternative endocrinologic mechanisms for risk associated with obesity and body fat distribution and for the biologic relevance of the increased risk associated with androstenedione in both premenopausal and postmenopausal disease. © Oxford University Press ARTICLES nationallicence Potischman Nancy Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut Hoover Robert N. Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut Brinton Louise A. Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut Siiteri Pentti Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut Dorgan Joanne F. Cancer Prevention Studies Branch, Division of Cancer Prevention and Control, National Cancer Institute Bethesda, MD aut Swanson Christine A. Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut Berman Michael L. Department of Obstetrics and Gynecology, University of California at Irvine Medical Center aut Mortel Rodrigue Department of Obstetrics and Gynecology, Milton S. Hershey Medical Center Hershey, PA aut Twiggs Leo B. Department of Obstetrics and Gynecology, University of Minnesota Medical School Minneapolis aut Barrett Rolland J. Department of Obstetrics and Gynecology, The Bowman Gray School of Medicine Winston-Salem, NC aut Wilbanks George D. Department of Obstetrics and Gynecology, Rush Medical College Chicago, IL aut Persky Victoria Division of Epidemiology-Biostatistics, School of Public Health, The University of Illinois Chicago aut Lurain John R. Department of Obstetrics and Gynecology, Northwestern University Medical School Chicago aut JNCI: Journal of the National Cancer Institute Oxford University Press 88/16(1996-08-21), 1127-1135 0027-8874 88:16<1127 1996 88 jnci https://doi.org/10.1093/jnci/88.16.1127 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1093/jnci/88.16.1127 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Potischman Nancy Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut NATIONALLICENCE 700 1- Hoover Robert N. Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut NATIONALLICENCE 700 1- Brinton Louise A. Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut NATIONALLICENCE 700 1- Siiteri Pentti Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut NATIONALLICENCE 700 1- Dorgan Joanne F. Cancer Prevention Studies Branch, Division of Cancer Prevention and Control, National Cancer Institute Bethesda, MD aut NATIONALLICENCE 700 1- Swanson Christine A. Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics Bethesda, MD aut NATIONALLICENCE 700 1- Berman Michael L. Department of Obstetrics and Gynecology, University of California at Irvine Medical Center aut NATIONALLICENCE 700 1- Mortel Rodrigue Department of Obstetrics and Gynecology, Milton S. Hershey Medical Center Hershey, PA aut NATIONALLICENCE 700 1- Twiggs Leo B. Department of Obstetrics and Gynecology, University of Minnesota Medical School Minneapolis aut NATIONALLICENCE 700 1- Barrett Rolland J. Department of Obstetrics and Gynecology, The Bowman Gray School of Medicine Winston-Salem, NC aut NATIONALLICENCE 700 1- Wilbanks George D. Department of Obstetrics and Gynecology, Rush Medical College Chicago, IL aut NATIONALLICENCE 700 1- Persky Victoria Division of Epidemiology-Biostatistics, School of Public Health, The University of Illinois Chicago aut NATIONALLICENCE 700 1- Lurain John R. Department of Obstetrics and Gynecology, Northwestern University Medical School Chicago aut NATIONALLICENCE 773 0- JNCI: Journal of the National Cancer Institute Oxford University Press 88/16(1996-08-21), 1127-1135 0027-8874 88:16<1127 1996 88 jnci Metadata rights reserved CC BY-NC-4.0 http://creativecommons.org/licenses/by-nc/4.0 nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-oxford