skip to content
National Cancer Institute U.S. National Institutes of Health www.cancer.gov
Pubications

Publications Search

Abstract

Title: Population-based analysis of pathologic data: A new approach to the investigation of uterine endometrial and ovarian endometrioid carcinomas.
Author: Henson DE, Schwartz AM, Tilara A, Grimley PM, Anderson WF
Journal: Arch Pathol Lab Med 131(9):1337-1342
Year: 2007
Month: September

Abstract: CONTEXT: Population-based analysis of the histopathology of endometrioid adenocarcinoma of the endometrium and ovary combined with epidemiologic techniques offer a new approach to exploring the relationship of tumors that share a similar range of morphologic phenotypes. OBJECTIVE: To evaluate the contribution of the Surveillance, Epidemiology, and End Results database to our understanding of gynecologic pathology. Specifically, to test and compare whether the etiology/pathogenesis of ovarian endometrioid cancer is as dependent upon the reproductive environment as uterine endometrial carcinoma. DESIGN: Graphic plots of the epidemiologic patterns were analyzed relating to incidence and age-specific rates of ovarian and uterine endometrioid carcinomas. The graphic analysis included evaluation of age frequency density plots and logarithmic plots (log-log) of age-specific incidence rates. RESULTS: At all ages, uterine endometrioid carcinomas have higher incidence rates than their ovarian homologues. Up to the age of 50 years, the log-log plots of age-specific incidence rates for each of these tumors remain essentially parallel. In contrast, after age 50 (menopause), the incidence rates begin to diverge: the rates for uterine endometrial carcinomas continue to rise, whereas the rates for ovarian endometrioid carcinomas plateau. This divergence persists even when the age-specific incidence is stratified according to histologic grade. Interestingly, endometrial stromal sarcomas follow an incidence rate pattern nearly identical to that of ovarian endometrioid carcinomas. CONCLUSIONS: The continuum of cellular and molecular events predisposing to gynecologic cancers of endometrioid phenotype apparently cease to operate in the ovary after menopause, but additional cellular and molecular events appear to occur in the ageing uterine endometrium.