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Principal Investigator
Amanda Black
Position Title
About this CDAS Project
PLCO (Learn more about this study)
Project ID
Obesity and Endometrial Cancer in Postmenopausal Women: Examining the Roles of Adiponectin, Leptin, and Estrone
Obesity is an increasing problem in the United States and an established risk factor for endometrial cancer (1), with greater than 50% of cases in the U.S. attributed to this factor (2). Obesity is thought to influence risk of disease via increased production of endogenous estrogens in adipose tissue of postmenopausal women, with risk mediated through estrogen-induced cellular proliferation and tumor growth (3, 4). Although obesity-related estrogens are clearly important, adipose tissue also produces bioactive adipocytokines, principally adiponectin and leptin, which act both locally and systemically and may also be involved in tumor growth (5, 6). To assess whether obesity increases endometrial cancer risk solely through estrogenic mechanisms or jointly through hormonal and non-hormonal influences, we propose the first prospective evaluation of obesity-related biomarkers and the estrogenic pathway in relation to risk for endometrial cancer. The study will be conducted in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial, evaluating prospectively collected serum samples from 200 endometrial cancer cases and 400 controls, for adiponectin and leptin (adipocytokines) and estrone (the major post-menopausal estrogen).

Our primary aim is: 1) To evaluate associations of adiponectin, leptin and estrone with risk of endometrial cancer. We hypothesize that decreased levels of adiponectin and increased levels of leptin are associated with an increased risk of endometrial cancer, independent of that imparted by increased estrone levels. Our secondary aims are: 2) To explore whether these associations are modified by other population characteristics and exposures (e.g. age, reproductive factors, postmenopausal hormone use, cigarette smoking). We hypothesize that the associations between adiponectin, leptin, estrone and endometrial cancer are modified by other factors shown to influence risk. 3) To explore predictors of serum levels of adiponectin, leptin, and estrone. We hypothesize that serum levels of adiponectin, leptin, and estrone are influenced by other population characteristics. In carrying out these studies we will first determine in pilot studies the assay variability for each of the examined biomarkers and whether a single measurement adequately captures a woman's postmenopausal exposure level (i.e. whether serum levels vary over time).


James Lacey (NCI, DCEG)
Chatterjee Nilanjan (NCI, DCEG)
Richard Hayes (NCI, DCEG)
Jocelyn Weiss (NCI, DCEG)

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