![]() ![]() These studies were combined in order to have a sufficient sample size to examine the rare outcome of EA/GCA. The current study leveraged the resources from three prospective parent cohort studies: Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial Alpha-Tocopherol, Beta-Carotene (ATBC) Cancer Prevention Study and Cancer Prevention Study II (CPS-II) Nutrition Cohort ( 30–32). Thus, we conducted a pooled, nested case–control study using prediagnostic serum samples from three large prospective cohort studies to evaluate associations between concentrations of circulating sex steroid hormones and future EA/GCA risks. To date, no study has been conducted of sex steroid hormones and EA/GCA risk with prediagnostically collected blood samples. One small prospective study reported lower concentrations of dehydroepiandrosterone (DHEA) and DHEA-sulfate among gastric cancer case participants (n = 13) than control participants (n = 52) ( 29), but the study did not report if any of the case participants were diagnosed with GCA. Additionally, a population-based case–control study found that androgen:estrogen balance was associated with increased odds of EA ( 44), and a small hospital-based study reported higher testosterone concentrations among EA case participants (n = 25) than control participants (n = 8) ( 28). This hypothesis is supported by sex steroid hormone involvement in the inflammatory process ( 11–14) expression of estrogen receptors (ERs) in esophageal and gastric cancer tissue ( 9, 15–20) lower rates of esophageal and gastric cancer among men with prostate cancer, who are likely to receive anti-androgen therapies ( 21–24) and in women, lower rates of esophageal and gastric cancer associated with reproductive factors and estrogen hormone replacement therapies ( 25–27). Sex hormones may potentially account for this sex disparity ( 9, 10). However, analyses of these factors have explained very little of the male predominance of these tumors ( 7, 8). ![]() These sex differences have been considered to be the result of established risk factors that differ in prevalence by sex, such as obesity, reflux, and smoking. EA and GCA are often considered a singular clinical entity since they both occur at or near the gastroesophageal junction and have similar overall and stage-specific five-year survival rates ( 4).Īge-adjusted incidence of EA/GCA is four to eight times higher in men than women ( 5, 6). The incidence of anatomically linked gastric cardia adenocarcinoma (GCA) has also increased but less rapidly than EA ( 3). Esophageal adenocarcinoma (EA) incidence has increased approximately 600% over the last 35 years in the United States, placing it among the most rapidly increasing cancer types ( 1, 2). ![]()
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