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Prenatal and Perinatal Risk Factors and Testicular Cancer: A Hospital-Based Case-Control Study

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Some evidence exists to support the hypothesis that elevated levels of circulating maternal estrogens during early pregnancy may increase risk of testicular germ cell cancer. However, the results from studies evaluating maternal factors have been mixed. We evaluated maternal factors, particularly those associated with excess estrogen levels, as risk factors for testicular cancer. We conducted a hospital-based case-control study at The University of Texas M. D. Anderson Cancer Center in Houston, Texas of 144 testicular cancer patients diagnosed between 1990 and 1996 and 86 friend controls matched to cases on age, race, and state of residence. Risk factor data about the mother, the son, and the pregnancy were obtained from the mothers by telephone interviews and from the sons by self-administered questionnaires. Extreme nausea during the first trimester of pregnancy was associated with an elevated risk of testicular cancer [odds ratio (OR) = 2.0; 95% confidence interval (CI) = 1.0–3.9]. Adjustment for potential confounders slightly lowered this risk (OR = 1.8; 95% CI = 0.9–3.8). Risks were modestly increased for other factors that are proxy measures for maternal estrogens, including preterm delivery (OR = 2.2; 95% CI = 0.4–12.9), birth weight <3000 g (OR = 2.4; 95% CI = 0.7–8.1), and birth weight >4000 g (OR = 1.7; 95% CI = 0.9–3.2), albeit nonsignificantly so. Our finding that severe nausea was associated with increased testicular cancer risk adds evidence to support the in utero estrogen exposure hypothesis because nausea early in pregnancy is related to rising levels of circulating estrogens. For other factors, which are less direct measures of maternal estrogens, the modest associations found indicate a suggestive pattern in support of the excess estrogen hypothesis.
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Keywords: Case-control studies; Estrogens; Maternal exposure; Risk factors; Testicular neoplasms

Document Type: Research Article

Affiliations: 1: Divisions of Cancer Epidemiology and Genetics and Cancer Prevention, National Cancer Institute, NIH, DHHS, Bethesda, MD, USA 2: Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA 3: ‡Department of Epidemiology, The University of Texas School of Public Health, Houston, TX, USA

Publication date: 2006-08-01

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