Abstract

Abstract A106 Although the incidence of testicular germ cell tumors (TGCT) has been rising worldwide, little known about the etiology. There is evidence, however, that TGCT is related to other male reproductive disorders, specifically, hypospadias, cryptorchidism and infertility. Because testosterone is responsible for the development and proliferation of testicular cells and testicular descent, it is plausible that testosterone and its binding protein, sex hormone binding globulin (SHBG), may be associated with TGCT risk. Using 512 case and 789 control participants from the U.S. Servicemen’s Testicular Tumor Environmental and Endocrine Determinants (STEED) Study, we assessed associations of pre-diagnostic serum SHBG and testosterone (measured total and calculated free) concentrations and risk of TGCT. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using adjusted logistic regression models. Among the controls, SHBG concentrations increased with age (p<0.01), while free testosterone concentrations decreased with age (p=0.02). Total testosterone concentrations, however, were not associated with age (p=0.84). SHBG and total testosterone concentrations decreased with increasing body mass index (p<0.01), however free testosterone did not (p=0.67). Overall, there were no statistically significant associations between SHBG and total testosterone concentrations and TGCT risk. There were suggestions that men had an increased risk of TGCT if they were in the highest quintile of SHBG (OR=1.41, 95% CI, 0.98-2.02) and free testosterone (OR=1.31, 95% CI, 0.91-1.88), but there were no statistically significant trends. Serum total testosterone concentrations were not associated with TGCT risk. There did not appear to be differences in risk by tumor subtype, seminoma versus nonseminoma, nor effect modification by body mass index. These results suggest that serum testosterone is not associated with risk of TGCT; other endogenous hormones, however, such as gonadotropins and estrogens, may provide additional clues to the etiology of TGCT. Citation Information: Cancer Prev Res 2008;1(7 Suppl):A106.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call