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polymorphisms modulate susceptibility to TGCT. The variants with higher activity of the FSHR are (TGCTs) and seminoma accounts for w50 % of them. idism, testi-cular atrophy, inguinal hernia and infertility (Horwich a genetic mutation. However, genetic polymorphisms Endocrine-Related Cancer (2008) 15 429–4371993, Swerdlow et al. 1998) but with striking geographicTGCTs represent the model of a curable malignancy (Horwich et al. 2006). However, successes in clinical aspects of TGCTs do not correspond to clear identifi-cation of molecular biology and carcinogenesis process of this tumour. Epidemiological hallmarks of TGCT include a peak incidence in a very young adult age, a markedly increasing incidence worldwide (Giwercman et al. might be responsible for ethnic differences in its prevalence as well as prevalence of other huma