Abstract

4590 Background: There is evidence that hereditary predisposition is important in the aetiology of testicular cancer but the mode of inheritance is unknown. Methods: To test the hypothesis that bilateral disease (5% of testis cancer) is a manifestation of hereditary predisposition, a family questionnaire was sent to patients with bilateral disease (cases) and responses compared with institutional controls with unilateral disease (two approached for every case), matched for year of first diagnosis. The primary outcome measure was the risk of testis cancer in the brothers of cases and controls, and a relative risk of between 4.1 and 5.0 was anticipated based on the model of Nicholson and Harland (BJC 1995 71:421–426). Results: Responses from 191 cases and 373 controls have been analysed. No evidence of reduced fertility was found in the parents or grandparents of cases compared to those of controls. Cases (48%) were less likely to have children than controls (64%). The mean (SD) age of onset of testicular cancer was lower in cases (31 (9)) than controls (35 (9)), p < 0.001. The incidence of testis cancer in the relatives of cases and controls are shown in the table . Conclusions: The 4.6-fold greater risk to brothers of cases confirms the role of a familial predisposition in bilateral testicular cancer. Given the incomplete ascertainment for brothers, there is likely to be a greater risk to brothers than fathers. No major effect of an X-linked gene is found. These findings are in keeping with previously described hereditary models for testicular cancer. [Table: see text] No significant financial relationships to disclose.

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