OBJECTIVES: Among women attending antenatal clinics during 1934-1944 a large intercristal diameter, the maximum distance between the pelvic iliac crests, was associated with a raised incidence of breast and ovarian cancer in the daughters in later life. At puberty, the intercristal diameter of girls enlarges rapidly under the influence of estrogen. We speculated that high maternal estrogen concentrations during pregnancy initiate hormonal cancers in their daughters. Here, we examine the association between the mothers' intercristal diameters and prostate cancer in their sons. METHODS: Using the national cancer registry we identified 221 cases of prostate cancer among 6,975 men born during 1934-1944 in Helsinki, Finland. Four thousand four hundred and one of these men had their mother's bony pelvic measurements recorded: there were 149 cases among them. RESULTS: Hazard ratios for prostate cancer rose as the mother's intercristal diameter increased; but this association was restricted to men who were born before 40 weeks of gestation. Among these men the hazard ratio was 1.27 (95% CI 1.09-1.48; P = 0.002). The hazard ratio was 2.2 (1.3-3.7; P < 0.001) in men whose mothers weighed more than 80 kg in late pregnancy compared with those whose mothers weighed 60 kg or less. CONCLUSIONS: These findings are consistent with a conceptual framework for the origins of hormonally dependent cancers that invokes exposure of embryonic tissue to maternal sex hormones followed by resetting of the fetal hypothalamic-gonadotropin axis in late gestation. We hypothesize that compensatory prepubertal growth among girls is associated with hormonal cancers in the next generation.
OBJECTIVES: Among women attending antenatal clinics during 1934-1944 a large intercristal diameter, the maximum distance between the pelvic iliac crests, was associated with a raised incidence of breast and ovarian cancer in the daughters in later life. At puberty, the intercristal diameter of girls enlarges rapidly under the influence of estrogen. We speculated that high maternal estrogen concentrations during pregnancy initiate hormonal cancers in their daughters. Here, we examine the association between the mothers' intercristal diameters and prostate cancer in their sons. METHODS: Using the national cancer registry we identified 221 cases of prostate cancer among 6,975 men born during 1934-1944 in Helsinki, Finland. Four thousand four hundred and one of these men had their mother's bony pelvic measurements recorded: there were 149 cases among them. RESULTS: Hazard ratios for prostate cancer rose as the mother's intercristal diameter increased; but this association was restricted to men who were born before 40 weeks of gestation. Among these men the hazard ratio was 1.27 (95% CI 1.09-1.48; P = 0.002). The hazard ratio was 2.2 (1.3-3.7; P < 0.001) in men whose mothers weighed more than 80 kg in late pregnancy compared with those whose mothers weighed 60 kg or less. CONCLUSIONS: These findings are consistent with a conceptual framework for the origins of hormonally dependent cancers that invokes exposure of embryonic tissue to maternal sex hormones followed by resetting of the fetal hypothalamic-gonadotropin axis in late gestation. We hypothesize that compensatory prepubertal growth among girls is associated with hormonal cancers in the next generation.
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