Do testicular seminoma and nonseminoma share the same etiology? Evidence from an age-period-cohort analysis of incidence trends in eight European countries.
Bray, Freddie;
Richiardi, Lorenzo;
Ekbom, Anders;
Forman, David;
Pukkala, Eero;
Cuninkova, Martina;
Møller, Henrik;
(2006)
Do testicular seminoma and nonseminoma share the same etiology? Evidence from an age-period-cohort analysis of incidence trends in eight European countries.
Cancer epidemiology, biomarkers & prevention, 15 (4).
pp. 652-658.
ISSN 1055-9965
DOI: https://doi.org/10.1158/1055-9965.EPI-05-0565
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The incidence of the two main clinical subentities of testicular germ cell cancer (seminoma and nonseminoma) is increasing throughout Europe. Most studies have revealed little variation in risk factors between the two subtypes. This study compared generation-specific trends in eight European countries, hypothesizing that similar temporal pattern by birth cohort implied that seminoma and nonseminoma had a largely comparable etiology. The results are presented using the age-period-cohort model and the nonidentifiability problem highlighted by partitioning the age, period, and cohort effects in terms of their linear and curvature component parts, assuming a priori that cohort effects predominated. Despite uniform overall increases by calendar period, declining rates of nonseminoma but not pure seminoma were observed in the majority of countries during the 1990s. The subtype trends were, however, largely analogous on a birth cohort scale. Notable observations were a decline in rates of both subtypes among recent birth cohorts in Switzerland and a short-term wartime effect in several countries, involving an attenuation of increasing risk of both subtypes in men born in 1940 to 1945. Departures from the steady increases in testicular cancer over time were likely to occur for nonseminomas some years ahead of seminoma on a period scale. The importance of birth cohort coincided with the view that given a short time interval of susceptibility to exposures earlier in life and a biologically constant time to diagnosis, all temporal changes in rate-limiting exposures should appear as generational effects. Trends in seminoma and nonseminoma conform to largely the same temporal patterns on this scale, implying that they share important etiologic factors.