Clues to the aetiological heterogeneity of testicular seminomas and non-seminomas: time trends and age-period-cohort effects

Citation
Sl. Liu et al., Clues to the aetiological heterogeneity of testicular seminomas and non-seminomas: time trends and age-period-cohort effects, INT J EPID, 29(5), 2000, pp. 826-831
Citations number
31
Categorie Soggetti
Envirnomentale Medicine & Public Health","Medical Research General Topics
Journal title
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
ISSN journal
03005771 → ACNP
Volume
29
Issue
5
Year of publication
2000
Pages
826 - 831
Database
ISI
SICI code
0300-5771(200010)29:5<826:CTTAHO>2.0.ZU;2-I
Abstract
Background Most previous epidemiological studies have treated testicular ca ncer as a single entity. However, some investigators suggest that testicula r seminomas and nonseminomas may have different risk profiles. We examine t he time trends in incidence of the two main histological types separately. Methods From 1970 through 1995, 7296 cases of testicular cancer were regist ered in the Canadian provinces of Ontario, Saskatchewan and British Columbi a. In addition to analyses of the secular trends by age group and birth coh ort, an age-period-cohort (APC) model with standard Poisson assumptions was fitted to the data to assess the time effects. Results The age-adjusted incidence rate for seminomas increased by 53%, fro m 1.5 per 100 000 males in 1970-1971 to 2.3 per 100 000 males in 1994-1995. Nonseminomas increased by 91%, from 1.1 to 2.1 per 100 000 males over the same period. Non-seminomas were more frequent at young ages whereas seminom as dominated in older ages. In contrast to seminomas, non-seminomas occurre d predominantly among adolescent men (15-19 years), with a fourfold increas e between 1970-1971 and 1994-1995. Age-period-cohort modelling showed that the increase in the risk of both seminomas and non-seminomas followed a bir th cohort pattern, but with differences in birth cohorts in addition to sig nificantly distinct age patterns. Conclusions Our findings support the hypothesis postulating aetiological he terogeneity in the development of seminomas and non-seminomas. We suggest t hat epidemiological studies of testicular cancer treat seminomas and non-se minomas separately.