Volume 65, Issue 6 pp. 723-729
Human Cancer

Continuing increase in incidence of germ-cell testis cancer in young adults: Experience from Connecticut, USA, 1935–1992

Tongzhang Zheng

Corresponding Author

Tongzhang Zheng

Departments of Epidemiology and Public Health and Surgery, Yale University School of Medicine, New Haven, CT, USA

Yale University School of Medicine, 200 College Street, Room C203, New Haven, CT 06510, USA. Fax: 203-764-9072Search for more papers by this author
Theodore R. Holford

Theodore R. Holford

Departments of Epidemiology and Public Health and Surgery, Yale University School of Medicine, New Haven, CT, USA

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Zheng Ma

Zheng Ma

Departments of Epidemiology and Public Health and Surgery, Yale University School of Medicine, New Haven, CT, USA

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Barbara A. Ward

Barbara A. Ward

Departments of Epidemiology and Public Health and Surgery, Yale University School of Medicine, New Haven, CT, USA

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John Flannery

John Flannery

Connecticut Tumor Registry, Hartford, CT, USA

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Peter Boyle

Peter Boyle

European Institute of Oncology, Milan, Italy

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Abstract

The current study is designed to examine long-term trends by histologic types of testis cancer in Connecticut. A regression model was used to identify age, period, or cohort as determinants of the time-trend on histologic types of testis cancer. The results from this descriptive epidemiologic study show that the overall age-adjusted incidence rate of testis cancer has increased 3.5-fold in Connecticut during the past nearly 60 years of cancer registration. The rates for seminoma and nonseminoma have been increasing since the mid-1950s and increase in a similar manner for those aged 15 to 49. The largest increase was observed in the age groups 20 to 44 for seminoma and 15 to 34 for non-seminoma. The observed increase was limited to whites. The results from age-period-cohort modeling suggest that the observed increase in seminoma before 1950s could be largely attributable to a period effect, while the increase for cohorts born after about 1910 both for seminoma and for non-seminoma are mainly explained by a strong birth-cohort effect. Therefore, the observed increase in germ-cell testis cancer in this population is likely to continue in the coming years. Thus far, the proposed hypotheses, such as exposure to DES in utero, earlier lifetime exposures to viruses, trauma or unusual amounts of heat to the testis, cannot adequately explain the observed incidence patterns of testis cancer. Analytical epidemiologic studies with large sample size are urgently needed to examine the risk factors responsible for the increase. © 1996 Wiley-Liss, Inc.

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