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Epstein‐barr virus and cytomegalovirus in relation to testicular‐cancer risk: a nested case‐control study
Author(s) -
Akre Olof,
Lipworth Loren,
Tretli Steinar,
Linde Annika,
Engstrand Lars,
Adami HansOlov,
Melbye Mads,
Andersen Aage,
Ekbom Anders
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990702)82:1<1::aid-ijc1>3.0.co;2-l
Subject(s) - testicular cancer , cytomegalovirus , seminoma , odds ratio , medicine , immunology , cancer , case control study , nested case control study , etiology , serology , antibody , virus , herpesviridae , viral disease , chemotherapy
An infectious etiology of testicular cancer has been suggested. We have evaluated seroreactivity against cytomegalovirus (CMV) and Epstein‐Barr virus (EBV) in relation to testicular‐cancer risk in a case‐control study, nested within a cohort of prospectively collected serum specimens from 293,692 individuals. For each of 81 cases of testicular cancer identified, 3 controls were randomly selected from the cohort. Serum IgG antibody titers against CMV and EBV were determined using enzyme‐linked immunosorbent assays (ELISAs) and immunofluorescence methods. Odds ratios (OR) were obtained from conditional logistic‐regression models. No association was found between CMV positivity and testicular cancer overall (OR = 1.08; 95% confidence interval 0.60–1.94); risk for testicular seminoma was increased among CMV seropositive [OR = 1.70 (0.80–3.59)], whereas seropositivity was associated with decreased risk for testicular non‐seminoma [OR = 0.54 (0.19–1.56)] ( p for heterogeneity, 0.09). For EBV, the risk for testicular cancer was increased among individuals seropositive for viral capsid antigen (VCA) [OR = 2.74 (0.62–12.12)]. The results lend some support to the hypothesis of an infectious etiology, and we propose that future studies should take into account age at infection. Int. J. Cancer 82:1–5, 1999. © 1999 Wiley‐Liss, Inc.