© 1997 by Oxford University Press
Journal Of The National Cancer Institute, Vol 89, 1293-1299, Copyright © 1997 by Oxford University Press
J Dillner, M Lehtinen, T Bjorge, T Luostarinen, L Youngman, E Jellum, P Koskela, RE Gislefoss, G Hallmans, J Paavonen, M Sapp, JT Schiller, T Hakulinen, S Thoresen and M Hakama
BACKGROUND: Major risk factors for invasive cervical cancer include
infection with human papillomavirus (HPV), infection with other sexually
transmitted pathogens (e.g., Chlamydia trachomatis), and smoking. Since
exposures to these risk factors can be related, the contribution of any
single factor to cervical carcinogenesis has been difficult to assess. We
conducted a prospective study to define the role of HPV infection in
cervical carcinogenesis, with invasive cancer as an end point. METHODS: A
nested case-control study within a joint cohort of 700,000 Nordic subjects
was performed. The 182 women who developed invasive cervical cancer during
a mean follow-up of 5 years were matched with 538 control women on the
basis of age and time of enrollment. Serum samples taken at enrollment were
analyzed for evidence of tobacco use (i.e., cotinine levels); for
antibodies against HPV types 16, 18, and 33; and for antibodies against C.
trachomatis. Relative risks (RRs) were estimated by use of conditional
logistic regression. RESULTS: Presence of antibodies against HPV in serum
(seropositivity) was associated with an increased risk of cervical cancer,
and adjustment for smoking and for C. trachomatis seropositivity did not
affect this finding (RR = 2.4; 95% confidence interval [CI] = 1.6-3.7).
HPV16 seropositivity was associated primarily with an increased risk of
squamous cell carcinoma (RR = 3.2; 95% CI = 1.7-6.2). In contrast, risk
associated with HPV18 seropositivity tended to be higher for cervical
adenocarcinoma (RR = 3.4; 95% CI = 0.8-14.9). In populations with a low
prevalence of antibodies against C. trachomatis, the HPV16-associated risk
of cervical cancer was very high (RR = 11.8; 95% CI = 3.7-37.0); in
contrast, in populations with a high prevalence of antibodies against C.
trachomatis, no excess risk was found. CONCLUSION: Past infection with
HPV16 increases the risk of invasive cervical squamous cell carcinoma, most
clearly seen in populations with a low prevalence of sexually transmitted
diseases.
ARTICLES
Prospective seroepidemiologic study of human papillomavirus infection as a risk factor for invasive cervical cancer
The Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden. joakim.dillner@mtc.ki.se
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