Prospective Seroepidemiologic Study of Human Papillomavirus and Other Risk Factors in Cervical Cancer
(2011) In Cancer Epidemiology Biomarkers & Prevention 20(12). p.2541-2550- Abstract
- Background: Several sexually transmitted infections (STI) have been reported to interact with human papillomavirus (HPV) in the etiology of cervical cancer. A large cohort study is required to obtain a both unbiased and stable estimate of their effects. Methods: Four major biobanks in the Nordic Countries containing samples from about 1,000,000 subjects were linked with nation-wide cancer registries. Serum samples from 604 women with invasive cervical cancer (ICC) diagnosed on average 10 years after sampling and 2,980 matched control women were retrieved and analyzed with serology for key STI. Results: Exposure to HPV16 was the strongest risk factor for cervical cancer [ OR = 2.4; 95% confidence interval (CI), 2.0-3.0], particularly for... (More)
- Background: Several sexually transmitted infections (STI) have been reported to interact with human papillomavirus (HPV) in the etiology of cervical cancer. A large cohort study is required to obtain a both unbiased and stable estimate of their effects. Methods: Four major biobanks in the Nordic Countries containing samples from about 1,000,000 subjects were linked with nation-wide cancer registries. Serum samples from 604 women with invasive cervical cancer (ICC) diagnosed on average 10 years after sampling and 2,980 matched control women were retrieved and analyzed with serology for key STI. Results: Exposure to HPV16 was the strongest risk factor for cervical cancer [ OR = 2.4; 95% confidence interval (CI), 2.0-3.0], particularly for squamous cell carcinoma (OR = 2.9; 95% CI, 2.2-3.7). HPV18 was strongly associated with increased risk for adenocarcinoma (OR = 2.3; 95% CI, 1.3-4.1). Baseline seropositivity for HPV16 did not confer any increased risk for HPV18 DNA-positive cancer and conversely HPV18 seropositivity had no association with HPV16 DNA-positive cancers. HPV6 had no effect on its own (OR = 1.1; 95% CI, 0.9-1.3), but had an antagonistic effect on the risk conferred by HPV16 (P < 0.01). Herpes simplex virus 2 had little or no association (OR = 1.1; 95% CI, 0.8-1.4). Previous exposure to Chlamydia trachomatis, as indicated by serum antibodies, had a strongly increased risk for cervical cancer (OR = 1.9; 95% CI, 1.5-2.3). Conclusions: A large prospective study has assessed the role of different STIs in cervical cancer. Impact: Prospective evidence supports cofactor role of some STI in cervical cancer. Cancer Epidemiol Biomarkers Prev; 20(12); 2541-50. (C) 2011 AACR. (Less)
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https://lup.lub.lu.se/record/2333293
- author
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Cancer Epidemiology Biomarkers & Prevention
- volume
- 20
- issue
- 12
- pages
- 2541 - 2550
- publisher
- American Association for Cancer Research
- external identifiers
-
- wos:000298234900010
- scopus:83055173763
- ISSN
- 1538-7755
- DOI
- 10.1158/1055-9965.EPI-11-0761
- language
- English
- LU publication?
- yes
- id
- 2bf58fa0-a99c-472a-a957-5a35f6958e59 (old id 2333293)
- date added to LUP
- 2016-04-01 13:25:35
- date last changed
- 2022-05-15 05:12:51
@article{2bf58fa0-a99c-472a-a957-5a35f6958e59,
abstract = {{Background: Several sexually transmitted infections (STI) have been reported to interact with human papillomavirus (HPV) in the etiology of cervical cancer. A large cohort study is required to obtain a both unbiased and stable estimate of their effects. Methods: Four major biobanks in the Nordic Countries containing samples from about 1,000,000 subjects were linked with nation-wide cancer registries. Serum samples from 604 women with invasive cervical cancer (ICC) diagnosed on average 10 years after sampling and 2,980 matched control women were retrieved and analyzed with serology for key STI. Results: Exposure to HPV16 was the strongest risk factor for cervical cancer [ OR = 2.4; 95% confidence interval (CI), 2.0-3.0], particularly for squamous cell carcinoma (OR = 2.9; 95% CI, 2.2-3.7). HPV18 was strongly associated with increased risk for adenocarcinoma (OR = 2.3; 95% CI, 1.3-4.1). Baseline seropositivity for HPV16 did not confer any increased risk for HPV18 DNA-positive cancer and conversely HPV18 seropositivity had no association with HPV16 DNA-positive cancers. HPV6 had no effect on its own (OR = 1.1; 95% CI, 0.9-1.3), but had an antagonistic effect on the risk conferred by HPV16 (P < 0.01). Herpes simplex virus 2 had little or no association (OR = 1.1; 95% CI, 0.8-1.4). Previous exposure to Chlamydia trachomatis, as indicated by serum antibodies, had a strongly increased risk for cervical cancer (OR = 1.9; 95% CI, 1.5-2.3). Conclusions: A large prospective study has assessed the role of different STIs in cervical cancer. Impact: Prospective evidence supports cofactor role of some STI in cervical cancer. Cancer Epidemiol Biomarkers Prev; 20(12); 2541-50. (C) 2011 AACR.}},
author = {{Dahlstrom, Lisen Arnheim and Andersson, Kristin and Luostarinen, Tapio and Thoresen, Steinar and Ogmundsdottir, Helga and Tryggvadottir, Laufey and Wiklund, Fredrik and Skare, Gry B. and Eklund, Carina and Sjölin, Kia and Jellum, Egil and Koskela, Pentti and Wadell, Goran and Lehtinen, Matti and Dillner, Joakim}},
issn = {{1538-7755}},
language = {{eng}},
number = {{12}},
pages = {{2541--2550}},
publisher = {{American Association for Cancer Research}},
series = {{Cancer Epidemiology Biomarkers & Prevention}},
title = {{Prospective Seroepidemiologic Study of Human Papillomavirus and Other Risk Factors in Cervical Cancer}},
url = {{http://dx.doi.org/10.1158/1055-9965.EPI-11-0761}},
doi = {{10.1158/1055-9965.EPI-11-0761}},
volume = {{20}},
year = {{2011}},
}