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By Martyn Plummer, O Herrero, Silvia Franceschi, Chris J. L. M. Meijer, Peter Snijders and F. Xavier Bosch


Background: Smoking has long been suspected to be a risk factor for cervical cancer. However, not all previous studies have properly controlled for the effect of human papillomavirus (HPV) infection, which has now been established as a virtually necessary cause of cervical cancer. To evaluate the role of smoking as a cofactor of progression from HPV infection to cancer, we performed a pooled analysis of 10 previously published case–control studies. This analysis is part of a series of analyses of cofactors of HPV in the aetiology of cervical cancer. Methods: Data were pooled from eight case–control studies of invasive cervical carcinoma (ICC) and two of carcinoma in situ (CIS) from four continents. All studies used a similar protocol and questionnaires and included a PCR-based evaluation of HPV DNA in cytological smears or biopsy specimens. Only subjects positive for HPV DNA were included in the analysis. A total of 1463 squamous cell ICC cases were analyzed, along with 211 CIS cases, 124 adeno- or adeno-squamous ICC cases and 254 control women. Pooled odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression models controlling for sexual and non-sexual confounding factors. Results: There was an excess risk for ever smoking among HPV positive women (OR 2.17 95%CI 1.46–3.22). When results were analyzed by histological type, an excess risk was observed among cases of squamous cell carcinoma fo

Year: 2003
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