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Ir J Med Sci. 2011 Jun;180(2):497-503. doi: 10.1007/s11845-011-0692-6. Epub 2011 Mar 12.

Human papillomavirus 16 or 18 infection and prostate cancer risk: a meta-analysis.

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Department of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou 310003, Zhejiang Province, China.



Whether the oncogenic human papillomavirus (HPV) infection, especially infection with the most common subtypes 16 or 18, is related to prostate carcinogenesis remains conflicting. A meta-analysis with updated data was performed to obtain a more precise estimate of the association between them.


Eligible studies were retrieved via both computer searches and review of references. The relation of HPV-16 or HPV-18 infection to prostate cancer (PC) was quantified separately. Stratified analyses based on HPV detection methods and geographic regions were also performed. Estimates of OR with 95% CI were summarized using the fixed-effect or random-effect models as appropriate.


Twenty-five eligible studies were retrieved. All the 25 studies were assigned for exploring the relation of HPV-16 infection to PC, while 13 studies provided additional information on HPV-18 simultaneously. In the overall estimates, the pooled OR indicated no significant increase of PC risk related with either HPV-16 (OR 1.09; 95% CI 0.97-1.23; P(heterogeneity) = 0.135) or HPV-18 (OR 1.05; 95% CI 0.89-1.24; P(heterogeneity) = 0.314) infection. Further quantitative assay of stratified data could also not yield any significant result, except the stratified analysis on HPV-16 DNA detection, which revealed higher HPV-16 DNA prevalence in PC cases (OR 1.54; 95% CI 1.07-2.20; P(heterogeneity) = 0.130).


Even though the overall estimates did not provide a supportive evidence for the causal role of HPV in prostate carcinogenesis, higher HPV-16 DNA prevalence in PC cases from the stratified analysis still indicated a potential association between HPV infection and PC risk in our meta-analysis.

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