Y Lin1, Q Mao, X Zheng, K Yang, H Chen, C Zhou, L Xie. 1. Department of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou 310003, Zhejiang Province, China. zjuckt@gmail.com
Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.
OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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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