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Human papillomavirus 16 infection as a potential risk factor for prostate cancer: an adaptive meta-analysis.

ABSTRACT: OBJECTIVES:Although an expert review published in 2013 concluded that an association between human papillomavirus (HPV) infection and prostate cancer (PCa) risk had not yet been firmly established, a 2011 systematic review of 14 articles revealed an increased prevalence of HPV-16 DNA in PCa tissues. Another meta-analysis of the related articles is needed to evaluate the potential link between HPV infection and PCa risk. METHODS:A snowballing search strategy was applied to the previously cited articles in the above-mentioned expert review and systematic review. Additional articles selected for this meta-analysis should fulfill all following inclusion criteria: (a) evaluation of detected HPV-16 DNA in tissue samples and the PCa risk and (b) report of the HPV-16 prevalence in both cancer and control tissues. Estimated summary odds ratios (sOR) with 95% confidence intervals (CI) were calculated using fixed effect or random-effect models. RESULTS:Hand searching identified 16 new articles. The sOR of the total 30 articles indicated a significant HPV-16 infection-related increase in the PCa risk (sOR, 1.851; 95% CI, 1.353 to 2.532, I(2)=37.82%). CONCLUSIONS:These facts provide additional supportive evidence for a causal role of HPV-16 infection in prostate carcinogenesis. As the PCa incidence rates have increased rapidly in Asian countries, including Korea, during the last several decades, further studies of HPV-related PCa carcinogenesis may be necessary.

SUBMITTER: Bae JM

PROVIDER: S-EPMC4371392 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Human papillomavirus 16 infection as a potential risk factor for prostate cancer: an adaptive meta-analysis.

Bae Jong-Myon JM

Epidemiology and health 20150211

<h4>Objectives</h4>Although an expert review published in 2013 concluded that an association between human papillomavirus (HPV) infection and prostate cancer (PCa) risk had not yet been firmly established, a 2011 systematic review of 14 articles revealed an increased prevalence of HPV-16 DNA in PCa tissues. Another meta-analysis of the related articles is needed to evaluate the potential link between HPV infection and PCa risk.<h4>Methods</h4>A snowballing search strategy was applied to the prev ...[more]

PMID: 25687950

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Project description:Persistent high-risk human papillomavirus (HPV) infection is the major causal factor in cervical and other anogenital cancers. Because there are currently no therapeutics capable of preventing neoplastic progression of HPV infections, understanding the mechanisms of HPV-mediated persistence, including immune evasion, is a major research priority. The multifunctional growth factor transforming growth factor beta (TGF?) has been shown to inhibit expression of early viral transcripts from cells harboring integrated HPV genomes or cells infected with retroviruses expressing HPV oncoproteins. However, the mechanism of TGF?-induced inhibition has not been fully defined. In this study, we have observed a previously uncharacterized ability of TGF? to repress the differentiation-induced upregulation of late HPV16 gene expression. In addition, interferon kappa (IFN-?), a keratinocyte-specific, constitutively expressed cytokine suppressed by differentiation, can be transcriptionally induced by TGF?1. TGF?-mediated IFN-? transcription only occurs in cells containing HPV16, and this is due to TGF?1-mediated reversal of HPV-induced methylation of the IFN-? promoter through active DNA demethylation mediated by thymine DNA glycosylase (TDG). This novel interaction between growth factor and innate immune signaling may shed light on the mechanisms of HPV persistence and how the virus manipulates both immune and growth factor signaling to promote its life cycle.IMPORTANCE Persistent infection by high-risk HPVs is the primary risk factor for development of HPV-induced cancers. Persistence involves viral evasion of the immune response, including the IFN response. HPV is also known to suppress TGF? signaling, which inhibits viral gene expression. Here, we show that the TGF? and IFN pathways are interrelated in the context of HPV16 infection through the upregulation of IFN-? by TGF?. The ability of TGF? to induce IFN-? promoter demethylation and transcriptional activation provides a new explanation for why HPV has evolved mechanisms to inhibit TGF? in infected cells.

Dataset Information

Human papillomavirus 16 infection as a potential risk factor for prostate cancer: an adaptive meta-analysis.

Publications

Human papillomavirus 16 infection as a potential risk factor for prostate cancer: an adaptive meta-analysis.

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