Abstract
BackgroundSeroepidemiological studies have reported associations between exposure to sexually transmitted organisms and prostate cancer risk. This study sought DNA evidence of candidate organisms in archival prostate cancer tissues with the aim of assessing if a subset of these cancers show any association with common genital infections.Methods221 archival paraffin-embedded tissue blocks representing 128 histopathologically confirmed prostate cancers comprising 52 “aggressive” (Gleason score ≥ 7) and 76 “non-aggressive” (Gleason score ≤ 6) TURP or radical prostatectomy specimens were examined, as well as unaffected adjacent tissue when available. Representative tissue sections were subjected to DNA extraction, quality tested and screened by PCR for HSV-1, HSV-2, XMRV, BKV, HPV, Chlamydia trachomatis, Ureaplasma parvum, Ureaplasma urealyticum, Mycoplasma genitalium, and Trichomonas vaginalis.Results195 of 221 DNA samples representing 49 “aggressive” and 66 “non-aggressive” prostate cancer cases were suitable for analysis after DNA quality assessment. Overall, 12.2% (6/49) aggressive and 7.6% (5/66) non-aggressive cases were positive for any of the candidate organisms. Mycoplasma genitalium DNA was detected in 4/66 non-aggressive, 5/49 aggressive cancers and in one cancer-unaffected adjacent tissue block of an aggressive case. Ureaplasma urealyticum DNA was detected in 0/66 non-aggressive and 1/49 aggressive cancers and HSV DNA in 1/66 non-aggressive and 0/49 aggressive cancers. This study did not detect BKV, XMRV, T. vaginalis, U. parvum, C. trachomatis or HPV DNA.ConclusionsThe low prevalence of detectable microbial DNA makes it unlikely that persistent infection by the selected candidate microorganisms contribute to prostate cancer risk, regardless of tumour phenotype.
Highlights
Seroepidemiological studies have reported associations between exposure to sexually transmitted organisms and prostate cancer risk
Common genetic variants of genes functionally linked to inflammation and immunity such as COX-2 [5], RNASEL [6] and TLR4 [7] have been associated with prostate cancer risk suggesting that infection and host response to infection may be involved in its development
Cases were drawn from three existing prostate cancer research projects, (1) the Melbourne Collaborative Cohort Study (MCCS) [11], a population-based prospective cohort study, recruited over the period 1990–1994, (2) the Risk Factors for Prostate Cancer Study (RFPCS) [12], a population-based case control study and (3) the Early Onset Prostate Cancer Study (EOPCS) [13], a population based case series of males diagnosed with prostate cancer aged ≤56 years of age
Summary
Seroepidemiological studies have reported associations between exposure to sexually transmitted organisms and prostate cancer risk. Many studies have sought associations between sexually transmitted infections (STIs) and prostate cancer risk but no clear association with a pathogen has been established. A meta-analysis of 29 case–control studies (1966–2003) reported associations between prostate cancer risk and any STI (OR 1.48 95% CI 1.26-1.73), gonorrhoea There is growing evidence of associations between prostate cancer risk and variants in genes involved in the response to infection and inflammation. Common genetic variants of genes functionally linked to inflammation and immunity such as COX-2 [5], RNASEL [6] and TLR4 [7] have been associated with prostate cancer risk suggesting that infection and host response to infection may be involved in its development
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