Background:  Like Breast and Cervix Cancer(CC), evidence linking Prostate cancer(PC) with early puberty is well established.  The importance of mutational events during the growth spurt in puberty is well established with respect of the link between smoking and lung cancer.  Since 1994, I have contributed literature on link between infection and PC. 
Objectives: This abstract review’s two aspects of PC epidemiology, roles of HPV and impact of microbial dysbiosis and compares the effect of the same agents in Breast and Cervical Cancer.
Methods: This abstract contains extract from previous publications and product of idea led literature searches
Results:  The role of HPV:  The most in-depth systematic review in PC was published in 2020. 12 of 26 reports had <50 subjects in each arm.  Of those with >= 50 subjects 8/11 had >% PC with positive HPV than controls.  There were 3 series with => 100 in each arm.  In these publications PC + HPV+ was 63/384 vs PC – HPV + 23/371 (X2 19.48  p=0.00001).  Possibly more significant is 3 studies where HPV positivity was higher in inflammatory BPH and in pre-cancer than with cancer, raising the concept of HPV acting as an initiator of malignant change and then being lost after more effective genetic events occur. The same observation has been reported in one breast cancer HPV study.  Microbial dysbiosis: Three cohort studies involving 289,089 healthy pubertal individuals have shown that puberty problems with Cutibacter acnes links to significant increased risk of PC after 30 years follow up [HR 1.67(0.79-3.55), RR 1.7(1.03-2.70), HR 1.45(1.06-1.92) ].  This facultative anaerobe seems to be playing a role similar to Helicobacter and stomach cancer.  At least 3 reports have shown that C. acnes bacteria in PC samples taken at prostatectomy and one in-vitro study demonstrated that C. acnes was able to inactivate the normal BRCA2 gene.  If this change was active in-vivo it could play a role in C. acnes persistence while facilitating PC development.  Currently, compared to Cervix cancer and the role of bacterial vaginosis in enhancing HPV induced malignancy, there is no similar consensus regarding PC and anaerobes.  Our study has shown linkage with microbiome and raised PSA possibly due to enhancing chronic inflammation prior to development of malignancy.
Conclusion/Implications:  This review has demonstrated the multiplicity of often subclinical infectious agents that potentially could contribute to the chronic inflammation that leads to malignancy.  There is increasing evidence for assays to identify chronic inflammation before cancer.  These could be deployed in screening programmes as a prognostic indicator and to monitor impact of diet change and even short course immunotherapy.  Given early BC and PC have similar reports of Spontaneous regression as do CIN 2&3 in Cervix cancer, those who fail this approach might be able to identify earlier the group who will most benefit from radical surgery.