The association between prostatitis and prostate cancer. Systematic review and meta-analysis

Perletti, Gianpaolo; Monti, Elena; Magri, Vittorio; Cai, Tommaso; Trinchieri, Alberto; Montanari, Emanuele

doi:10.4081/aiua.2017.4.259

Cited by 41 publications

(41 citation statements)

References 32 publications

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“…program and induction of pluripotency, as would occur in noncancerous cells to promote wound healing and maintain tissue homeostasis 15,16,66 . Viewed in this way and given the association of prostatitis with EMT 67,68 and prostate cancer 69 , prolonged activation of MUC1-C in settings of chronic inflammation and, in turn, the induction of stemness and reprogramming could hold important implications for PC progression and treatment. In this respect and of potential clinical relevance, targeting MUC1-C in PC cells with the GO-203 inhibitor, which blocks MUC1-C homodimerization and nuclear localization [42][43][44] , phenocopied the effects of MUC1-C silencing, including downregulation of (i) MYC→BRN2 signaling, (ii) MYCN, EZH2 and NE markers, and (iii) the OSKM pluripotency factors.…”

Section: Discussionmentioning

confidence: 99%

MUC1-C regulates lineage plasticity driving progression to neuroendocrine prostate cancer

et al. 2020

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Neuroendocrine prostate cancer (NEPC) is an aggressive malignancy with no effective targeted therapies. The oncogenic MUC1-C protein is overexpressed in castration-resistant prostate cancer (CRPC) and NEPC, but its specific role is unknown. Here, we demonstrate that upregulation of MUC1-C in androgen-dependent PC cells suppresses androgen receptor (AR) axis signaling and induces the neural BRN2 transcription factor. MUC1-C activates a MYC→BRN2 pathway in association with induction of MYCN, EZH2 and NE differentiation markers (ASCL1, AURKA and SYP) linked to NEPC progression. Moreover, MUC1-C suppresses the p53 pathway, induces the Yamanaka pluripotency factors (OCT4, SOX2, KLF4 and MYC) and drives stemness. Targeting MUC1-C decreases PC self-renewal capacity and tumorigenicity, suggesting a potential therapeutic approach for CRPC and NEPC. In PC tissues, MUC1 expression associates with suppression of AR signaling and increases in BRN2 expression and NEPC score. These results highlight MUC1-C as a master effector of lineage plasticity driving progression to NEPC.

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Section: Discussionmentioning

confidence: 99%

MUC1-C regulates lineage plasticity driving progression to neuroendocrine prostate cancer

et al. 2020

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“…Overall, meta-analyses of these studies have observed strong positive associations between clinical prostatitis and prostate cancer, supporting a role for prostate inflammation in prostate cancer development. [5][6][7][8] . However, none of these meta-analyses took into consideration the potential for detection bias in their pooled estimates.…”

Section: Introductionmentioning

confidence: 99%

A Systematic Review and Meta-analysis of Associations between Clinical Prostatitis and Prostate Cancer: New Estimates Accounting for Detection Bias

Langston

Horn

Khan

et al. 2019

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Previous meta-analyses have estimated summary positive associations between clinical prostatitis and prostate cancer. However, none have accounted for detection bias, the possibility for increased prostate cancer screening and detection in men with clinical prostatitis, in their pooled estimates. Methods: We searched for studies that investigated the relation between clinical prostatitis and prostate cancer through November 2018. Random-effects meta-analysis was used to calculate summary odds ratios (ORs) among all studies and in strata defined by methods used to reduce detection bias. Results: Although an increased odds of prostate cancer was seen among men with a history of clinical prostatitis in all 38 eligible studies combined (OR=2.05, 95% CI: 1.64-2.57), this estimate attenuated to null among studies that performed the most rigorous analyses to limit detection bias (OR=1.16, 95% CI: 0.77-1.74). Conclusions: Our findings indicate that previously reported positive associations between clinical prostatitis and prostate cancer are likely due to detection bias. Impact: Studies using rigorous detection bias methods are warranted to replicate these findings, as well as to examine the possible relation between prostate inflammation and prostate cancer

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“…13 Whether clinical prostatitis is a prostate cancer risk factor is unclear. [14][15][16] In our recent study, we found clinical prostatitis was associated with a lower prostate cancer risk in African American men. 17 Evidence also exists of unequal PSA amounts between white and African American men with prostate cancer.…”

Section: Introductionmentioning

confidence: 85%

Potential effect of anti‐inflammatory drug use on PSA kinetics and subsequent prostate cancer diagnosis: Risk stratification in black and white men with benign prostate biopsy

et al. 2019

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Background Rising prostate‐specific antigen (PSA) levels are associated with both increased risk of prostate cancer and prostatic inflammation. The confounding effects of inflammation on the utility of PSA kinetics to predict prostate cancer may be partially mitigated by anti‐inflammatory drug use. We investigated the influence of anti‐inflammatory drug use on the association of PSA kinetics with prostate cancer risk. Methods We studied 488 prostate cancer case‐control pairs (290 white, 198 African American (AA)) nested in a retrospective cohort of men with a benign prostate biopsy. A series of multivariable models estimated prostate cancer risk associated with PSA velocity (PSAV) at different levels of anti‐inflammatory drug use while adjusting for the presence of both clinical and histologic prostatitis. Results In men with one, two, or three or more courses of anti‐inflammatory drug use, for each ng/mL/year increase in PSAV, prostate cancer risk increased 1.21‐fold, 1.83‐fold, and 1.97‐fold, respectively ( P < 0.0001). In controls with histologic prostatitis, anti‐inflammatory drug use was associated with a significantly lower PSAV ( P < 0.0001). This association was not observed in men with histologic prostatitis who were subsequently diagnosed with prostate cancer. A positive interaction between anti‐inflammatory drug use and PSAV‐associated prostate cancer risk was only observed in AA men, as well as a strong positive association between any anti‐inflammatory drug use and clinical prostatitis ( P = 0.004). Conclusions In men with benign prostate biopsy, accounting for the presence of histologic prostatitis and anti‐inflammatory drug use, particularly in AA men, may help distinguish between men with rising PSA because of prostatitis vs undiagnosed cancer.

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The association between prostatitis and prostate cancer. Systematic review and meta-analysis

Abstract: Meta-analysis of 15 case-control studies shows that a history of clinical chronic prostatitis can significantly increase the odds for prostate cancer in the general population, whereas such association in African-American individuals remains uncertain.

Cited by 41 publications

References 32 publications

MUC1-C regulates lineage plasticity driving progression to neuroendocrine prostate cancer

MUC1-C regulates lineage plasticity driving progression to neuroendocrine prostate cancer

A Systematic Review and Meta-analysis of Associations between Clinical Prostatitis and Prostate Cancer: New Estimates Accounting for Detection Bias

Potential effect of anti‐inflammatory drug use on PSA kinetics and subsequent prostate cancer diagnosis: Risk stratification in black and white men with benign prostate biopsy

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