Abstract
Simple SummaryProstatitis, or the inflammation of the prostate, is frequently observed in the clinic and by research studies, but its relevance to a man’s risk of being diagnosed with prostate cancer, or to his survival after the diagnosis, is not completely understood. In this review, we summarize the current knowledge on the causes of prostate inflammation, as well as the relationship with prostate cancer, with a particular focus on aggressive, defined as a high Gleason score or clinical stage, and lethal stages of disease. We also describe the strengths and weaknesses of the various technologies used to evaluate prostate inflammation in human studies, and we consider the potential of immune therapy and lifestyle interventions to prevent lethal disease and improve outcomes for prostate cancer patients. Future research is needed to better understand the role of prostate inflammation in lethal prostate cancer, and to provide evidence to guide the development of new treatment and prevention strategies to reduce prostate inflammation and improve survival.Prostate cancer is a major cause of disease for men globally. Inflammation, an established hallmark of cancer, is frequently observed in the prostate, though its contribution to prostate cancer risks and outcomes is not fully understood. Prostate cancer is biologically and clinically heterogeneous, and there is now evidence that inflammation and immunological characteristics vary by the genomic and mutational landscape of the tumor. Moreover, it is now recognized that risk factor profiles vary between tumor subgroups, as defined by histopathological and molecular features. Here, we provide a review centered around the relationship between inflammation and prostate cancer, with a consideration of molecular tumor features and a particular focus on the advanced and lethal stages of disease. We summarize findings from epidemiological studies of the etiology and role of inflammation in prostate cancer. We discuss the pathology of prostate inflammation, and consider approaches for assessing the tumor immune microenvironment in epidemiological studies. We review emerging clinical therapies targeting immune biology within the context of prostate cancer. Finally, we consider potentially modifiable risk factors and corresponding lifestyle interventions that may affect prostate inflammation, impacting outcomes. These emerging insights will provide some hints for the development of treatment and prevention strategies for advanced and lethal prostate cancer.
Highlights
Prostate cancer is a major cause of disease among men, notable for its geographic variation, ranking the second most common men’s cancer for incidence and the fifth for mortality globally, with 1,414,259 new cases and 375,304 deaths estimated in 2020 [1].Prostate cancer is biologically and clinically heterogeneous, and a major challenge lies in identifying, at the time of diagnosis, which cancers will be lethal
Health Professionals Follow-Up Study reported no association between gonorrhea and Cancers 2022, 14, 1367 the total prostate cancer risk (RR 1.04; 95% confidence interval (CI) 0.79–1.36), but found a suggestion of a positive association for advanced (RR 1.37; 95% CI 0.64–2.95), relative to organ-confined (RR 0.99; 95% CI 0.71–1.38), prostate cancer risk, there were no differences in Gleason scores (
In a phase III trial of Ipilimumab in the first-line treatment of patients with chemotherapy-naïve metastatic castration-resistant prostate cancer (mCRPC), no significant difference was found between the Ipilimumab group and the placebo group in terms of overall survival, but an improvement in progression-free survival
Summary
Prostate cancer is a major cause of disease among men, notable for its geographic variation, ranking the second most common men’s cancer for incidence and the fifth for mortality globally, with 1,414,259 new cases and 375,304 deaths estimated in 2020 [1]. It is intriguing that a relatively low proportion of patients achieve a response from currently available immunotherapies [11–13], suggesting that much of prostate cancer is likely to be immunologically “cold”. This could be characterized by lack of T-cells within tumor, or failed T-cell priming, such as ineffective antigen presentation [14]. Understanding the immune microenvironment across histological and molecular subgroups of prostate cancer may identify patients that could benefit from immunotherapy, as well as informing our understanding of lethal prostate cancer etiology to identify lifestyle interventions and prevention strategies. We identify some future research directions, for patient subgroups who may benefit from immune therapy and/or lifestyle interventions that target inflammation
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