Prostate cancer (PCa) is considered as the one most prevalent types of cancer affecting men all over the world [1]. The disease affected 1.4 million people in 2020 and a higher rate of 75 % of prevalence was identified in men over 65 years old. Besides, in Brazil, the disease was responsible for the amount of 15,841 deaths in 2020 in the United States; the incidence rate for PCa increased 3 % between 2014 and 2019, which was predicted 72,000 new cases per year in the next three years [2].

The pathogenesis of PCa is complex in that many factors are involved in the disease risk development. One of these contributors is the diet composed by high rates of saturated fatty acids from animal-derived foods and poor fiber ingestion, in addition to overweight and obesity, the positive familiar history for PCa and the inflammatory status of the prostate [3].

In fact, the progression of PCa is highly affected by immune players, such as: the tumor necrosis factor α (TNF-α) and cyclooxygenase (COX-2). TNF-α is a relevant immune-mediator involved in the differentiation of B-lymphocytes in bone marrow which previous data suggested the levels of TNF-α as a considerable parameter for estimation of tumor mass presence in patients with multiple myeloma [4].

Besides, the interleukins (ILs) also are involved in the several aspects of tumor development [5], [6]. We may cite the IL-6, responsible for up-regulating pathways of DNA-repair by Ataxia-Telangiectasia Mutated (ATM) and Breast Cancer (BRCA) 1, leading to PCa radiotherapy resistance [7]. In addition, IL-8 also is involved in the tumor microenvironment and the expression of this IL is related to aggressive PCa [8].

Other factors that influence the pathogenesis and progression of PCa are genetic variations. A genetic predisposition was identified in 12 % of men with metastatic prostate cancer and 6 % in men diagnosed with the limited disease in the prostate [9]. Variations in the BRCA1 and BRCA2 genes are commonly related to the prostate cancer risk, being suggested as a more personalized genetic source of estimation for the disease [10]. Moreover, genetic variations in the ATM, Checkpoint Kinase 2 (CHEK2) and Nijmegen breakage syndrome (NBM) genes were also associated with prostate cancer risk, but less frequently [11].

Besides, the literature brings a relevant amount of data for genetic polymorphisms in immune mediator genes and PCa risk. The rs1143627 [12] in IL1B, the rs1800795, rs1800796, rs1800797 polymorphisms in IL6 [13], the rs4073 polymorphism in IL8 [14] and the rs1800871 and rs1800872 polymorphisms in IL10 [15] are significant genetic variations associated with a greater risk of developing or a greater severity or even as protective factor against PCa, reinforcing the role of immune mediator genes and their functional products in tumor progression.

Many of the case-control studies available in the literature on this topic were the subject of meta-analyses that seek to gather published data to increase the sample number and better evaluate the association between these polymorphisms and the risk of PCa [16], [17]. However, meta-analyses may present limitations related to the use of the P value as a reliability threshold and the only point of precision, resulting in possible false positive results in meta-analysis studies [18].

To solve this problem, Bayesian calculations such as FRPR (False-Positive Report Probability) [19] and BDFP (Bayesian Phase Discovery Probability) [20] were developed to verify the rate of false positives in meta-analysis studies. This approach becomes necessary to better assess the reliability of meta-analysis studies.

Therefore, the importance of understanding the impact of genetic polymorphisms in immunological mediators and the risk of PCa through meta-analytic data is clear. Thus, this work aims to analyze the notoriety of the results of meta-analyses published on genetic variants in immunological mediator genes and the risk of developing PCa.