Deciphering the role of zinc in prostate health: From mechanism to therapeutic application.

Self-validating quasi-BIC Metasensors for reusable, ultrasensitive, and label-free biosensing.

A0210 Angioneurectomy: A pre-endocrine concept in the early medical treatment of prostatic disease (Albarrán & Motz, 1897)

Prostate inflammation is a common condition in men characterized by swelling of the prostate gland, often associated with other prostate diseases. Understanding the role of chronic inflammation in prostatic diseases is important due to the changes in prostatic cells and the persistence when undiagnosed. The evaluation and management of chronic prostatitis (CP) and chronic pelvic pain (CPP) involve specific diagnostic tests. This study aimed to evaluate the efficiency of the polymerase chain reaction (PCR) detection kits that use multiplex real-time PCR in comparison to standard microbiology sperm culture for detecting pathogens in individuals with CP and CPP. This retrospective observational study analyzed data from a database of 68 patients, aged 50.1 ± 17.8 years and treated at a secondary care urology center. PCR testing detected at least one microorganism in 63/68 samples (92.6%), while conventional culture yielded positive results in 12/68 cases (17.6%). The most detected microorganisms by PCR were the Bacteroides/Porphyromonas/Prevotella group (61.8%). Most of the samples were found to be polymicrobial, with the most common high-order combination consisting of Anaerococcus spp., Atopobium cluster, Bacteroides/Porphyromonas/Prevotella, Megasphaera/Veillonella/Dialister, and Peptostreptococcus/Parvimonas. This study concluded that PCR is more effective than traditional sperm culture in detecting organisms (p < .05), especially in identifying polymicrobial infections and fastidious microorganisms in patients with CP and CPP. PCR has higher sensitivity in detecting pathogens, including those often missed by standard culture techniques, leading to improved clinical outcomes, particularly in cases of polymicrobial infection.

Monosodium glutamate (MSG) is a widely used flavor enhancer with controversial health effects. While high doses have been associated with oxidative stress and repro ductive toxicity, low doses may exert protective effects. The objectives of this study were to investigate the effects of monosodium glutamate (MSG) on serum markers of prostate cancer and semen quality in male Wistar rats. Thirty-six male Wistar rats were randomly grouped into six groups (n = 6 per group) and orally administered varying doses of MSG (0, 15, 50, 100, 500, and 1000 mg/kg body weight) for 28 days. Serum total Prostate Specific Antigen (tPSA), free PSA (fPSA), Total Acid Phos phatase (TAP), Prostatic Acid Phosphatase (PAP), and Gamma-Glutamyl Transferase (GGT) were measured using ELISA. Sperm count, motility, viability, and morphology were assessed from epididymal samples. Our results showed that MSG exhibited a biphasic (hormetic) response. 15 mg/kg MSG reduced TAP by -64% (p &lt; 0.001), fPSA by -60% (p &lt; 0.001) and tPSA by -60% (p &lt; 0.001), GGT by -19.4% (p&lt;0.05) while 50–100 mg/kg MSG improved semen quality, boosting sperm count by +110% and +170% (p &lt; 0.01, p &lt; 0.001), sperm motility by +108% and +77% (p &lt; 0.001, p &lt; 0.01), and viability by +7% and +16% (ns, p &lt; 0.05), respectively. In contrast, 1000 mg/kg MSG caused severe repro ductive toxicity, with –65% sperm count, –100% motility, –23% morphology, and –37% viability (all p &lt; 0.05). These results confirm MSG’s hormetic behavior: low doses improved prostate health and fertility, while high doses induced prostate pathology and impaired spermatogenesis. Low-dose MSG (15–100 mg/kg) demonstrated protective effects on prostate health and male fertility, while higher doses (≥ 500 mg/kg) showed potential for prostate pathology induction and reproductive toxicity. These findings suggest MSG’s dual potential as both a therapeutic candidate for prostate cancer and a model compound for inducing prostate disease in experimental settings

The article discusses the causes that contribute to the development of inflammatory processes in the body, as well as disorders in the assimilation of nutrients and immunity, which can lead to infections, including those in the pelvic area, which is located in close proximity to the prostate gland. Matirials and methods. Retrospectively analyzed and/or in patients. Assessed the parameters of the known AVD, used the SF-36 scale, scales of urological pathology, the results of consultations of the surgeon and gastroenterologist to determine the indications for operative rehabilitation and the development of a program of conservative. Conducted statistical processing of the obtained data. The results of the study of electrolytes and a number of trace elements (especially zinc, vitamins, and, in particular, B 6, which is involved in neuromuscular function and promotes relaxation of the smooth muscles of the intestines), as well as the frequency of gastroenterological symptoms and urological manifestations (diagnostic scales are used), are evaluated. As a result of compliance with the regimen, manifestations of physical activity, and avoidance of stress, the risk of exacerbations is reduced and the patient's quality of life improves. Conclusions. 1. There is a relationship between prostate diseases and gastrointestinal symptoms. 2. A comprehensive approach to the rehabilitation of such patients should include the correction of nutrition.

Abstract The decline in prostate cancer screening in recent years has led to a 6% annual increase in patients diagnosed with distant prostate cancer, where the 5-year survival rate is only 38%, demonstrating the urgent need to improve prostate cancer screening practices. Prostate cancer is highly heritable and presents a unique opportunity to implement risk-stratified screening. Accordingly, we have identified many strong genetic risk factors of prostate cancer and developed a polygenic risk score (PRS) that is highly predictive of prostate cancer risk across diverse populations, which could inform the decision to initiate screening, along with the optimal age and frequency of screening. Several of these genetic factors have implications beyond screening—for instance, among patients diagnosed with low-risk prostate cancer being monitored on active surveillance, the PRS was predictive of risk of upgrading or extreme upgrading (i.e., to grade group 3 or higher) along with a higher percentage of cancerous biopsy cores. In recent work, we demonstrated that it is possible to improve the ability of the PRS to distinguish risk of advanced from indolent prostate cancer. This has launched an effort to characterize the common genetic architecture of aggressive prostate cancer by undertaking a large-scale multi-ancestry genome-wide association study (GWAS) focused on prostate cancer aggressiveness. This work is anticipated to identify new genetic mechanisms contributing to the etiology of lethal prostate cancer while also advancing PRS and clinical models to inform prostate cancer screening and treatment decisions. Citation Format: Burcu F. Darst. Advances in using germline genetics to inform prostate cancer risk assessment and disease progression [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr IA003.

Abstract Group-based variations in prostate cancer (PCa) outcomes represents a critical healthcare challenge in the USA. African American (AA) men face the highest incidence of PCa and are twice as likely to succumb to their disease compared to their Caucasian American (CA) counterparts. This disparity stems from a complex interplay involving social, environmental, and biological factors. While inequitable access to quality healthcare is a key contributor, even in settings with equal care, AA patients more often present with advanced disease at diagnosis, suggesting unique tumor biology. While some understanding of the epigenomic landscape has been recently identified, the full extent of the contribution of global chromatin remodeling towards differences in health outcomes across population groups remains poorly understood. To better elucidate how chromatin remodeling and gene regulation influences PCa development across CA and AA population groups, we employed single-cell spatial transposase-accessible chromatin technology followed by sequencing (spatial scATAC-seq) using samples from men who underwent prostatectomy at the Center for Prostate Disease Research/Walter-Reed National Military Medical Center. Our current analysis reveals a similar distribution of genome wide accessible locations between AA and CA men. Leveraging a machine learning-based computational cell typing method called Cellcano to annotate scATACseq data, we identify one immune cluster and three stroma and epithelial subclusters. Focusing on the three epithelial subclusters, we observe clear heterogeneity in each patient independent of race. However, motif analysis indicates a race dependent set of transcription factors. Most significant was a dramatic loss of the CCCTC-binding factor (CTCF) motif in AA men. CTCF is a critical zinc finger protein crucial for regulating gene expression, and organizing 3-dimensional structure of chromatin. This finding was validated by CTCF immunohistochemistry staining in an independent TMA that includes 99 patients including both CA and AA prostatectomy samples. Our current findings provide critical insights into the divergent chromatin accessibility profiles between AA and CA men with localized PCa, which likely underlie distinct transcriptional responses that can determine therapeutic resistance and tumor progression. These data shed light on the complex epigenomic mechanisms driving the group-basedvariations in PCa outcomes and may inform the development of personalized treatment strategies to address this critical healthcare challenge. Citation Format: Beatriz German, Kun-Lin Ho, Tri Truong, Jennifer Garbarino, Amina Ali, William Azadze, Sally Elsamanoudi, Colin Ng, Greg Chesnut, Leigh Ellis. Spatial Mapping of Accessible Chromatin Landscapes in Prostate Cancer [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr PR011.

Abstract Background: Natural Killer (NK) cells play a vital role in anti-tumor immunity through direct tumor cell lysis. Recent studies indicate immune microenvironment differences in prostate tumors between African American (AA) and Caucasian American (CA) men; however, the contribution of NK cell-associated genes to these disparities remains incompletely understood. The NK cell receptor gene, KLRC2, is of particular intertest, as prior work from our group demonstrated significantly lower KLRC2 expression in AA prostate tumors compared to CA tumors. Given that germline KLRC2 deletion polymorphisms differ across global populations, including East and West African ancestry groups, investigating its deletion status may provide insight into downstream expression differences and associated immune variation. Purpose: The purpose of this study was to gain a deeper understanding of immunobiological differences between AA and CA men with prostate cancer (PCa) by evaluating an NK cell-relevant gene, KLRC2, in racially diverse genomic datasets. We hypothesized that germline deletion may contribute to its variability in downstream expression and ultimately contribute to observed racial disparities in PCa. Methods: We analyzed germline whole genome sequencing data from a large Center for Prostate Disease Research (CPDR) cohort matched for AA (n=259) and CA (n=272) men. Bioinformatics workflows were applied to accurately infer KLRC2 deletion status, including copy-number calling and quality control filtering. Results: We identified a significant difference in the heterozygous deletion status of KLRC2 between AA and CA men in this robust CPDR cohort. These findings suggest population-level variation in KLRC2 copy number that may account for reduced KLRC2 expression previously observed in AA prostate tumors. Conclusions: Germline deletions in the KLRC2 gene may contribute to alterations in NK cell-mediated immune function in the tumor microenvironment of AA men with PCa. Our findings provide foundational evidence that KLRC2 status may play a role in racial immune disparities and highlight KLRC2 as a potential biomarker and candidate target for NK cell-based immunotherapeutic strategies. Conflict of Interest Disclaimer Statement: The contents of this publication are the sole responsibility of the author(s) and do not necessarily reflect the views, opinions or policies of Uniformed Services University of the Health Sciences (USUHS), the Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., the Department of War (DoW) or the Departments of the Army, Navy, or Air Force. Mention of trade names, commercial products, or organizations does not imply endorsement by the U.S. Citation Format: Laila N. Scroggins, Paula O. Cooper, Stefan DiFazio, Kun L. Ho, Ayesha A. Shafi, Cara Schafer. Evaluation of KLRC2 deletion in a racially diverse cohort of prostate cancer patients [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr A058.

Prostate-specific antigen (PSA) is widely used clinically to diagnose and monitor prostate cancer (PCa) and benign prostatic hyperplasia (BPH). Although PSA has long been used in forensic science for semen identification, its utility as a postmortem serum biomarker has not been systematically evaluated in a forensic autopsy context. This study explored whether postmortem serum PSA levels may reflect underlying prostatic pathology in forensic autopsy practice. A total of 101 male autopsy cases (PCa, n = 3; BPH, n = 16; non-prostatic malignancies, n = 36; controls, n = 46) examined between 2015 and 2024 were included. Postmortem cardiac blood was collected, and serum PSA levels were measured using chemiluminescent enzyme immunoassays. Group comparisons were performed using the Kruskal-Wallis test with Dunn's post-hoc analysis, and relationships between PSA levels, age, and postmortem interval (PMI) were examined using simple linear regression. Median PSA levels were 0.87 ng/mL in controls, 234.0 ng/mL in PCa, and 3.82 ng/mL in BPH, while PSA levels in non-prostatic malignancies were comparable to controls. Markedly elevated PSA values were observed in PCa cases compared with controls; however, all PCa-related findings were interpreted strictly as exploratory owing to the extremely small number of PCa cases (n = 3). In the BPH group, the PSA values showed only a modest tendency toward elevation relative to controls, with substantial overlap between groups. PSA levels in controls showed no significant correlation with age or PMI. Postmortem serum PSA may serve as a supportive adjunctive indicator of underlying prostatic pathology in forensic autopsies; however, its diagnostic performance - particularly for distinguishing benign disease from normal aging - appears limited. These findings should be regarded as hypothesis-generating and require confirmation in larger multicenter cohorts. The primary objective was to explore whether postmortem serum PSA differs among PCa, BPH, and control cases, and the secondary objectives were to examine its relationships with age and PMI and the postmortem stability of PSA.

ObjectiveTo assess plasma levels of heat shock protein 90α (Hsp90α) and inflammatory markers, and evaluate their diagnostic potential in prostate cancer (PCa).Patients and methodsPatients were divided into two groups based on histopathological diagnosis: PCa group and benign prostatic disease group. The levels of plasma Hsp90α and inflammatory markers were compared between groups. Diagnostic performance was evaluated using receiver operating characteristic (ROC) curve analysis. Bioinformatics analysis (Gene Set Enrichment Analysis, GSEA) was further performed to explore the potential Hsp90α-related signaling pathways in PCa.ResultsPlasma Hsp90α levels were significantly higher in PCa patients compared to benign prostatic disease patients (102.8 ± 89.77vs.62.57 ± 34.82 ng/mL, p < 0.001), while PLT (213 ± 58.95vs.266 ± 70.62 *109/L, p < 0.05) and platelet-to-neutrophil ratio (PNR, 62.48 ± 24.01vs.74.33 ± 25.19, p < 0.05) were significantly lower. Plasma Hsp90α levels showed strong correlations with the M stage (p < 0.001), N stage (p < 0.01) and Clinical stage (p < 0.001), PNR was negatively correlated with M stage (p < 0.01), decreasing with tumor progression. ROC curve analysis revealed moderate diagnostic value for Hsp90α (AUC = 0.661), PLT (AUC = 0.601), and PNR (AUC = 0.590). GSEA indicated that significant correlation between Hsp90 levels and protein secretion-related pathways and cell cycle regulation signaling pathways.ConclusionsIn summary, this study demonstrates the potential clinical utility of plasma Hsp90α as an auxiliary diagnostic biomarker for PCa, particularly in advanced or metastatic disease. Furthermore, we are the first to report the diagnostic and distant metastasis risk assessment potential of PNR in PCa. Notably, diagnostic models integrating Hsp90α and PNR with prostate-specific antigen (PSA) exhibited superior performance compared to PSA alone, suggesting their complementary role. Through integrated bioinformatics analyses, we have elucidated the molecular mechanisms by which Hsp90α drives PCa progression. These findings provide novel mechanistic insights into the pathophysiology of PCa and establish a foundation for developing future diagnostic strategies and targeted therapies focusing on Hsp90α or its associated pathways.

Association between periodontal disease and prostatic disease: a systematic review and meta-analysis of observational studies

Amyloid bodies (corpora amylacea) are found in the prostate and other organs, and their abnormal accumulation can lead to amyloidosis. However, it remains unclear how the constituents and pathological significance of amyloid bodies differ between tissues. We performed pathological, proteomic, and biochemical analyzes of prostatic amyloid bodies isolated from 53 consecutive patients who underwent pathological autopsy at Kumamoto University from 2006 to 2017. Amyloid bodies were isolated using laser microdissection, and their constituents were analyzed by liquid chromatography-tandem mass spectrometry, immunohistochemistry, and immunoblotting. Prostatic amyloid bodies were found in samples from 47 of the 53 patients (89%). The most frequently detected proteins were lactoferrin (100%), S100-A9 (90.9%), prostate-specific antigen (90.9%), and cytoskeleton-associated protein 2-like (90.9%). Amyloid-associated proteins, such as apolipoprotein E (72.7%), vitronectin (54.5%), and serum amyloid P component (36.4%), were also present but were less prevalent. Prostatic amyloid bodies were more common in patients with benign prostatic hyperplasia (N = 25) than in other patients (N = 28). These results suggest that amyloid bodies from different tissues may share some constituents. Our findings support further investigation to determine the relationship between the constituents of prostatic amyloid bodies and the pathophysiology of prostatic diseases.

Background: Benign prostatic hyperplasia (BPH) and prostate cancer (PCa) are the most common prostatic diseases in elderly men. Cost-effective methods are required to accurately differentiate benign hyperplasia from prostatic adenocarcinoma. Methods: This is an analytical, cross-sectional study conducted on 109 archival paraffin-embedded prostate tissue samples obtained from Omdurman Teaching Hospital. Data collected included histopathological diagnosis, lesion type, patient age, and Gleason score for malignant cases. Three sections were prepared from each sample and stained using Periodic Acid–Schiff, Alcian blue (pH 2.5), and Feulgen reaction to assess mucin types and DNA intensity. The diagnostic value of these histochemical stains in differentiating benign and malignant prostatic lesions and their association with Gleason grading were evaluated. Results: All 53 BPH cases showed positive staining for neutral mucins with complete absence of acidic mucins. In contrast, PCa samples demonstrated acidic mucin positivity in 22 cases (39.21%), neutral mucin positivity in 2 cases (3.5%), positivity for both mucin types in 17 cases (30.35%), and negativity for all mucins in 15 cases (26.78%). Statistically significant differences were observed between benign and malignant groups regarding mucin type and DNA staining intensity (p &lt; 0.001). Additionally, Gleason score showed a significant association with both mucin type and DNA intensity in malignant cases (p &lt; 0.001). Conclusion: Mucin histochemical stain can be used as a useful biomarker in differentiating BPH from PCa. The intensity of DNA expression using Feulgen reaction may provide valuable prognostic information in prostate cancer.

Benign prostatic hyperplasia (BPH) and prostate cancer (PCa) are common urological conditions among aging men, characterized by benign enlargement and malignant progression of the prostate gland, respectively. This study was designed to answer the question of whether adropin, irisin, and preptin serum levels have an impact on the development of prostate disease in a total of 90 participants, including BPH (n=30), localized PCa (n=30), and healthy controls (n=30). The serum concentrations of these peptides were determined using enzyme-linked immunosorbent assay (ELISA). According to the findings, adropin and irisin levels were significantly lower in the BPH and PCa groups compared to the control group (p

A 77-year-old man with a prior diagnosis of prostate adenocarcinoma, previously treated with radiotherapy and hormone therapy, presented with rising PSA levels suggestive of biochemical recurrence. While no evidence of metastatic prostate disease was detected, the PET/CT (positron emission tomography–computed tomography) scan incidentally revealed an area of abnormal radiotracer uptake in the left temporal lobe of the brain, unrelated to the patient’s known malignancy. The imaging characteristics raised the suspicion of a meningioma. A subsequent brain MRI confirmed the presence of an extra-axial lesion consistent with a meningioma. This unexpected finding highlights the additional diagnostic value of 18F-fluorocholine PET/CT beyond its primary role in prostate cancer imaging, particularly in detecting clinically significant incidental intracranial lesions. This case underscores the importance of careful and systematic interpretation of imaging studies during oncologic evaluations, even in regions outside the primary area of concern.

Recent studies have highlighted the effects of educational attainment (EA) and obesity on health, but their exact causal associations with prostate diseases remain unclear. Therefore, in this study, we performed a Mendelian randomization study to explore these potential relationships. Instrumental variables (IVs) for EA, obesity-related indicators (waist-to-hip ratio [WHR], body mass index, and leptin, and adiponectin [APN] levels), and 3 prostate diseases (benign prostatic hyperplasia [BPH], prostate cancer [PCa], and prostatitis) were selected from genome-wide association studies. Univariate and multivariate Mendelian randomization analyses were performed to investigate and verify the causal relationships. Univariate Mendelian randomization revealed that higher EA levels were related with a lower risk of prostatitis (odds ratio [OR] = 0.819; 95% confidence interval (CI): 0.742–0.905) and a higher risk of PCa (OR = 1.112; 95% CI: 1.060–1.167) and BPH (OR = 1.071; 95% CI: 1.019–1.126). WHR was positively correlated with BPH (OR = 1.13; 95% CI: 1.035–1.352), and leptin was negatively related with PCa (OR = 0.834; 95% CI: 0.912–1.160). Sensitivity analysis revealed little evidence of bias. Multivariate Mendelian randomization further clarified that EA exerted directly on prostatitis after adjusting for alcohol consumption (OR = 0.799; 95% CI: 0.691–0.923) and smoking (OR = 0.784; 95% CI: 0.662–0.927). After accounting for drinking, WHR was found to have a detrimental effect on prostatitis (OR = 1.184; 95% CI: 1.032–1.359) and BPH (OR = 1.177; 95% CI: 1.035–1.338). Leptin demonstrated a protective role against PCa (OR = 0.788, 95% CI: 0.619–1.004, adjusted for alcohol consumption), while APN was not associated with PCa, which may differ from previous studies. Our study highlights the role of EA and obesity in the progression of prostate disease, provides novel insights into the mechanisms of the relationship between central obesity, leptin, APN, and prostate disease, and indicated that leptin receptor antagonists are promising treatments for PCa.

The causal relationship between neuropsychiatric disorders and prostate diseases remains unclear, hindering early identification and intervention for affected patients. This study aims to elucidate the causal relationship between neuropsychiatric disorders and prostate diseases. Sixteen neuropsychiatric disorders and 3 prostate disorders including prostate cancer (PCa), benign prostatic hyperplasia, and prostatitis, were analyzed. Summary statistics of exposures and outcomes were derived from genome-wide association studies, and genetic tools associated with exposures at the genome-wide significance level (P < 5 × 10−8) were extracted for analysis. The inverse variance weighting method was used as the primary approach for Mendelian randomization (MR) analysis, and a mediation MR analysis was conducted to assess the mediating effect of body mass index (BMI) and its proportion. A suggestive causal link was identified between bipolar disorder and a heightened risk of PCa (odds ratio = 1.072, P = .039). Dementia was suggestively causally associated with a reduced risk of PCa (odds ratio = 0.960, P = .014). BMI mediated 4.544% and 4.449% of the respective causal relationships. Furthermore, suggestive causal associations were observed between autism spectrum disorder and an elevated risk of PCa, major depressive disorder and an increased likelihood of benign prostatic hyperplasia, as well as Parkinson’s disease and demyelinating diseases of the central nervous system with an elevated risk of prostatitis. No causal association with prostate disease was identified for the remaining conditions. Our study identified suggestive causal associations, indicating that BMI mediates the increased risk of PCa in individuals with bipolar disorder and the decreased risk in those with dementia. Our MR study revealed a potential causal link between neuropsychiatric disorders and the risk of PCa, providing new insights for the screening and prevention of PCa patients.

&amp;lt;p class=&amp;quot;cvGsUA direction-ltr align-justify para-style-body&amp;quot; style=&amp;quot;text-align: justify;&amp;quot;&amp;gt;&amp;lt;span class=&amp;quot;a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none&amp;quot;&amp;gt;Benign prostatic hyperplasia (BPH), chronic prostatitis (CP), and prostate cancer (PC) are frequently occurring conditions that affect the prostate gland, with overlapping clinical features and potentially shared pathogenetic mechanisms. A growing body of research indicates that oxidative stress (OS) is a critical factor in both the onset and advancement of these disorders. Xanthine oxidase (XO) is a known enzymatic source of reactive oxygen species (ROS), however, its involvement in prostate disease pathogenesis remains underexplored. &amp;lt;/span&amp;gt;&amp;lt;span class=&amp;quot;a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none&amp;quot;&amp;gt;The study included 17 patients with CP, 10 with BPH, and 15 with PC. Ten healthy individuals served as controls. Serum samples were collected for BPH and CP groups, while PC samples were obtained from surgical tissues. OS was assessed by measuring thiobarbituric acid-reactive substances (TBARS) and advanced oxidation protein products (AOPP). XO activity was determined spectrophotometrically in plasma and tissue homogenates. &amp;lt;/span&amp;gt;&amp;lt;span class=&amp;quot;a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none&amp;quot;&amp;gt;Serum concentrations of TBARS and AOPP were markedly higher in individuals diagnosed with BPH and CP relative to those in the healthy control group (p &amp;amp;lt; 0.001). Similarly, XO activity was markedly increased in these groups. In PC tissue, both TBARS and AOPP concentrations, as well as XO activity, were significantly higher than in non-tumor prostate tissue (p &amp;amp;lt; 0.001), indicating local OS and enzymatic ROS production. &amp;lt;/span&amp;gt;&amp;lt;span class=&amp;quot;a_GcMg font-feature-liga-off font-feature-clig-off font-feature-calt-off text-decoration-none text-strikethrough-none&amp;quot;&amp;gt;These findings confirm that systemic and tissue-level OS is elevated in BPH, CP, and PC. XO may represent a shared mechanism linking inflammation and carcinogenesis. The study supports further investigation into the therapeutic potential of antioxidants and XO inhibitors as adjunct strategies in prostate disease management.&amp;lt;/span&amp;gt;&amp;lt;/p&amp;gt;

Prostate adenocarcinoma is mainly diagnosed based on serum PSA levels, but elevated PSA levels can also be caused by BPH, which weakens its specificity. Recent scientific studies have demonstrated that specific microRNAs regulate cancer cell proliferation by modulating the Wnt/β-catenin pathway. To date, no published literature has provided a comprehensive assessment of the interactions between miR-106a-5p and miR-375-3p and components of the Wnt/β-catenin pathway in prostate cancer. Therefore, the aim of the present study was to perform a pilot evaluation of the expression of miRNAs 106a-5p and 375-3p, as well as β-catenin, Fzd8, Wnt5a, and cyclin D1 in prostate adenocarcinoma compared with BPH. The study material consisted of samples collected from 30 patients with prostate cancer and 30 with BPH. Protein expression was analyzed using IHC and qRT-PCR methods, while miRNA levels were quantified by dPCR. Our study results revealed lower immunoreactivity and expression of genes encoding β-catenin, Fzd8, Wnt5a, and cyclin D1 and significantly higher fluorescence intensity of miRNA 106a-5p and 375-3p with prostate adenocarcinoma compared to BPH. These parallel alterations in miRNA expression and Wnt/β-catenin-related components reflect disease-specific expression patterns and warrant further investigation in larger cohorts to determine their potential utility as diagnostic biomarkers in prostate diseases.