Introduction: Systemic inflammation is increasingly recognized for its role in cancer prognosis. Inflammatory markers such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic inflammation index (SII) are emerging as relevant factors in oncology. This study evaluates their associations with established prognostic classifications in prostate cancer (PCa): the Cambridge Prognostic Groups (CPG) and the International Society of Urological Pathology (ISUP) grading system.Methods: A retrospective cohort study was conducted on 272 prostate cancer patients using systematically collected clinical data. We calculated and analyzed NLR, PLR, and SII concerning CPG and ISUP scores.Results: Statistically significant relationships were found between NLR, SII, and prognostic classifications. PLR did not demonstrate any significant association.Conclusion: NLR and SII may be helpful to prognostic factors in PCa, particularly in outpatient settings. However, further multi-center validation and establishing standardized cut-off values are necessary.

Cancer is a major cause of morbidity worldwide. Prostate cancer (PCa) is one of the most commonly diagnosed malignancies in men and is clinically heterogeneous, highlighting the need for additional biomarkers that may improve risk stratification. Lipoprotein(a) [Lp(a)] is a genetically determined and increasingly available biomarker, but its relationship with PCa remains uncertain. This systematic review aimed to synthesize observational, genetic, and Mendelian randomization evidence on the associations of circulating Lp(a), LPA-related genetic variants, and genetically predicted Lp(a) with prostate cancer incidence, mortality, and clinicopathological features, and to assess the potential clinical implications of the available evidence. We conducted this review in accordance with PRISMA guidelines. PubMed, Scopus, and Web of Science databases were searched from inception to May 2026. Eligible studies were original, peer-reviewed studies in English that assessed circulating Lp(a), LPA-related genetic variants, or genetically predicted Lp(a) in relation to prostate cancer incidence, mortality, or clinicopathological features. Certainty of evidence was assessed using GRADE. Due to heterogeneity in study designs, exposure assessments, endpoints, and effect measures, results were synthesized narratively; no meta-analysis was performed. The search identified 489 records. After duplicate removal, 253 records were screened, 15 full-text reports were assessed, and 12 studies were included. These comprised prospective cohort or biobank-observational studies, observational studies, one genetic cohort study, and Mendelian randomization studies. Studies of circulating Lp(a) showed inconsistent findings for prostate cancer incidence and mortality. One cohort reported a positive association in a categorical analysis, whereas other studies found no association or a non-significant inverse association. The genetic cohort study found no robust association between LPAL2–LPA variants and prostate cancer incidence after correction for multiple testing. Mendelian randomization findings were mixed. Although several analyses yielded directionally positive or statistically significant estimates, several primary analyses were null or borderline, and estimates varied across methods and datasets. Overall, the Mendelian randomization evidence was of low certainty and does not establish a causal association between genetically predicted Lp(a) and PCa risk. Evidence for clinicopathological features was limited and inconsistent. Certainty of evidence was low for Mendelian randomization studies and very low for circulating Lp(a), genetic cohort evidence, and clinicopathological outcomes. Current evidence regarding Lp(a), LPA genetic variants, and genetically predicted Lp(a) in PCa remains heterogeneous and clinically inconclusive. Although some studies reported positive associations, the overall evidence linking Lp(a) to prostate cancer is inconsistent and of low certainty, and does not currently support a clear association.

Introduction: Clinical staging based on digital rectal examination is imprecise, leading to pathological upstaging in patients with prostate cancer (PCa). Accurate preoperative assessment remains a challenge despite the use of multiparametric magnetic resonance imaging (mpMRI) and fusion-guided biopsy. This study aims to identify key predictors of upstaging in preoperative patients. Materials and Methods: A retrospective analysis of 924 patients who underwent radical prostatectomy between July 2012 and January 2025 was performed. Variables included prostate-specific antigen, prostate volume, biopsy type, MRI, body mass index and age. Upstaging was defined as ≥pT3 in patients staged clinically as cT1–2. Optimal cut-offs for continuous variables were defined statistically. Multivariable logistic regression was applied to identify independent predictors of upstaging and minor staging upgrading (MSU)—defined as any upward shift in the pathological T stage relative to the clinical T stage. Model performance was evaluated using the area under the Receiver Operating Characteristic (ROC) curve (AUC). Results: Upstaging occurred in 31.9% and MSU in 50.6% of patients. The mean age was 65 years. Cut-off values for PSA density (PSAD) were 0.29 for upstaging and 0.28 for MSU. In the full-cohort model (AUC = 0.628), PSAD (odds ratio (OR) = 2.55), age (OR = 1.04), and hypertension (HT) (OR = 1.47) were associated with upstaging. In PIRADS-based models, PIRADS 5 and PSAD predicted both upstaging (OR = 1.62 and 6.10, respectively; AUC = 0.664) and MSU (OR = 1.75 and 4.67, respectively; AUC = 0.659). MSU was also associated with HT and a lack of fusion biopsy (AUC = 0.622). Conclusions: PSAD and PIRADS 5 lesions are strong determinants of pathological upstaging and MSU in PCa. These factors should be considered in preoperative risk stratification to improve staging accuracy. Despite advances in imaging and biopsy techniques, upstaging remains a common phenomenon, underlining the need for further refinement of diagnostic protocols.

Robot-assisted radical prostatectomy (RARP) requires a balance between complete cancer excision and preservation of urinary continence and erectile function. Because the preservation of neurovascular bundles adjacent to the prostate surface contributes to postoperative functional recovery, intraoperative margin assessment and surgeon-guidance technologies may help refine resection and support individualized nerve-sparing decision-making. Neurovascular structure-adjacent frozen-section examination remains the most studied and clinically established method, with evidence supporting reduced positive surgical margins and broader nerve preservation, but its use is limited by cost, workflow complexity, and pathology infrastructure. Fluorescence confocal microscopy is promising but remains limited by short and apical margins; its improved accuracy for longer margins raises concerns about its reliability for routine intraoperative margin assessment. Other optical, spectroscopic, and prostate-specific membrane antigen-targeted molecular margin assessment techniques have demonstrated inconsistent diagnostic performance, with particularly low sensitivity for assessment approaches remain investigational, whereas intraoperative ultrasound, three-dimensional and augmented-reality models, fluorescence guidance, and image-enhancement systems should be viewed as surgical guidance tools rather than direct margin-assessment methods. Intraoperative technologies may improve surgical decision-making during RARP, but prospective multicenter studies with standardized oncological and functional endpoints are needed before broader adoption.