Objective: We aimed to investigate the diagnostic value of different laboratory indicators in combination with total prostate-specific antigen (TPSA) for prostate cancer (PCa). Methods: In this retrospective study, we selected 291 patients who underwent prostate biopsy. Patients were divided into the benign prostatic hyperplasia group and the PCa group. In both groups, patients were again divided into a group with TPSA 4.0–10.0 ng/mL and a group with TPSA >10.0 ng/mL. Clinical data including age, pre-puncture TPSA, free prostate-specific antigen (FPSA), and prostate volume (PV) were collected from all patients. We calculated the metrics PSA/PV (prostate-specific antigen density, PSAD), age/PV (AVR), age × PV/TPSA (PSA-AV), and (FPSA/TPSA)/PSAD [(F/T)/PSAD]). We plotted receiver operating characteristic (ROC) curves and calculated the area under the ROC curve (AUC). Results: We found statistically significant differences in PV, PSAD, AVR, PSA-AV, and (F/T) PSAD for patients with TPSA 4.0–10.0 ng/mL and TPSA >10 ng/mL. We further plotted the ROC of individual or combined indices in different subgroups and calculated the AUC. We found that the diagnostic efficacy of the combined indices was higher with TPSA >10 ng/mL. Conclusion: The combination of TPSA with multiple indicators may improve diagnostic accuracy for PCa.

Purpose The purpose of this study was to evaluate the nature of ultrasound characteristics during mpMRI/TRUS cognitive fusion targeted biopsy (cTB). Methods From 2023 to 2024, data from 502 lesions in 426 men who underwent targeted combined systematic biopsy were analyzed. All lesions had a Prostate Imaging Reporting and Data System (PI-RADS) score of ≥ 3. The primary endpoint was the detection rate of prostate cancer (PCa) according to the PI-RADS score/ultrasound characteristics, categorized as benign or invisible (Bi), hypoechoic only (Ho), and hypoechoic with microcalcification (Hm), assessed through cross-stratification. The secondary endpoints included the distribution of ultrasound characteristics across PI-RADS scores, prostate zones, and histological types. Finally, associations between ultrasound characteristics and clinically significant PCa (csPCa) were assessed using multivariate logistic regression analysis (MVA). Results Among lesions, 233 (46%) were Bi, 210 (42%) Ho, and 59 (12%) Hm. First, Bi lesions had a 64% (103/161) non-cancer rate in PI-RADS 3, while Ho + Hm lesions showed the highest csPCa rate in PI-RADS 5 at 82% (102/124). Additionally, Ho + Hm lesions were predominantly observed in PI-RADS 5 (92% [114/124]) and in the peripheral zone (64% [179/278]). Notably, Hm lesions had a significantly higher percentage of cribriform morphology than Ho lesions (32% vs. 14%, P = 0.001). Finally, MVA confirmed Ho ([Ref Bi] OR 4.95, P < 0.001) and Hm ([Ref Bi] OR 27.7, P < 0.001) as independent predictors of csPCa. Conclusion In cTB, the identification of Ho and Hm lesions on TRUS enhances the diagnostic yield of csPCa by facilitating more precise localization compared to Bi lesions. Clinical Trial Registration No. 2023-272-002, July 14, 2023.

Bladder cancer is one of the most prevalent cancers worldwide, and its morbidity and mortality rates have been increasing over the years. However, how RAC family small GTPase 3 (RAC3) affects the proliferation, migration and invasion of cisplatin‐resistant bladder cancer cells remains unclear. Bioinformatics techniques were used to investigate the expression of RAC3 in bladder cancer tissues. Influences of RAC3 in the grade, stage, distant metastasis, and survival rate of bladder cancer were also examined. Analysis of the relationship between RAC3 expression and the immune microenvironment (TIME), genomic mutations, and stemness index. In normal bladder cancer cells (T24, 5637, and BIU‐87) and cisplatin‐resistant bladder cancer cells (BIU‐87‐DDP), the expression of RAC3 was detected separately with Western blotting. Plasmid transfection was used to overexpress or silence the expression of RAC3 in bladder cancer cells resistant to cisplatin (BIU‐87‐DDP). By adding activators and inhibitors, the activities of the JNK/MAPK signalling pathway were altered. Cell viability, invasion, and its level of apoptosis were measured in vitro using CCK‐8, transwell, and flow cytometry. The bioinformatics analyses found RAC3 levels were elevated in bladder cancer tissues and were associated with a poor prognosis in bladder cancer. RAC3 in BIU‐87‐DDP cells expressed a higher level than normal bladder cancer cells. RAC3 overexpression promoted BIU‐87‐DDP proliferation. The growth of BIU‐87‐DDP cells slowed after the knockdown of RAC3, and RAC3 may have had an impact on the activation of the JNK/MAPK pathway.