Prostate最新文献

{"title":"Evidence and Rationale for Prostate Cancer Screening.","authors":"Takeshi Takahashi","doi":"10.1002/pros.70002","DOIUrl":"10.1002/pros.70002","url":null,"abstract":"","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":"1245-1247"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144369555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Annexin A1-Targeted d-Peptide-Monomethyl Auristatin E Conjugate Enhanced Antitumor Effect of Monomethyl Auristatin E for Chemotherapy of Prostate Cancer.","authors":"Kai Ozaki, Tohru Yoneyama, Yuka Kubota, Mihoko Sutoh Yoneyama, Motohiro Nonaka, Tomonori Suzuki, Ryuma Tanaka, Chikara Ohyama, Shingo Hatakeyama","doi":"10.1002/pros.70007","DOIUrl":"10.1002/pros.70007","url":null,"abstract":"<p><strong>Background: </strong>N-terminus 15 amino acid (MC16) of Annexin A1 (ANXA1) is an effective therapeutic target for tumors and tumor vasculature as it specifically localizes to the cell surface of tumor cells and tumor vascular endothelial cells. We identified the d-type peptide (hpnevrs, dhp7) by mirror-image phage display targeting l-type MC16 and tested the hypothesis that intravenously injected c(vcMMAE)dhp7 eradicates prostate tumor in mice with less adverse side effects than that of mc-Val-Cit-PAB-monomethyl auristatin (vcMMAE) alone.</p><p><strong>Methods: </strong>The binding affinity of dhp7 to MC16 of ANXA1 was analyzed by biolayer interferometry and in silico conformational analysis. c(vcMMAE)dhp7 was synthesized by coupling dhp7 to vcMMAE to evaluate the antitumor effects. A subcutaneous tumor model was generated by inoculating the luciferase-expressing prostate cancer PC-3 cell line, PC-3-hLuc-PSMA, into the nude mice. 1.25 mg/kg vcMMAE or 2.14 mg/kg c(vcMMAE)dhp7, the equal dose as 1.25 mg/kg vcMMAE, was administered intravenously every 3 or 4 days and growth of tumors was assessed by photon count using an IVIS system.</p><p><strong>Results: </strong>The dhp7 bound specifically to l-type MC16 (KD 0.48 μM) but not bound to d-type MC16 and mutant l-type MC16. Both in vitro and in silico interaction analysis indicating the α-helix of the l-type MC16 may be important for dhp7 binding. Fluorescence labeled-dhp7 accumulated in both ANXA1 positive cells and subcutaneous prostate tumor. To evaluate the antitumor effect, c(vcMMAE)dhp7 was synthesized by coupling dhp7 with mc-Val-Cit-PAB-monomethyl auristatin E (vcMMAE) as a payload. The IC50 s of vcMMAE (129.9 ng) and c(vcMMAE)dhp7 (122.7 ng) against prostate cancer cells showed almost equivalent in vitro drug sensitivity. The c(vcMMAE)dhp7-treated mice showed significant antitumor effects including complete responses at the same dose of MMAE (1.25 mg/kg) as mice treated with vcMMAE alone. Pathological analysis of the residual tumor showed that CD31 density of the c(vcMMAE)dhp7 treated group was significantly higher than that of the vcMMAE group, and the Ki-67 index was significantly lower than that of the vcMMAE alone. Clinical chemistry tests showed side effects of MMAE significantly improved in terms of hepatic/biliary toxicity in c(vcMMAE)dhp7-treated group.</p><p><strong>Conclusions: </strong>The c(vcMMAE)dhp7 conjugate exerts a better antitumor effect than vcMMAE on ANXA1-positive prostate cancer.</p>","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":"1208-1221"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144576978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRMT5:MEP50 Are Mediators of Treatment-Induced Neuroendocrine Differentiation in Prostate Cancer.","authors":"Hye Seung Nam, Andrew Michael Asberry, Xuehong Deng, Sheng Liu, Jiaoti Huang, Chang-Deng Hu, Jun Wan, Michael K Wendt","doi":"10.1002/pros.70006","DOIUrl":"10.1002/pros.70006","url":null,"abstract":"<p><strong>Background: </strong>Neuroendocrine prostate cancer (NEPC) is a lethal subtype of prostate cancer responsible for an estimated 20%-30% of castration-resistant prostate cancer (CRPC) deaths. While NEPC can arise spontaneously, the majority of these cases emerge as treatment-induced NEPC (tNEPC). Our clinical and computational analyses identified increased expression of protein methyltransferase 5 (PRMT5) and its cofactor methylosome protein 50 (MEP50) in tNEPC.</p><p><strong>Methods: </strong>Here we generated an in vitro cell culture and mouse model of prostate cancer to recapitulate tNEPC induced upon treatment with the androgen receptor (AR) inhibitor, enzalutamide. The role of PRMT5 and its cofactor MEP50 were determined by overexpression. Depletion of these genes and pharmacological inhibition of PRMT5 were followed by analysis of cell viability, neurite growth, and effects on neuroendocrine-related gene transcription using immunofluorescence, immunohistochemistry, and Western blot. PRMT5 and MEP50 protein expression levels were comprehensively analyzed for clinical correlation in NEPC patient prostate tissue samples.</p><p><strong>Results: </strong>Elevated PRMT5 and MEP50 correlated with increased recurrence in prostate cancer patients receiving androgen deprivation therapy. Depletion of PRMT5 and MEP50 prevented neuroendocrine differentiation (NED)-induced by enzalutamide both in vitro and in a xenograft mouse model. Conversely, overexpression of PRMT5 and MEP50 was sufficient to induce NED in prostate cancer cells. Evaluation of a genetically engineered mouse model, in which PRMT5 and MEP50 were overexpressed in the prostate, similarly indicated NEPC development.</p><p><strong>Conclusions: </strong>Our data suggest that PRMT5:MEP50 are regulators of tNEPC. PRMT5/MEP50 expression could serve as a predictive biomarker and therapeutic target for aggressive forms of prostate cancer.</p>","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":"1196-1207"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Late Bowel Symptoms in Long-Term Survivors of Prostate Cancer Following Radiotherapy.","authors":"Isabella Gruber, Oliver Koelbl, Maria M Meier","doi":"10.1002/pros.70004","DOIUrl":"10.1002/pros.70004","url":null,"abstract":"<p><strong>Background: </strong>Despite advances in radiotherapy planning, some long-term prostate cancer survivors experience persistent symptoms. Although overall quality of life appears comparable between patients treated with definitive and salvage radiotherapy and aligns with normative data, prostate-specific deficits-particularly bowel symptoms-may persist.</p><p><strong>Methods: </strong>This study assessed prostate-specific quality of life using the EORTC QLQ-PR25 questionnaire in 141 patients with localized or locally advanced prostate cancer (T1-4 N0 M0) treated with external radiotherapy between 2011 and 2021. After a median follow-up of 63.6 months, bowel symptom scores and radiation doses to the anal canal and rectum were analyzed in 71 patients who received definitive radiotherapy (median dose: 78 Gy) and 70 who received salvage radiotherapy (median dose: 70 Gy). Bowel symptom scores were correlated with previously reported global health status scores (EORTC QLQ-C30) from the same cohort and compared to those of a reference population.</p><p><strong>Results: </strong>Tumor stage distribution (localized vs. locally advanced) was similar between groups. Patients in the definitive group were older at the time of survey than those in the salvage group (79 years vs. 75 years; p = 0.009). Mean doses to the anal canal and rectum were comparable between groups, reflecting consistent application of dose constraints across treatment intents. EORTC QLQ-PR25 scores, including bowel symptom scores, did not differ significantly between the groups. Patients reporting bowel symptoms (n = 92) received significantly higher mean doses to the anal canal (41.0 Gy vs. 35.1 Gy; p < 0.001), whereas rectal doses were similar. Mean anal canal dose (Dmean) correlated with bowel symptom scores (r = 0.307; p < 0.001), whereas no correlation was observed for mean rectal doses. A Dmean threshold of 32 Gy to the anal canal differentiated patients with and without bowel symptoms. Higher bowel symptom scores were associated with lower global health status (r = -0.469; p < 0.001). Compared to the reference population, patients showed significantly and clinically relevant higher bowel symptom scores, indicating a greater symptom burden.</p><p><strong>Conclusions: </strong>Bowel symptoms are a significant concern after radiotherapy for prostate cancer and are associated with reduced quality of life. Since higher anal canal doses correlate with increased symptom burden, greater efforts to spare this structure during treatment are warranted.</p><p><strong>Trial registration: </strong>This study was retrospectively registered.</p>","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":"1181-1188"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329166/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of NONO Suppresses Proliferation, Migration, and Invasion in Metastatic Prostate Cancer.","authors":"Anna-Lena Lemster, Sarah Grünhagen, Sarah Schmalfeld, Florian Lenz, Anna Natzius, Anne Offermann, Sven Perner, Jiong Zhang, Verena Sailer, Jutta Kirfel","doi":"10.1002/pros.24925","DOIUrl":"10.1002/pros.24925","url":null,"abstract":"<p><strong>Background: </strong>As prostate cancer (PCa) remains one of the leading causes of cancer-related death in men, it is important to develop effective therapeutic approaches for the treatment of metastatic PCa and to improve the accuracy of prognosis for aggressive tumors. Non-POU domain-containing octamer-binding (NONO) is involved in RNA transport and almost all steps of gene regulation, and aberrant expression is associated with tumorigenesis in various tumor entities.</p><p><strong>Methods: </strong>Immunohistochemical analysis of the expression of NONO was performed in a cohort of 405 patient samples, including 54 benign prostate tissues, 250 primary prostate tumors, and 101 metastatic tissue samples. To assess the role of NONO in PCa cells, siRNA-mediated knockdown of NONO in the metastatic PCa cell lines PC3 and DU145, followed by a series of functional assays including proliferation, transwell, western blotting, and real-time quantitative PCR, was used.</p><p><strong>Results: </strong>The current study showed that the nuclear expression of NONO increases during the progression of PCa and is highest in distant metastases. NONO regulates cell proliferation by increasing the expression of cell cycle-related genes. In addition, NONO modulates migration and invasion in PCa cells.</p><p><strong>Conclusion: </strong>Overall, these results suggest inhibition of NONO may be a promising approach for the treatment of metastatic PCa.</p>","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":"1121-1133"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12278708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144287082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Multimarker Model for Prostate Cancer Risk Assessment: Improving Diagnostic Accuracy Beyond PSA.","authors":"Penglu Yang, Bin Yang","doi":"10.1002/pros.24920","DOIUrl":"10.1002/pros.24920","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the association between biochemical markers and prostate cancer (PCa) risk by analyzing patients with benign prostatic hyperplasia (BPH) and PCa. Additionally, the study sought to assess the diagnostic accuracy of a multimarker model compared to prostate-specific antigen (PSA) alone.</p><p><strong>Methods: </strong>A cross-sectional study was conducted with data from 2931 patients (1374 with BPH and 1557 with PCa) from the Prostate Cancer Data Set of the National Population Health Data Center. Biochemical markers, including PSA, apolipoproteins, lipid profiles, and metabolic markers (calcium and phosphate), were analyzed. Univariate and multivariate logistic regression analyses were performed to assess the associations with PCa risk. The diagnostic performance of the multimarker model was evaluated using receiver operating characteristic (ROC) curve analysis.</p><p><strong>Results: </strong>Total PSA levels were significantly higher in PCa patients, and the free/total PSA ratio was lower (p < 0.001). Apolipoprotein A1, LDL cholesterol, calcium, and phosphate were also significantly associated with PCa risk (p < 0.001). The multivariate logistic regression model, incorporating multiple markers, showed improved diagnostic accuracy (AUC 0.731, 95% CI: 0.713-0.749), with sensitivity of 68.4% and specificity of 65.8%.</p><p><strong>Conclusions: </strong>Combining multiple biochemical markers with PSA enhances the diagnostic accuracy for PCa, offering additional predictive value. This multimarker approach has the potential to improve PCa screening and reduce unnecessary biopsies.</p>","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":"1096-1103"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12278700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive Analysis of Fraction of Genome Altered in Prostate Cancer Treatment.","authors":"Kazuma Yukihiro, Yohei Sekino, Go Kobayashi, Tomoya Hatayama, Hiroyuki Shikuma, Ryo Tasaka, Yuki Kohada, Kenshiro Takemoto, Miki Naito, Shunsuke Miyamoto, Kohei Kobatake, Hiroyuki Kitano, Keisuke Goto, Akihiro Goriki, Keisuke Hieda, Nobuyuki Hinata","doi":"10.1002/pros.70042","DOIUrl":"https://doi.org/10.1002/pros.70042","url":null,"abstract":"<p><strong>Background: </strong>Genomic instability is a key feature of cancer and plays a central role in tumor progression. One emerging metric for genomic instability is the fraction of genome altered (FGA), which quantifies the proportion of the genome affected by copy number alterations. Previous studies in various solid tumors have shown that high FGA is associated with aggressive disease and adverse clinical outcomes. However, the clinical significance of FGA in prostate cancer (PC) remains unclear. In this study, we investigated the role of FGA as a potential biomarker of tumor aggressiveness and a poor prognosis in PC using several large-scale public databases.</p><p><strong>Methods: </strong>We analyzed the processed data from previous large-scale PC studies available through the cBioPortal database: MSK CHORD 2024 (n = 3211), MSK 2021 (n = 2069), MSK 2020 mCSPC (n = 424), SU2C/PCF mCRPC (n = 444), and AACR Project GENIE (n = 5306). Associations between FGA and clinical parameters such as T stage, Gleason score (GS), tumor volume, metastatic burden, pathological subtype, and treatment history were evaluated. Kaplan-Meier survival analysis was used to assess the prognostic value of FGA.</p><p><strong>Results: </strong>High FGA was significantly associated with aggressive clinical features, including higher T stage, GS, metastatic burden, and neuroendocrine prostate cancer histology. FGA increased after most therapeutic interventions. Patients with high FGA had significantly poorer overall survival across nearly all treatment modalities. An oncoplot analysis revealed a higher frequency of somatic alterations in key driver genes, including AR, PTEN, and TP53, in high-FGA tumors.</p><p><strong>Conclusions: </strong>FGA was closely associated with tumor aggressiveness, therapy-induced genomic instability, and a poor prognosis in PC. It may serve as a clinically relevant biomarker across diverse treatment contexts.</p>","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical-Inflammatory Protection: Explaining Favorable Oncological Outcomes in Large Prostates.","authors":"Yu-Hsiang Lin, Jau-Yuan Chen, Chun-Te Wu","doi":"10.1002/pros.70041","DOIUrl":"https://doi.org/10.1002/pros.70041","url":null,"abstract":"","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Directed Evolution Restored Castrate Sensitivity in a Patient With Castrate Resistant Metastatic Prostate Cancer.","authors":"Robert A Gatenby, Alexander R A Anderson, Joel S Brown, Jill Gallaher, Jeffrey Krolick, Dawn Lemanne","doi":"10.1002/pros.70038","DOIUrl":"https://doi.org/10.1002/pros.70038","url":null,"abstract":"<p><strong>Objective: </strong>For centuries, humans have used directed evolution to promote desired traits in domesticated animals. We hypothesized similar strategies may be employed to steer castrate resistant prostate cancer cells to a castrate sensitive phenotype allowing resumption of Androgen Deprivation therapy (ADT) and prolonging survival.</p><p><strong>Methods: </strong>Our interdisciplinary team investigated directed evolution to restore castrate sensitivity in a patient with metastatic castrate resistant prostate cancer who could not tolerate available therapeutic agents for castrate resistant disease. Guided by an evolutionary mathematical model and using the PSA/testosterone ratio as a biomarker for intra-tumoral population dynamics, we applied a sequence of testosterone injections as evolutionary selection forces to suppress resistant androgen receptor-upregulated clones and promote proliferation of ADT-responsive clones.</p><p><strong>Results: </strong>When the PSA/testosterone ratio indicated successful transition to dominant castrate sensitive population, reinstitution of adaptive dosing of ADT has resulted in three stable cycles.</p><p><strong>Conclusion: </strong>This case suggests that evolution-informed strategies using population-based biomarkers to manipulate intra-tumoral evolution can restore castrate sensitivity in select patients.</p>","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144979126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prostate Volume and PSA-Density Estimation by Transabdominal Ultrasound: Prospective Evidence of Comparative Accuracy to MRI and Transrectal Ultrasound in Prostate Cancer Early Diagnostics.","authors":"Liza M Kurucz, Tiziano Natali, Sanne Westerhout, Marias Hagens, Jeroen J Visser, Erik A M van Muilekom, Jolien D van Kesteren, Ivo Schoots, Thierry N Boellaard, Georgios Agrotis, Behdad Dashtbozorg, Theo J M Ruers, Pim J van Leeuwen, Laura S Mertens","doi":"10.1002/pros.70036","DOIUrl":"10.1002/pros.70036","url":null,"abstract":"<p><strong>Background: </strong>Prostate-specific antigen (PSA) density is an easily available predictor for clinically significant PCa. While transrectal ultrasound (TRUS) is utilized for PSA density (PSAD) estimation, transabdominal ultrasound (TAUS) is a more accessible, noninvasive alternative that can be used to decide if follow-up diagnostics are necessary. This study aims to compare prostate volume (PV) and PSAD across TAUS, TRUS and MRI, comparing the clinical utility of TAUS and TRUS for PSAD-based risk stratification.</p><p><strong>Methods: </strong>Hundred and eighty men undergoing PCa diagnostics were included by collecting serum PSA, TRUS, MRI, and TAUS PV examinations. PV was calculated blindly by all operators and image quality was assessed. Agreement in PV measurements of all imaging modalities was analyzed in Bland-Altman diagrams. PCa risk derived from PSAD_TAUS and PSAD_TRUS was compared against MRI outcomes in Sankey diagrams and the percentage of misclassified PCa risk was reported.</p><p><strong>Results: </strong>After excluding 33 inadequate TAUS acquisitions, 147 patients were included. The average volume difference between TAUS and MRI was 2.5 mL (standard deviation (SD): 16.4), between TAUS and TRUS 11.5 mL (SD: 20.4), and between TRUS and MRI -9.0 mL (SD: 21.1). TAUS and TRUS underestimate PCa risk in 3%-4%, while the percentage of men with overestimated risk decreased when TAUS was used (7% vs. 13%).</p><p><strong>Conclusions: </strong>PVs obtained with TAUS are equivalent to MRI. Still, image quality varies with experience and interobserver variability needs further exploration, ensuring generalizable outcomes. Nevertheless, TAUS represents a valid alternative for PV and PSAD estimation, enabling a patient-friendly alternative for PCa risk assessment.</p>","PeriodicalId":54544,"journal":{"name":"Prostate","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144876883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}