Purpose: Magnetic resonance imaging (MRI) targeted prostate biopsy has been shown to find many high-grade prostate cancers in men with concurrent negative transrectal ultrasound (TRUS) systematic biopsy. The oncologic risk of such tumors can be explored by looking at long-term outcomes of men with negative TRUS biopsy followed without MRI. The aim was to analyze the mortality after initial and second negative TRUS biopsy.
miR-615-3p has previously been described as up-regulated in prostate cancer (PC) tissue samples compared with nonmalignant controls; however, its prognostic potential and functional role in PC remain largely unknown. In this study, we investigated the clinical and biological relevance of miR-615-3p in PC. The expression of miR-615-3p was measured in PC tissue specimens from 239 men who underwent radical prostatectomy (RP), and it was investigated if miR-615-3p could predict postoperative biochemical recurrence (BCR). These findings were subsequently validated in three independent RP cohorts (n Z 222, n Z 273, and n Z 387) and functional overexpression studies conducted in PC cells (PC3M). High miR-615-3p expression was significantly associated with BCR in four independent PC patient cohorts (P < 0.05, log-rank test). In addition, high miR-615-3p expression was a significant predictor of PC-specific survival in univariate (hazard ratio, 3.75; P < 0.001) and multivariate (hazard ratio, 2.66; P Z 0.008) analysis after adjustment for the Cancer of the Prostate Risk Assessment Post-Surgical (CAPRA-S) nomogram in a merged RP cohort (n Z 734). Moreover, overexpression of miR-615-3p in PC cells (PC3M) significantly increased cell viability, proliferation, apoptosis, and migration. Together, our results suggest that miR-615-3p is a significant predictor of postoperative BCR and PC-specific survival and has oncogenic functions in PC cells.
AimsZinc-alpha 2-glycoprotein (AZGP1) is a promising tissue biomarker to predict outcomes in men undergoing treatment for localised prostate cancer (PCa). We aimed to examine the association between AZGP1 expression and the endpoints: risk of biochemical failure (BF), initiating castration-based treatment, developing castration-resistant PCa (CRPC) and PCa-specific mortality following radical prostatectomy (RP).MethodsThe study included a prospective cohort of 302 patients who underwent RP for PCa from 2002 to 2005. AZGP1 expression was analysed using immunohistochemistry on tissue microarray RP specimens and was scored semiquantitively as low or high expression. Risk of all endpoints was analysed using stratified cumulative incidences and cause-specific Cox regression, and validated with receiver operating curves, calibration and discrimination in competing-risk analyses. A meta-analysis was performed including previous studies investigating AZGP1 expression and risk of BF following RP.ResultsMedian time of follow-up was 14.0 years. The cumulative incidence of all endpoints was significantly higher in patients with low AZGP1 expression compared with patients with high AZGP1 expression (p<0.001). In a multivariate analysis, low AZGP1 expression increases the risk of BF (HR 2.7; 95% CI 1.9 to 3.8; p<0.0001), castration-based treatment (HR 2.2; 95% CI 1.2 to 4.2; p=0.01) and CRPC (HR 2.3; 95% CI 1.1 to 5.0; p=0.03). Validation showed a low risk of prediction error and a high model performance for all endpoints. In a meta-analysis, low AZGP1 was associated with BF (HR 1.7; 95% CI 1.2 to 2.5).ConclusionsLow AZGP1 expression is associated with the risk of aggressive time-dependent outcomes in men undergoing RP for localised PCa.
Postembolization syndrome (PES) is the most common side effect of vascular embolization of solid organs. The aim of this review was to determine the incidence of PES and its individual components after prostatic artery embolization (PAE). A systematic review with a pre-specified search strategy for PubMed, Embase, Web of Science and Cochrane Library was performed according to PRISMA guidelines. Studies in English regarding PAE in humans with 10 or more participants were eligible for inclusion. No restrictions on participant demographics or PAE technique were imposed. The search returned 378 references, of which 32 studies with a total of 2116 patients met the inclusion criteria. The results for overall PES frequency and individual PES components were presented as median (interquartile range, (IQR)). Overall median PES frequency was 25.5% (12.5–45.8). The two most frequent individual PES components were dysuria/urethral burning and local pain, with a median frequency of 21.7% (13.8–33.3) and 20% (5.4–29.4), respectively. Most outcome measures were characterized by a marked lack of uniformity and inconsistency in reporting across studies. Development of a uniform reporting system would help the clinicians recognize and treat PES accordingly.
Improved prostate cancer prognostic biomarkers are urgently needed. We previously identified the four-miRnA prognostic biomarker panel MiCaP ((miR-23a-3p × miR-10b-5p)/(miR-133a-3p × miR-374b-5p)) for prediction of biochemical recurrence (BCR) after radical prostatectomy (RP). Here, we identified an optimal numerical cutoff for MiCaP dichotomisation using a training cohort of 475 RP patients and tested this in an independent cohort of 281 RP patients (PCA281). Kaplan-Meier, uni-and multivariate Cox regression analyses were conducted for multiple endpoints: BCR, metastatic-(mPC) and castration-resistant prostate cancer (CRPC), prostate cancer-specific (PCSS) and overall survival (OS). Functional effects of the four MiCaP miRNAs were assessed by overexpression and inhibition experiments in prostate cancer cell lines. We found the numerical value 5.709 optimal for MiCaP dichotomisation. This was independently validated in PCA281, where a high MiCaP score significantly [and independent of the Cancer of the Prostate Risk Assessment Postsurgical (CAPRA-S) score] predicted BCR, progression to mPC and CRPC, and PCSS, but not OS. Harrell's C-index increased upon addition of MiCaP to CAPRA-S for all endpoints. Inhibition of miR-23a-3p and miR-10b-5p, and overexpression of miR-133a-3p and miR-374b-5p significantly reduced cell survival. Our results may promote future implementation of a MiCaP-based test for improved prostate cancer risk stratification. Prostate cancer is a significant healthcare problem, globally causing > 300,000 deaths/year 1. While many prostate cancers are indolent, a subset progress to metastatic (mPC) and castration-resistant (CRPC) disease, causing significant morbidity and mortality. Routine prognostic tools for early-stage prostate cancer are suboptimal, causing overtreatment of indolent prostate cancer and undertreatment of aggressive prostate cancer 2. Thus, novel prognostic biomarkers are urgently needed to improve risk stratification and guide individualised treatment. MicroRNAs (miRNAs) are small noncoding RNAs that bind complementary sequences in target messenger RNAs (mRNAs), inhibiting mRNA translation and stability 3. miRNAs regulate genes involved in key cellular processes, including differentiation, cell-cycle control, and migration. Furthermore, dysregulation of miRNA expression is a hallmark of cancer development and progression 3,4 , and miRNAs have shown promising prognostic biomarker potential in prostate cancer 5-9. We recently identified the four-miRNA prognostic model MiCaP ((miR-23a-3p × miR-10b-5p)/(miR-133a-3p × miR-374b-5p)) 9 as an independent predictor of biochemical recurrence (BCR) in radical prostatectomy (RP) patients 9. Here, to promote future clinical implementation of a MiCaP test, we identified an optimal numerical cutoff value for MiCaP dichotomisation using a merged training cohort of 475 RP patients (PCA475)
BACKGROUND:The oncological risks after benign histology on a transurethral resection of the prostate (TURP) remain largely unknown.Here, the risk of prostate cancer incidence and mortality following a benign histological assessment of TURP is investigated in a populationbased setting. METHODS: Between 1995 and 2016, 64,059 men in Denmark underwent TURP without prior biopsy of the prostate; 42,558 of these men had benign histology. The risks of prostate cancer, prostate cancer with a Gleason score ≥ 3 + 4, and prostate cancer-specific death were assessed with competing risks. Specific risks for pre-TURP prostate-specific antigen (PSA) levels at 10 and 15 years were visualized by locally estimated scatterplot smoothing. RESULTS: The median age at TURP was 72 years (interquartile range [IQR], 65-78 years), and the median follow-up was 15 years (IQR, 10-19 years). The 10-year risks of any prostate cancer and prostate cancer with a Gleason score ≥ 3 + 4 and the 15-year risk of prostate cancer death showed clear visual relations with increasing PSA. The 15-year cumulative incidence of prostate cancer-specific death after benign TURP was 1.4% (95% confidence interval [CI], 1.3%-1.6%) for all men and 0.8% (95% CI, 0.6%-1.1%) for men with PSA levels <10 ng/ml. The primary limitation was exclusion due to missing PSA data. CONCLUSIONS: Men with low PSA levels and a benign TURP can be reassured about their cancer risk and do not need to be monitored differently than any other men. Patients with high PSA levels can be considered for further follow-up with prostate magnetic resonance imaging. These findings add to the literature suggesting that normal histology from the prostate entails a low risk of death from the disease.
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