Oligometastatic prostate cancer (OMPC) has been proposed as an intermediary state between localised disease and widespread metastases, with varying definitions including 1, 3, or ≤5 visceral or bone metastasis. Traditional definitions of OMPC are based on staging with conventional imaging, such as computerised tomography (CT) and whole-body bone scan (WBBS). Novel imaging modalities such as prostate-specific membrane antigen positron emission tomography (PSMA PET) have improved diagnostic utility in detecting early metastatic prostate cancer (PC) metastases compared with conventional imaging. Specifically, meta-analytical data suggest that PSMA PET is sensitive in detecting oligometastatic disease in patients with biochemical recurrence (BCR) post-radical treatment of PC. Recent trials have evaluated PSMA PET-guided metastases-directed therapy (MDT) in oligometastatic recurrent disease, typically with salvage surgery or radiotherapy (RT). To date, these preliminary studies demonstrate promising results, potentially delaying the need for systemic therapy. We aim to report a comprehensive, multidisciplinary review of PSMA-guided MDT in OMPC. In this review, we highlight the utility of PMSA PET in biochemically recurrent disease and impact of PSMA PET on the definition of oligometastatic disease and outline data pertaining to PSMA-guided MDT.

Prostate cancer is the second most frequent cancer in men, with increasing prevalence due to an ageing population. Advanced prostate cancer is diagnosed in up to 20% of patients, and, therefore, it is important to understand evolving mechanisms of progression. Significant morbidity and mortality can occur in advanced prostate cancer where treatment options are intrinsically related to lipid metabolism. Dysfunctional lipid metabolism has long been known to have a relationship to prostate cancer development; however, only recently have studies attempted to elucidate the exact mechanism relating genetic abnormalities and lipid metabolic pathways. Contemporary research has established the pathways leading to prostate cancer development, including dysregulated lipid metabolism-associated de novo lipogenesis through steroid hormone biogenesis and β-oxidation of fatty acids. These pathways, in relation to treatment, have formed potential novel targets for management of advanced prostate cancer via androgen deprivation. We review basic lipid metabolism pathways and their relation to hypogonadism, and further explore prostate cancer development with a cellular emphasis.

Objectives: This study aimed to compare long‐term (≥ 5 years) functional outcomes and reoperation rates following holmium laser enucleation of prostate (HoLEP) vs GreenLight photoselective vaporisation of prostate (GLPVP).Methods: MEDLINE, Embase and Cochrane databases were searched from inception to December 2023. Included were randomised controlled trials (RCTs), cohort studies and case series studying HoLEP and/or GLPVP, where functional outcomes and reoperation rates were reported. Studies with <5‐year follow‐up were excluded. Evidence was synthesised as a comparison across all parameters. Quality of evidence was assessed with the Newcastle–Ottawa Scale.Results: Of 3047 records identified, 25 were eligible, including two RCTs, two cohort studies, one cross‐sectional study and 20 case series. Twenty‐three studies focused on HoLEP or GLPVP, whilst two were comparative studies. HoLEP demonstrated long‐term durability of outcomes and low reoperation rates (mean 4.1%, range 2.0%–6.3%) at a mean follow‐up of 7.3 years. GLPVP also had durable outcomes at 5‐year follow‐up, but inconclusive evidence for improvements at 10 years. Reoperation rates were also higher (mean 12.6%, range 3.8%–33.3%). This is in keeping with findings of comparative studies, where HoLEP demonstrated greater improvements in all functional parameters except PVR, and lower reoperation rates. Findings are limited by patient attrition, lack of comparative studies and long‐term data beyond 10 years. Three studies examined the 180‐W GLPVP model at 5 years showed superior durability to earlier 80‐W/120‐W models.Conclusions: Current evidence suggests that HoLEP provides significantly greater functional improvements and a lower reoperation rate when compared with the GLPVP 80‐W/120‐W model at 5‐year follow‐up. The 180‐W model is comparable with HoLEP based on limited data at 5 years, but there is a lack of data beyond 10 years for longer‐term functional outcomes.

Introduction: Urological cancers account for a significant portion of cancer diagnoses and mortality rates worldwide. The traditional treatment options of surgery and chemoradiation can have significant morbidity and become ineffective in refractory disease. The discovery of the CRISPR system has opened up new avenues for cancer research by targeting specific genes or mutations that play a role in cancer development and progression. In this review, we summarise the current state of research on CRISPR in urology and discuss its potential for improving the diagnosis and treatment of urological cancers. Methods: A comprehensive literature search was conducted on databases including PubMed, Embase, and Cochrane Library. The keywords included CRISPR and urology OR prostate OR renal OR bladder OR testicular cancer. Results: CRISPR has been used extensively in a preclinical setting to identify and target genes in prostate cancer, including AR, NANOG, ERβ, TP53, PTEN, and PD-1. Targeting PRRX2 and PTEN has also been shown to overcome enzalutamide and docetaxel resistance in vitro. In bladder cancer, CBP, p300, hTERT, lncRNA SNGH3, SMAD7e, and FOXA1 have been targeted, with HNRNPU knockout demonstrating tumour inhibition, increased apoptosis and enhanced cisplatin sensitivity both in vitro and in vivo. Renal cancer has seen CRISPR target VHL, TWIST1, PTEN, and CD70, with the first in-human clinical trial of Anti-CD70 CAR T cell therapy showing an excellent safety profile and durable oncological results. Lastly, testicular cancer modelling has utilised CRISPR to knockout FLNA, ASH2L, HMGB4, CD24, and VIRMA, with NAE1 found to be over-expressed in cisplatin-resistant germ cell colonies. Conclusions: CRISPR is a cutting-edge technology that has been used extensively in the pre-clinical setting to identify new genetic targets, enhance drug sensitivity, and inhibit cancer progression in animal models. Although CAR T cell therapy has shown promising results in RCC, CRISPR-based therapeutics are far from mainstream, with further studies needed across all urological malignancies.