Intraductal carcinoma of the prostate (IDC) and invasive cribriform carcinoma (invasive Crib) are closely related high-risk morphologies that frequently coexist and are associated with adverse pathology, early metastasis and disease-specific mortality across the prostate cancer continuum. These morphologies are common in intermediate- and high-risk disease, but remain under-recognized and inconsistently reported, contributing to undergrading and potentially inappropriate selection of patients for de-escalation strategies such as active surveillance or focal therapy. Biopsy detects these patterns in only about half of affected men, and magnetic resonance imaging (MRI)-targeted sampling does not reliably close this gap. These tumours are enriched for loss of the tumour-suppressor gene PTEN, DNA-damage-repair alterations and genomic instability, and are associated with immunologically 'cold', fibroblast-rich tumour niches. These findings provide a rationale for evaluating biomarker-directed strategies, including inhibition of the PARP and AKT pathways and therapies targeting B7-H3 (also known as CD276). However, definitive evidence that either IDC or invasive Crib predicts benefit from any of these treatments has not been established. A deeper understanding of the biological and clinical behaviour of these tumours, together with rigorous, standardized reporting, is essential for accurate risk stratification, rational use of active surveillance and focal approaches, selection of patients for intensified local and systemic treatment, and the design of biomarker-driven trials for this aggressive disease subset.

Lower urinary tract dysfunction (LUTD) substantially affects quality of life and is increasingly associated with metabolic syndrome (MetS). An intricate relationship exists between MetS components, such as obesity, diabetes, dyslipidaemia and hypertension, and bladder dysfunction. Insights from preclinical models show that MetS-driven autonomic dysfunction, increased intra-abdominal pressure, chronic bladder ischaemia, low-grade inflammation, dysregulated nutrient-sensing pathways and an altered oestrogen-to-testosterone ratio contribute to lower urinary tract symptoms. Diabetic models, such as streptozotocin-induced rodents and polygenic TallyHo mice, show biphasic diabetic LUTD progression, from detrusor hyperactivity to underactivity, driven by hyperglycaemia and neural degeneration. Obesity models, such as leptin-deficient ob/ob mice, undergo prostate and urethral changes exacerbating lower urinary tract symptoms, whereas dyslipidaemia models, such as Apoe[-/-] mice, show ischaemia-induced bladder remodelling. Hypertension and early-life stress further worsen LUTD through angiotensin-mediated pathways and visceral adiposity, respectively. Preclinical models provide important insights in this context but face limitations, including non-physiological bladder filling rates and interspecies differences, necessitating advanced approaches such as multi-omics and patient-derived urinoids. These tools could facilitate personalized therapies by elucidating disease mechanisms and enabling longitudinal monitoring but ethical challenges associated with clinical translation persist.

[This corrects the article DOI: 10.1177/17562872261449901.].