Conventionally, transrectal ultrasound guided prostate biopsy (TRUS-Bx) was the main technique used for the diagnosis of prostate cancer since it was first described in 1989 [1]. However, the PROMIS trial showed that this random, nontargeted approach could miss up to 18% of clinically significant cancer (csPCa) [2]. Furthermore, risk of sepsis post TRUS-Bx can be as high as 2.4% [3]. Understanding the demerits of TR-biopsy have led to the introduction of transperineal prostate biopsy (TP-Bx). The incorporation of mpMRI revolutionized prostate cancer diagnostics, allowing visualization of areas likely to harbor csPCa whilst permitting some men to avoid an immediate biopsy. Furthermore, the advent of prostate specific membrane antigen-positron emission tomography (PSMA-PET) is highly promising, because of its role in primary diagnosis of prostate cancer and its higher diagnostic accuracy over conventional imaging in detecting nodal and metastatic lesions. Our narrative review provides an overview on prostate biopsy techniques and an update on prostate imaging, with particular focus on PSMA-PET.
Urothelial bladder cancer is a major cause of morbidity and mortality worldwide, causing an estimated 150 000 deaths per year. Whilst non-muscle-invasive bladder tumours can be effectively treated, with high survival rates, many tumours recur, and some will progress to muscle-invasive disease with a much poorer long-term prognosis. Thus, there is a pressing need to understand the molecular transitions occurring within the progression of bladder cancer to an invasive disease. Tumour invasion is often associated with a down-regulation of E-cadherin expression concomitant with a suppression of cell:cell junctions, and decreased levels of E-cadherin expression have been reported in higher grade urothelial bladder tumours. We find that expression of E-cadherin in a panel of bladder cancer cell lines correlated with the presence of cell:cell junctions and the level of PAK5 expression. Interestingly, exogenous PAK5 has recently been described to be associated with cell:cell junctions and we now find that endogenous PAK5 is localised to cell junctions and interacts with an E-cadherin complex. Moreover, depletion of PAK5 expression significantly reduced junctional integrity. These data suggest a role for PAK5 in maintaining junctional stability and we find that, in both our own patient samples and a commercially available dataset, PAK5mRNA levels are reduced in human bladder cancer compared with normal controls. Taken together, the present study proposes that PAK5 expression levels could be used as a novel prognostic marker for bladder cancer progression.