Genito-urinary Cancer

These findings suggest that CacyBP/SIP may play a critical role in urothelial carcinoma progression by modulating ERK1/2 and p38 kinase activity.

The analysis covers conventional NK-based strategies, the engineering and 'armouring' of CAR-NK platforms to overcome the immunosuppressive tumour microenvironment, and preclinical and early clinical advances with target antigens like CAIX, CD70, PSMA, and nectin-4 across different urological malignancies. We conclude that while CAR-NK therapy represents a promising 'off-the-shelf' modality for these cancers, its success in solid tumours hinges on next-generation designs that solve critical challenges of in vivo persistence, efficient tumour homing, and resistance to local metabolic and immunosuppressive pressures.

In contrast, under standard low-Cu conditions, CTR1 remains required for cellular Cu uptake and CuCOX metallation. Together, these findings define context-dependent Cu trafficking pathways in renal cancer and establish SEC-ICP-MS as a sensitive platform for assessing CuCOX metallation and mitochondrial metabolism, with potential applications in biomarker discovery and therapeutic targeting in RCC.

All patients with follow-up data were alive without evidence of disease progression. Our findings expand the clinical, histologic, immunohistochemical, and molecular spectrum of ELOC-mutated RCC and further support its classification as a distinct renal neoplasm.

Our work further demonstrates that M1C integrates L1 and HERV-K activation with induction of APOBEC3 (A3) genes that evolved to restrain genomic instability induced by these retrotransposons. Of translational relevance, these findings demonstrate that M1C (i) is essential for inducing L1, HERV-K and A3 expression and resistance of CRPC cells to olaparib, and (ii) is a target for advancing the treatment of HR-competent CRPC with PARP inhibitors.

Moreover, KCNN4 knockdown suppresses tumor growth and synergizes with enzalutamide in xenograft models, underscoring the therapeutic potential of targeting the p300-KCNN4 axis. Collectively, our findings reveal a previously unrecognized epigenetic regulatory mechanism coupling p300-mediated acetylation to potassium channel stability, providing a promising therapeutic strategy to overcome chemoresistance in advanced prostate cancer.

Third, we perform a cistrome-wide association study in ccRCC, validating five established RCC risk loci and identifying six novel loci, including a locus at 12q24 linked to SCARB1 that was functionally validated. These datasets provide new perspectives on the role of developmental pathways in ccRCC tumorigenesis, insights into epigenetic mechanisms of ccRCC heritability, and a comprehensive epigenomic atlas for the research community.

P=N/A, N=450, Recruiting, Origin Sciences | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Jun 2025 --> Jul 2027

A 10% failure rate related to pre-analytical artifacts was observed and is an area for improvement in our practices. Thus, the effectiveness of digital pathology and the use of AI models are closely dependent on pre-analytical quality and its organizational integration.

For HRRm-positive mCRPC, TALA+ENZA provided survival and QALY gains compared with ENZA alone but at higher cost, resulting in an ICER exceeding typical U.S. WTP thresholds.