Bladder Cancer

P=N/A, N=150, Recruiting, Janssen Research & Development, LLC | Not yet recruiting --> Recruiting

P1, N=19, Completed, Memorial Sloan Kettering Cancer Center | Active, not recruiting --> Completed

P=N/A, N=8000, Recruiting, UMC Utrecht | Trial completion date: May 2025 --> Aug 2030 | Trial primary completion date: Feb 2024 --> Feb 2030

Furthermore, the platform was extended to achieve site-specific m6A quantification, revealing upregulated methylation at specific sites of CDCP1 mRNA in bladder cancer cells and let-7a-5p miRNA in colorectal cancer cells compared with normal epithelial cells. Overall, this IDNP-mediated nFCM assay platform provides a powerful and versatile approach for rapid, simple, and multiplexed biochemical analysis, showing broad potential in biomedical and clinical applications.

Both in vitro and in vivo experiments confirmed that targeted inhibition of CALR effectively suppresses BLCA growth. This study not only elucidates the mechanism by which CALR maintains high expression through the CALR/HIF-1α positive feedback loop and promotes malignant progression in BLCA but also provides a theoretical foundation for its potential use as a prognostic biomarker and therapeutic target.

High clinical suspicion is required in patients with BCG therapy history presenting with spinal symptoms. Early recognition and appropriate treatment are crucial, though surgical intervention may be necessary for progressive deformity.

The findings of this study suggest that the presence of TLS-like lymphocyte aggregates observed on routinely used hematoxylin and eosin-stained slides of RC specimens may be an important predictor of survival outcomes after RC.

P=N/A, N=72, Active, not recruiting, University College Cork | Recruiting --> Active, not recruiting | Trial primary completion date: Nov 2025 --> Mar 2026

In particular, the dynamic interplay between tumor cell metabolic reprogramming and the immune suppressive tumor microenvironment, collectively termed the "metabolic-immune axis", constitutes a major challenge underlying drug resistance. This review summarizes how this axis, through mechanisms such as enhanced glycolysis and abnormal amino acid/lipid metabolism, influences bladder cancer progression and treatment responsiveness, thereby establishing a theoretical framework for future research directions.

P2, N=131, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Feb 2026 --> Feb 2027 | Trial primary completion date: Feb 2026 --> Feb 2027

In vitro experiments demonstrated that ARHGEF18 knockdown and YPEL5 overexpression led to decreased cell proliferation, migration, invasion, and increased apoptosis in T24 and 5637 bladder cancer cells. Our findings identify ARHGEF18 and YPEL5 as genetically and transcriptionally supported regulators of bladder cancer, highlighting a scalable strategy for linking genetic risk to cell-type-specific mechanisms.