Among cisplatin-ineligible patients with MIBC, nivolumab alone was well tolerated. Ipilimumab/nivolumab caused toxicity that delayed cystectomy. Cases of progression before cystectomy indicated insufficient efficacy of pure neoadjuvant immunotherapy for unselected patients. Despite low response rates, some patients experienced sustained clinical CRs without cystectomy.
P2, N=82, Active, not recruiting, Canadian Cancer Trials Group | Trial completion date: Mar 2026 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Jun 2026
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Trial completion date • Trial primary completion date
In vivo studies using mouse models further supported these findings, showing that ERBB2 mutations promote tumor growth, metastasis, and macrophage infiltration. Collectively, these results suggest that ERBB2 mutations drive NMIBC progression by stabilizing HIF-1 through phosphorylation, thereby facilitating tumor development and immune modulation, and underscore the potential of ERBB2 as a therapeutic target for preventing NMIBC recurrence and metastasis.
Remarkably, nanoscale multivalent assemblies of R11 amplify these effects through enhanced multivalent binding to actin. This study unveils a new strategy for cytoskeleton-targeted intervention through peptide-based precision materials, highlighting R11 assemblies as a promising therapeutic platform for the treatment of metastatic BCa and potentially other cytoskeleton-dependent malignancies.
Functional characterization showed that RNF11 regulates proliferation and migration of bladder cancer. These findings highlight the prognostic value of CAF signatures and provide a framework for precision medicine approaches in bladder cancer management.
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FOXA1 (Forkhead Box A1) • LRIG1 (Leucine Rich Repeats And Immunoglobulin Like Domains 1)
Functional assays further demonstrate that YTHDF3 knockdown enhances cisplatin sensitivity in bladder cancer cells and xenograft tumors, whereas enforced expression of KDM6B or CDKN1A phenocopies the cisplatin-sensitizing effect of YTHDF3 knockdown. Collectively, our findings define a lactate-AARS2-YTHDF3-KDM6B-CDKN1A axis that integrates metabolic reprogramming, m6A-dependent epitranscriptomic regulation, and epigenetic chromatin remodeling to drive cisplatin resistance in bladder cancer.
This was confirmed by pathway inhibitors (Dorsomorphin, ESI-09) and siRNA knockdown, which reversed cell cycle arrest and reduced cytotoxicity...Crucially, AMPK inhibition attenuated Ad-VT's antitumor effects. These results demonstrate that Ad-VT exerts potent, tumor-selective activity against bladder cancer by inducing cAMP-dependent AMPK-Raptor-mTOR signaling and G2/M arrest, supporting its therapeutic potential.