Bladder Cancer

The patient was managed by transurethral resection of bladder tumor (TURBT) followed by targeted therapy with sunitinib (37.5 mg)...ccRCC can metastasize to unusual sites, including the urinary bladder. Early recognition through comprehensive imaging and immunohistochemical evaluation is essential for timely diagnosis and management.

Despite treatment with corticosteroids, plasma exchange, cyclophosphamide and eculizumab he remained dialysis-dependent. PD-1 inhibitors, such as pembrolizumab, are known to predispose to loss of tolerance and generation of autoantibodies. In this case, factor B autoantibodies were detected in association with C3GN.

Additionally, copy number variations (CNVs) were evaluated, identifying chromosomal losses (e.g., Y chromosome, 1p12, 9p21.2-p21.3) and gains (e.g., 1q21.3, 6p22.3). This study establishes a foundational dataset for Bangladeshi bladder cancer patients, paving the way for further validation experiments in vitro, and the possibility of developing population-specific molecular biomarker panels, these insights may also contribute to personalized treatment strategies and help combat rising morbidity and recurrence rates of bladder cancer in Bangladesh.

Notably, combination therapy targeting B7x alongside PD-1/PD-L1 or CTLA-4 blockade reduced tumor burden and overcame resistance to monotherapy. These findings establish B7x as a substantial driver of immune evasion in bladder cancer and highlight its potential as a therapeutic target to improve immune checkpoint blockade efficacy in MIBC.

Genetic depletion of IGF2BP3 or CCN2 abrogates THAP7-AS1-driven invasive and metastatic phenotypes, whereas CCN2 re-expression partially rescues the effects of THAP7-AS1 silencing. Collectively, these findings define a THAP7-AS1-IGF2BP3-m6A-CCN2 axis that couples post-transcriptional mRNA stabilization to lymphatic metastasis and nominate THAP7-AS1 as a potential biomarker and therapeutic target in BCa.

These exploratory data support that pre-BCG microbial features may be related to early response, and post-BCG profiles may reflect durability and survival. Urine immune-microbiome profiling could be a feasible, noninvasive adjunct for monitoring and risk stratification in NMIBC.

Crucially, the TIMP1 inhibitor FXR agonist 3 suppressed MSCs-driven BC proliferation in vitro and attenuated tumor growth in PDX models by disrupting the cMet-RAP1 signaling pathway without systemic toxicity. Our findings propose targeting the MSCs-TIMP1-RAP1 axis as a novel therapeutic strategy for BC.

Our findings demonstrate that ATAD3A drives BCa progression by promoting USP10-mediated stabilization of MYC and enhancing glycolytic reprogramming. The ATAD3A-USP10-MYC axis represents a potential therapeutic target for BCa.

We identified cytarabine and methotrexate as significantly more effective in the 9p21 compromised BLCA cells. Analysis of morphological alterations further supported a genotype-specific activity of nucleoside analogs, nominating gemcitabine as a drug with greater efficacy in this context...Synergy between cytarabine and inhibitors of PRMT5 (MRTX1719) and MAT2A (AG-270) was mediated by a differential activation of DNA damage and replication stress markers, suggesting an exploitable vulnerability. In fact, rational drug combinations with ATR/CHK1 pathway inhibitors increased efficacy while maintaining 9p21-specificity. Finally, we confirmed the effectiveness of these combinations in cell models of pancreatic adenocarcinoma and pleural mesothelioma, two tumor types with high prevalence of MTAP loss and, most notably, in bladder cancer patient-derived organoids, underscoring the strong translational potential of our findings.

These findings advance our understanding of genetic susceptibility to different cancers. Future work in larger, more diverse GWAS, coupled with more comprehensive annotation atlases, is essential to expand upon and validate our results.

Cancer cachexia is highly prevalent in patients with bladder cancer receiving first-line chemotherapy and is independently associated with reduced survival, regardless of onset timing. Early identification may improve risk stratification and guide supportive interventions.

Bioinformatic and experimental analyses further showed that NUPR1 was associated with immunosuppressive infiltration and promoted M2 macrophage polarization. Together, our findings uncover an ARIH2-NUPR1 regulatory axis that drives BLCA progression by suppressing ferroptosis and favouring an immunosuppressive microenvironment, highlighting this pathway as a potential therapeutic target in BLCA.