Bladder Cancer

Muscle-invasive bladder cancer(MIBC)carries a high risk of recurrence.The standard treatment has been cisplatin-based neoadjuvant chemotherapy(NAC)followed by radical cystectomy(RC), but nearly half of patients are cisplatin-ineligible and unable to receive optimal NAC.Furthermore, recurrence after NAC plus RC remains common, highlighting the need for effective adjuvant strategies.Recent advances in immune checkpoint inhibitors(ICIs)have revolutionized perioperative treatment paradigms.The phase Ⅲ CheckMate 274 trial demonstrated that adjuvant nivolumab significantly prolonged disease-free survival(DFS), particularly in PD-L1-positive patients.In the IMvigor010 trial, adjuvant atezolizumab did not improve DFS in the overall population, but a biomarker-driven subanalysis revealed marked benefit in patients with postoperative circulating tumor DNA(ctDNA)positivity.Based on these findings, the ongoing IMvigor011 trial restricts adjuvant atezolizumab to ctDNA-positive patients.The NIAGARA trial evaluated a comprehensive perioperative approach using neoadjuvant gemcitabine-cisplatin plus durvalumab followed by adjuvant durvalumab for 1 year.This regimen significantly improved DFS, overall survival(OS), and pathological complete response(pCR)rates without increasing Grade ≥3 toxicities.ctDNA has emerged as a promising biomarker for risk stratification and treatment monitoring, potentially enabling precision perioperative immunotherapy.This review summarizes pivotal phase Ⅲ trials of perioperative ICI therapy in MIBC and discusses the role of ctDNA-guided strategies, envisioning a shift from universal ICI administration to biomarker-driven, individualized perioperative approaches.

This suggests that besides SMARCA4 deficiency, alterations in other genes may cooperatively contribute to the tumorigenesis of bladder undifferentiated tumors. These findings provide a reference for subsequent exploration of precise diagnostic and prognostic assessment and treatment strategies for this disease.

Its structure is highly complex and comprises a Bicycle connected to microtubule inhibitor monomethyl aurostatin-E (MMAE) via a molecular spacer and a cleavable linker. This provides a unique challenge in structural elucidation, and this report shows a strategy to overcome this using an incremental, nuclear magnetic resonance spectroscopy-based approach, which may be applied to complex structures of a similar nature.

Compared with the distal approach, the pubic superior ramus approach for obturator nerve block provides more efficient blockade and superior multidimensional perioperative benefits, making it an optimal technique for TURBT within enhanced recovery protocols.

Therefore, further investigation of how PRIM1 is regulated in this cancer type is essential. This association between PRIM1 and advanced urothelial carcinoma highlights the crosstalk between DNA replication machinery and genetic mutations in bladder cancer, which may open new possibilities for targeted therapies and biomarker discovery.

Both components showed concordant aberrant tumor-suppressor immunoprofiles (p53 overexpression and Rb loss), and high-risk HPV RNA in situ hybridization (RNAscope) was negative. This case expands the recognized morphologic spectrum of bladder neuroendocrine carcinoma to include POU2F3-defined non-small cell neuroendocrine carcinoma with basaloid architecture, supporting the practical value of incorporating POU2F3 into immunohistochemical panels for poorly differentiated basaloid bladder tumors.

In vivo, AGTR1 facilitated early tumor engraftment and promoted tumor progression, accompanied by reduced E-cadherin and elevated N-cadherin expression, with most of these changes suppressed by LOS treatment. In conclusion, our findings highlight the crucial role of AGTR1 in bladder cancer and support the repositioning of ARBs, such as LOS, as therapeutics for AGTR1-upregulated bladder cancer, while underscoring the importance of AGTR1 stratification for future clinical evaluation.

Finally, we propose a novel treatment strategy involving the synergistic inhibition of bladder cancer cell growth by combining TAK-901 with Afatinib. Our research strongly suggests that Aurora A and Aurora B are promising epigenetic therapeutic targets in bladder cancer. Furthermore, TAK-901 can function as a targeted kinase inhibitor and EGFR inhibitor for the treatment of bladder cancer by activating the FOXO signaling pathway, which induces apoptosis in bladder cancer cells.

Addition of DV to BCG provided favorable early response and superior intermediate-term RFS for BCG-naïve HER2-expressing HR-NMIBC, highlighting its prospect in HR-NMIBC management.

P=N/A, N=105, Recruiting, AstraZeneca | N=384 --> 105

Primary and secondary pseudo-stability/progression occur in a non-trivial proportion of patients across cancer types. Outcomes after pseudo-stability/progression are dependent on cancer type and initial response. Uncovering the clinical and molecular features of pseudo-stability/progression subtypes may guide treatment decisions and identify patients who may benefit from continued immunotherapy despite radiographic progression.

POSTN+ CAFs drive BCa progression by enhancing angiogenesis, migration, and immune suppression, mediated partly by the IL1B/IL1R1 axis.