cisplatin

This combinatorial strategy not only reduced tumor cell proliferation and promoted apoptosis but also enhanced autophagy. Collectively, our findings highlight the potential of combining Pla B with cisplatin as a novel and promising therapeutic approach for the treatment of HCC.

Here, it is demonstrated that tumor necrosis factor superfamily member 4 (TNFSF4/OX40L) significantly upregulates in proximal tubular cells (PTCs) from patients with CKD and in murine models of AKI-CKD transition induced by unilateral ischemia-reperfusion injury (uIRI) or repeated low-dose cisplatin...TNFSF4 blocks synaptotagmin-like protein 4 (SYTL4)-mediated ubiquitination of GSK-3α, prolongs its half-life, and sustains profibrotic signaling, effects reversed by GSK-3α knockdown. Collectively, these results uncover a previously unrecognized TNFSF4-GSK-3α axis as a key proximal tubule-intrinsic driver of AKI-CKD progression, and propose targeting this pathway as a promising therapeutic strategy to mitigate renal fibrosis and halt AKI-CKD transition.

Additionally, three cancer cell subpopulations with distinct chemosensitivity profiles were identified; Subpopulation 2, characterized by high expression of CCNA2, UBE2C, and CENPF, demonstrated significantly reduced sensitivity to methotrexate, doxorubicin, cisplatin, ifosfamide, and etoposide. This study provides a preliminary characterization of the metabolic landscape of OS and its associated immune microenvironment. Targeting SLC7A7-deficient monocytes may represent promising strategies for enhancing the efficacy of immunotherapy in OS.

Several derivatives, including spirooxindole-pyrrolidine hybrids, thiazolo-pyrrolidine-spirooxindolines, and dispirooxindolines, demonstrate superior activity compared with cisplatin and doxorubicin. Emerging synthetic strategies, particularly multicomponent reactions and click chemistry, further expand the scope of these molecules. Collectively, current findings underscore their potential as anticancer agents and the importance of future in vivo and pharmacokinetic studies to advance clinical translation.

In addition, silencing of CREB3L4 promoted apoptosis and inhibited cell proliferation, which was also associated with decreased BAG3 expression. Taken together, these findings indicate that depletion of CREB3L4 suppressed autophagy and reduced cisplatin resistance in GC cells by downregulating BAG3.

In vivo, onalespib remodels the tumor immune microenvironment, promotes CD8+ effector T-cell infiltration, and enhances the antitumor efficacy of cisplatin without compromising tolerability. Collectively, these findings define a functional HSP90-IDO1 regulatory axis and provide a mechanistic rationale for combination strategies targeting metabolic immune tolerance.

Our study reveals that H. pylori contribute to gastric carcinogenesis by activating the B4GALT5/YWHAZ/FOXO3a axis via specific glycosylation, suggesting YWHAZ N95 glycosylation as a potential therapeutic target for GC.

P1, N=288, Active, not recruiting, AbbVie | Trial completion date: Jun 2026 --> Nov 2027 | Trial primary completion date: Jun 2026 --> Nov 2027

P3, N=212, Recruiting, Sun Yat-sen University | Trial primary completion date: Dec 2025 --> Dec 2026

P2, N=30, Active, not recruiting, Columbia University | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026 | Recruiting --> Active, not recruiting

Treatments include surgery, radiation, and chemotherapy, with ongoing trials investigating agents like cetuximab, cisplatin, and Tazemetostat. Tazemetostat, targeting KMT2D-related DNA (deoxyribonucleic acid) methylation, and cetuximab, targeting the PIK3CA signaling cascade, may offer therapeutic benefits. Further research on mutation-specific therapies could improve treatment strategies.

Here, we show that direct physical contact between small cell lung cancer (SCLC) cells and lung fibroblasts induces early resistance to standard-of-care chemotherapeutic agents, etoposide and cisplatin. A high-throughput drug screening identified idarubicin as a compound that retains efficacy despite fibroblast-mediated protection, suggesting it could bypass microenvironment-induced resistance early on. Together, our findings identify direct tumor-fibroblasts contact as an early driver of chemoresistance and highlight a potential therapeutic strategy targeting cell-cell interactions within the tumor microenvironment.