cisplatin

DLL1 drives cisplatin resistance in OV by enhancing ferroptosis resistance via the Notch-Nrf2/GPX4 axis. Targeting DLL1 alongside ferroptosis induction represents a promising therapeutic strategy, positioning DLL1 as a potential biomarker and target in drug-resistant OV.

ANXA3 plays a critical role in maintaining CSC‑like traits in osteosarcoma by up‑regulating the HIF‑1α/VEGF pathway in a PI3K/Akt/mTOR‑dependent manner. Targeting ANXA3 or its downstream signaling components may represent a promising therapeutic strategy for reversing CSC phenotypes and overcoming chemoresistance in osteosarcoma.

In vitro and in vivo experiments demonstrated the ability of C-L@F-siA4 to reverse the resistance and restore the effectiveness of cisplatin in treatment of esophageal cancer. This study provides a target for treating esophageal cancer with acquired cisplatin resistance and offers a strategy as an adjuvant method for chemotherapy of esophageal cancer.

In vivo, capivasertib significantly suppressed tumor growth and its combination with cisplatin significantly prolonged survival in xenograft models without inducing overt systemic toxicity. Mechanistically, capivasertib treatment increased AKT phosphorylation, consistent with pharmacodynamic target engagement, while suppressing downstream mTOR/4EBP1 signaling and inducing pro-apoptotic levels. Collectively, these findings demonstrate that Akt/mTOR inhibition by capivasertib enhances therapeutic efficacy in preclinical NPC models and provides rationale for further clinical evaluation of capivasertib in advanced NPC.

HET dose- and time-dependently reduced SAS-CR viability, inhibited clonogenic growth, and exhibited stronger cytotoxicity than cisplatin or 5-fluorouracil...Additionally, HET increased reactive oxygen species (ROS) production, whereas ROS scavenger N-acetylcysteine (NAC) attenuated HET-induced apoptosis and restored cuproptosis-related markers. In a zebrafish model, HET demonstrated negligible toxicity while reducing tumor-associated fluorescence and FDX1 expression. Collectively, HET effectively suppresses chemoresistant OSCC through coordinated ROS-dependent apoptosis and cuproptosis-associated mitochondrial stress, supporting its development as a therapeutic candidate for refractory OSCC.

P2, N=18, Completed, Memorial Sloan Kettering Cancer Center | Active, not recruiting --> Completed

P2, N=468, Completed, Bristol-Myers Squibb | Active, not recruiting --> Completed

P2, N=70, Recruiting, Innate Pharma | Trial completion date: Sep 2026 --> Jun 2027 | Trial primary completion date: Jun 2025 --> Jun 2027

P2, N=41, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: May 2026 --> May 2027 | Trial primary completion date: May 2026 --> May 2027

It also considerably reduced NF-kB p65 and inflammatory markers in comparison with cisplatin alone. Our study demonstrated that rhIGFBP-3 enhanced cisplatin efficacy by promoting apoptosis and attenuating inflammation, highlighting its potential as both a cisplatin adjuvant and a monotherapy in HeLa cells.

Tumor tissue and serial plasma samples were collected from 15 patients with aUC treated with dose-dense methotrexate, vinblastine, doxorubicin, and cisplatin (ddMVAC). While the NOIR-SS-based assay proved sensitive and informative, limitations include the cost and time required for sequencing, potential temporal discordance between tissue and plasma sampling, and the absence of correction for clonal hematopoiesis of indeterminate potential. Overall, ctDNA profiling using this targeted panel and NOIR-SS suggested the feasibility of sensitive, non-invasive molecular monitoring in aUC, and may have future clinical applicability if validated prospectively in larger cohorts.

Collectively, our findings establish the H3K18la-HNRNPF-Parkin axis as a previously unrecognized signaling cascade that bridges epigenetic reprogramming and mitochondrial quality control in chemoresistance. Targeting this axis, particularly the HNRNPF-Parkin interaction or mitophagy activation, presents a novel therapeutic strategy to overcome cisplatin resistance in BCa.