P2, N=220, Active, not recruiting, Janssen Research & Development, LLC | Trial completion date: Jul 2027 --> Sep 2027 | Trial primary completion date: Sep 2024 --> Jul 2025

This study provides a comprehensive multi-omics-based framework for understanding cisplatin resistance in OSCC. DUSP3 was identified as a key prognostic indicator, and the proposed nomogram may enhance precision oncology efforts for cisplatin-resistant OSCC patients.

Furthermore, combining TNK2/ACK1 inhibitors with anti-PD-1 immunotherapy or with nab-paclitaxel plus gemcitabine demonstrates promising antitumor efficacy in both allograft and spontaneous PDAC models. Overall, our findings reveal a mechanism of immune evasion and provide a potential framework for developing tailored immunotherapeutic strategies in PDAC.

Since cellular senescence is a key event induced by temozolomide and radiation in GBM cells, it is reasonable to conclude that glioma cells cannot be completely eliminated, neither by radiation or chemotherapy alone nor in combination. Based on the data, new treatment options with senopreventics, senolytics and senostatics/senomorphics as important supportive medication during or after radiochemotherapie are discussed.

Given its crucial role in mediating DNA damage responses, we analyzed the p53 protein functionality and downstream target activation in a panel of UM cell lines in response to standard-of-care treatments (i.e., cisplatin and proton-beam irradiation)...Our results indicated a correlation between higher expression levels of Δ40p53α or Δ133p53γ isoforms and the development of more aggressive cancers. Our findings suggest that shorter p53 isoforms can promote cancer aggressiveness and therapy resistance, thereby providing crucial insights into UM pathogenesis.

Moreover, NR significantly potentiated gemcitabine efficacy both in vitro and in subcutaneous PDAC models, demonstrating synergistic enhancement of chemotherapy-induced tumor cell death. These findings establish NR as a promising SIRT3-targeting adjuvant that both enhances the efficacy of standard chemotherapy and delays carcinogenesis, thereby overcoming therapeutic resistance in established PDAC and potentially impeding its development.

Exploratory analysis indicates that responders show significantly higher tumor PD-L1 expression than non-responders do, with median tumor proportion scores of 8% and 2%, respectively. The study is registered at ClinicalTrials.gov (NCT05236699).

As a primary chemotherapy agent for NSCLC, gemcitabine (GEM) suppresses RNA/DNA synthesis to trigger cancer cell apoptosis...In vivo assessment substantiated significantly enhanced tumor regression with ferroptosis promotion. These findings nominate BT-GEM/MZ1@NP as a promising clinical candidate for NSCLC therapy.

Administering after CDK4/6i and capecitabine, VNR-GEMQ2W regimen shows activity in HR + /HER2- ABC and a manageable safety profile. This regimen should be considered as a potential control arm in the design of future clinical trials targeting HR + /HER2- ABC.

At the last follow-up in August 2025, the patient had a progression-free survival (PFS) of 29.8 months, with no evidence of recurrence in the lung lesions. This case demonstrates the efficacy of a multimodal induction chemoimmunotherapy in achieving complete response and preserving organ function, thereby providing a promising therapeutic option for patients with synchronous lung and base-of-tongue SCC.

Adjuvant chemotherapy with TMZ (Temozolomide) does not improve the survival of patients suffering from GBM (Glioblastoma)...Increased XBP-1s expression might contribute to the enhanced TMZ sensitivity. This combination therapy is promising for TMZ-resistant cancers, but it needs further investigation.

TSN selectively sensitized bladder cancer cells to UVC-induced cytotoxicity (IC50 decreased 35%, P = 0.026, n = 3), without affecting the viability of human urothelial cell SV-HUC-1 cells or lung adenocarcinoma A549 cells (both P > 0.05, n = 3). TSN inhibits FA DNA repair signaling in bladder cancer by suppressing JAK/STAT1-mediated FA core gene transcription, supporting its potential as a combinatorial agent to overcome cisplatin resistance.