Furthermore, we identify a synergistic antitumor effect between KPT-330 and translation inhibitors, including everolimus and homoharringtonine. Notably, the disruptive impact of KPT-330 on CRC homeostasis extends to other cancer cell lineages, underscoring its broad mechanistic relevance. Collectively, our findings elucidate a novel mechanism through which KPT-330 destabilizes CRC via translational dysregulation and highlight its potential therapeutic utility in combination regimens for DDLPS.

Importantly, LUCAT1 overexpression attenuates the MYCi975 anti-tumor effects on HNSCC, confirming its role in therapeutic resistance. These results establish LUCAT1 as both a biomarker of aggressive disease and a mediator of MYC-driven oncogenesis, proposing LUCAT1 as a candidate synergistic therapeutic target in the treatment of HNSCC with MYC inhibition.

P1, N=94, Not yet recruiting, Zhongda Hospital

P2, N=40, Enrolling by invitation, Guangdong Second Provincial General Hospital

PLD1-inhibitor remodeled phospholipid metabolism, induced ferroptosis and restored QUIZOM response in LSC. Our findings provided the therapeutic and resistant mechanisms of QUIZOM and paved the way for targeted interventions in this AML subtype.

P2, N=61, Not yet recruiting, First People's Hospital of Hangzhou

P2, N=35, Not yet recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University

In vivo, RRx-001 significantly inhibits tumor growth, enhances T-cell infiltration, promotes M1 macrophage polarization, downregulates PD-L1 expression, and strengthens anti-tumor immunity through T cell-related pathways. With both metabolic and immunomodulatory effects, RRx-001 provides a basis for novel HCC therapies, and future research could explore its synergistic effects with immune checkpoint inhibitors.

P1, N=12, Recruiting, OHSU Knight Cancer Institute | Not yet recruiting --> Recruiting | Initiation date: Aug 2025 --> Jan 2026

P1, N=6, Completed, University of Illinois at Chicago | Active, not recruiting --> Completed

All patients remained disease-free, with no events of measurable residual disease (MRD) positivity by flow cytometry or molecular analysis documented. These findings preliminarily confirm that venetoclax, cytarabine, and homoharringtonine-based cytoreductive therapy is a safe and effective bridging therapy for allo-HSCT in patients with refractory/relapsed AML and RUNX1::RUNX1T1 fusion gene.

Additionally, HHT inhibits NSCLC migration by modulating epithelial-mesenchymal transition (EMT) signaling. These findings highlight PDIA4 as a critical mediator of HHT efficacy against NSCLC, provide novel insights into PDIA4-associated therapy, and support the translational potential of HHT in NSCLC treatment.