cytarabine

Given persistent cholestasis and bleeding risk, the patient underwent Roux-en-Y choledochojejunostomy for biliary decompression, followed by initiation of rituximab-cyclophosphamide-vincristine-doxorubicin-high-dose methotrexate/rituximab-ifosfamide-etoposide-high-dose cytarabine (R-CODOX-M/R-IVAC) with central nervous system prophylaxis...Ampullary BL should be considered in pediatric patients with obstructive jaundice and upper gastrointestinal bleeding. Surgical biliary decompression can stabilize cholestasis and facilitate timely multi-agent chemotherapy.

Venetoclax-based regimens, combined venetoclax with either hypomethylating agents or low-dose cytarabine, have markedly improved treatment outcomes in elderly patients with acute myeloid leukemia (AML). Importantly, the combination of bortezomib and venetoclax significantly prolongs the survival of mice inoculated with venetoclax-resistant AML cell line harboring BAX mutations, which are commonly observed in relapsed AML following venetoclax-based regimens and confer resistance to venetoclax by inhibiting BAX-dependent apoptotic pathway. Collectively, this study provides a rationale for venetoclax-bortezomib combination as a potential strategy to overcome venetoclax resistance in certain AML subsets.

P3, N=300, Not yet recruiting, Institute of Hematology & Blood Diseases Hospital, China | Initiation date: Jan 2026 --> Apr 2026

P=N/A, N=100, Not yet recruiting, Institute of Hematology & Blood Diseases Hospital, China

P3, N=468, Recruiting, Syndax Pharmaceuticals

These findings underscore the potential of GNL as a hepatoprotective drug against cytarabine-induced hepatotoxicity, mediated by its antioxidant and anti-inflammatory effects through modulation of the PI3K/AKT and NF-κB pathways. Future research should investigate its therapeutic potential in alleviating chemotherapy-induced liver damage.

Using an unbiased approach, we identify Src-family kinase member LYN, and guanine nucleotide-binding protein G(i) alpha subunit proteins, GNAI1, GNAI2, and GNAI3 as novel binding partners of MSLN in AML and show that pharmacological or genetic inhibition of LYN signaling restores NOMO-1 cell sensitivity to Ara-C. Together, these findings demonstrate that MSLN functions as an oncogenic driver in AML and reveal a previously unrecognized MSLN-LYN signaling axis, the therapeutic targeting of which may enhance responses to chemotherapy.

P2, N=20, Suspended, University of Michigan Rogel Cancer Center | Recruiting --> Suspended

P2, N=160, Active, not recruiting, Chinese PLA General Hospital | Recruiting --> Active, not recruiting | Trial primary completion date: Apr 2026 --> Sep 2025

P2, N=45, Recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University

P2, N=227, Completed, International Extranodal Lymphoma Study Group (IELSG) | N=126 --> 227

Analysis of primary AML samples or cell lines revealed that BMPR1B and TAZ/TEAD but not YAP levels were higher after patient relapse or in cells resistant to cytarabine or venetoclax. Finally, using a 3D human bone marrow-like model, we showed that targeting BMPR1B or TAZ/TEAD in combination with cytarabine impaired persistence of AML primary cells within the AML niche. Future therapeutic approaches could involve BMPR1B and/or TAZ/TEAD targeting in the context of AML patients refractory to chemotherapy or after relapse.