ArticleLeukemia2024
Combination of menin and kinase inhibitors as an effective treatment for leukemia with NUP98 translocations.
Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Discovery and preclinical activity of the menin-KMT2A inhibitor ziftomenib in acute leukemia models.Blood · 2026Article
- Menin inhibitors as a treatment for acute leukemia: from bench to the clinic.Blood neoplasia · 2026Review
- Menin Inhibition in Acute Myeloid Leukemia: Rewiring Leukemic Transcriptional Networks.International journal of molecular sciences · 2026Review
- Advances in targeted therapies for pediatric tumors.Acta pharmacologica Sinica · 2026Article
- [Prognostic analysis of NUP98 rearrangement in patients with pediatric acute myeloid leukemia undergoing allogeneic hematopoietic stem cell transplantation].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- Targeted therapies reshape extracellular matrix remodeling and microenvironmental regulation in pediatric acute myeloid leukemia.Discover oncology · 2026Article
- Strategies for identifyingHaematologica · 2026Article
- Targeting the Menin-KMT2A interaction in leukemia: Lessons learned and future directions.International journal of cancer · 2026Review
- RareAmerican journal of cancer research · 2026Article
- The promise of menin inhibitors: from approval to triplet regimens.Hematology. American Society of Hematology. Education Program · 2025Review
- Targeting menin in lysine methyltransferase 2A/nucleophosmin-mutated leukemia: A novel strategy from epigenetic dysregulation to clinical therapy (Review).Oncology letters · 2025Review
- Transcriptional condensates and the nuclear pore complex regulate gene expression and 3D genome architecture in response to stress.Biochemical Society transactions · 2025Review
- Inhibition of EYA family tyrosine phosphatase activity reveals a therapeutic vulnerability and enhances Menin and DOT1L inhibitor efficacy in KMT2A-rearranged leukemia.Experimental hematology & oncology · 2025Article
- One step further in targeting acute leukemia by combining antibody-based immunotherapies and small molecule inhibitors.Cancer cell international · 2025Review
- Menin: from molecular insights to clinical impact.Epigenomics · 2025Review
- Complete remission ofHaematologica · 2025Article
- Review
- Menin Inhibitors: New Targeted Therapies for Specific Genetic Subtypes of Difficult-to-Treat Acute Leukemias.Cancers · 2025Review
- NUP98 is rearranged in 5.0% of adult East Asian patients with AML.Blood advances · 2024Article
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Authors and funding
9 authors.
Funding
Abstract
Chromosomal translocations of the nucleoporin 98 (NUP98) gene are found in acute myeloid leukemia (AML) patients leading to very poor outcomes. The oncogenic activity of NUP98 fusion proteins is dependent on the interaction between Mixed Lineage Leukemia 1 and menin. NUP98-rearranged (NUP98-r) leukemia cells also rely on specific kinases, including CDK6 and/or FLT3, suggesting that simultaneous targeting of these kinases and menin could overcome limited sensitivity to single agents. Here, we found that combinations of menin inhibitor, MI-3454, with kinase inhibitors targeting either CDK6 (Palbociclib) or FLT3 (Gilteritinib) strongly enhance the anti-leukemic effect of menin inhibition in NUP98-r leukemia models. We found strong synergistic effects of both combinations on cell growth, colony formation and differentiation in patient samples with NUP98 translocations. These combinations also markedly augmented anti-leukemic efficacy of menin inhibitor in Patient Derived Xenograft models of NUP98-r leukemia. Despite inhibiting two unrelated kinases, when Palbociclib or Gilteritinib were combined with the menin inhibitor, they affected similar pathways relevant to leukemogenesis, including cell cycle regulation, cell proliferation and differentiation. This study provides strong rationale for clinical translation of the combination of menin and kinase inhibitors as novel treatments for NUP98-r leukemia, supporting the unexplored combinations of epigenetic drugs with kinase inhibitors.
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