ArticleProceedings of the National Academy of Sciences of the United States of America2020
Combined inhibition of JAK/STAT pathway and lysine-specific demethylase 1 as a therapeutic strategy in CSF3R/CEBPA mutant acute myeloid leukemia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- The dual roles of lysine-specific demethylase 1 (KDM1A/LSD1) in the modulation of tumor immune microenvironment and its inhibitors in colorectal cancer.Journal of molecular medicine (Berlin, Germany) · 2026Review
- CSF3R Mutations Imply Adverse Prognostic Impact in Adult Acute Myeloid Leukemia Patients: A Single-Center Retrospective Study.Cancer medicine · 2025Article
- Research progress on the mechanisms of CSF3R mutations in leukemogenesis and treatment strategies.Cancer cell international · 2025Review
- JAK/STAT in human diseases: a common axis in immunodeficiencies and hematological disorders.Frontiers in immunology · 2025Review
- A bibliometric analysis of drug resistance in immunotherapy for breast cancer: trends, themes, and research focus.Frontiers in immunology · 2024Article
- JAK/STAT blockade reverses the malignant phenotype of Hodgkin and Reed-Sternberg cells.Blood advances · 2023Article
- Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia.Molecular cancer research : MCR · 2023Article
- Pharmacological inhibition of LSD1 suppresses growth of hepatocellular carcinoma by inducing GADD45B.MedComm · 2023Article
- Spermatogenesis associated serine rich 2 like plays a prognostic factor and therapeutic target in acute myeloid leukemia by regulating the JAK2/STAT3/STAT5 axis.Journal of translational medicine · 2023Article
- LSD1 inhibition modulates transcription factor networks in myeloid malignancies.Frontiers in oncology · 2023Review
- Article
- PU.1 and MYC transcriptional network defines synergistic drug responses to KIT and LSD1 inhibition in acute myeloid leukemia.Leukemia · 2022Article
- Acute Myeloid Leukemia WithFrontiers in oncology · 2022Review
- The Ups and Downs of STAT Inhibition in Acute Myeloid Leukemia.Biomedicines · 2021Review
- From the (Epi)Genome to Metabolism and Vice Versa; Examples from Hematologic Malignancy.International journal of molecular sciences · 2021Review
- Risk Stratification of Cytogenetically Normal Acute Myeloid Leukemia With BiallelicFrontiers in oncology · 2021Article
- Review
- Epigenetic crosstalk between hypoxia and tumor driven by HIF regulation.Journal of experimental & clinical cancer research : CR · 2020Review
- JAK Inhibitors and Modulation of B Cell Immune Responses in Rheumatoid Arthritis.Frontiers in medicine · 2020Review
- Lysine-specific demethylase 1 as a therapeutic cancer target: observations from preclinical study.Expert opinion on therapeutic targetsArticle
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) is a deadly hematologic malignancy with poor prognosis, particularly in the elderly. Even among individuals with favorable-risk disease, approximately half will relapse with conventional therapy. In this clinical circumstance, the determinants of relapse are unclear, and there are no therapeutic interventions that can prevent recurrent disease. Mutations in the transcription factor CEBPA are associated with favorable risk in AML. However, mutations in the growth factor receptor CSF3R are commonly co-occurrent in CEBPA mutant AML and are associated with an increased risk of relapse. To develop therapeutic strategies for this disease subset, we performed medium-throughput drug screening on CEBPA/CSF3R mutant leukemia cells and identified sensitivity to inhibitors of lysine-specific demethylase 1 (LSD1). Treatment of CSF3R/CEBPA mutant leukemia cells with LSD1 inhibitors reactivates differentiation-associated enhancers driving immunophenotypic and morphologic differentiation. LSD1 inhibition is ineffective as monotherapy but demonstrates synergy with inhibitors of JAK/STAT signaling, doubling median survival in vivo. These results demonstrate that combined inhibition of JAK/STAT signaling and LSD1 is a promising therapeutic strategy for CEBPA/CSF3R mutant AML.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.