ArticleLeukemia2022
PU.1 and MYC transcriptional network defines synergistic drug responses to KIT and LSD1 inhibition in acute myeloid leukemia.
Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- KIT-dependent acute myeloid leukemias are responsive to LSD1 inhibition.Clinical epigenetics · 2026Article
- Spi-1 proto-oncogene regulates mRNA hypertranscription and malignant progression in head and neck cancer.Signal transduction and targeted therapy · 2026Article
- Intracellular protein editing enables incorporation of noncanonical residues in endogenous proteins.Science (New York, N.Y.) · 2025Article
- Targeting senescent stemlike subpopulations in Philadelphia chromosome-like acute lymphoblastic leukemia.Blood · 2025Article
- PSPC1 exerts an oncogenic role in AML by regulating a leukemic transcription program in cooperation with PU.1.Cell stem cell · 2025Article
- Single-cell CRISPR screening characterizes transcriptional deregulation in T-cell acute lymphoblastic leukemia.Haematologica · 2024Article
- The ncBAF Complex Regulates Transcription in AML Through H3K27ac Sensing by BRD9.Cancer research communications · 2024Article
- Article
- ARHGAP4 promotes leukemogenesis in acute myeloid leukemia by inhibiting DRAM1 signaling.Oncogene · 2023Article
- Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia.Molecular cancer research : MCR · 2023Article
- SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia.Cancer research · 2023Article
- LSD1 inhibition modulates transcription factor networks in myeloid malignancies.Frontiers in oncology · 2023Review
- Article
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Responses to kinase-inhibitor therapy in AML are frequently short-lived due to the rapid development of resistance, limiting the clinical efficacy. Combination therapy may improve initial therapeutic responses by targeting pathways used by leukemia cells to escape monotherapy. Here we report that combined inhibition of KIT and lysine-specific demethylase 1 (LSD1) produces synergistic cell death in KIT-mutant AML cell lines and primary patient samples. This drug combination evicts both MYC and PU.1 from chromatin driving cell cycle exit. Using a live cell biosensor for AKT activity, we identify early adaptive changes in kinase signaling following KIT inhibition that are reversed with the addition of LSD1 inhibitor via modulation of the GSK3a/b axis. Multi-omic analyses, including scRNA-seq, ATAC-seq and CUT&Tag, confirm these mechanisms in primary KIT-mutant AML. Collectively, this work provides rational for a clinical trial to assess the efficacy of KIT and LSD1 inhibition in patients with KIT-mutant AML.
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Registered trials
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.