ArticleBlood2020
Human erythroleukemia genetics and transcriptomes identify master transcription factors as functional disease drivers.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 61 citations in OpenAlex.
- Disruption of methionine metabolism drives erythroid cell fate reprogramming by remodeling the H3K4me3 landscape.The Journal of clinical investigation · 2026Article
- Development and Characterization of a Novel Congenital Acute Erythroid Leukemia Cell Line with Unique Features.Cancers · 2026Article
- The fluoroquinoline compound exerts anti-erythroleukemic effects by dual-targeting GLUT1 and the PI3K/AKT signaling pathway.Scientific reports · 2026Article
- Lactate-mediated macrophage polarization promotes splenomegaly in acute erythroleukemia.Cell death & disease · 2026Article
- Diagnosis and management of rare acute erythroid leukemia with hemophagocytic lymphohistiocytosis: a case report.Frontiers in oncology · 2026Article
- Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q.Blood cancer discovery · 2025Article
- Novel Mutations in Acute Erythroid Leukemia-A Case Report with Review of Literature.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025Article
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- Acute Erythroid Leukemia Post-Chemo-Radiotherapy and Autologous Stem Cell Transplantation Due to Multiple Myeloma: Tracing the Paths to Leukemic Transformation.International journal of molecular sciences · 2024Article
- Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes.International journal of molecular sciences · 2024Review
- The ETO2 transcriptional cofactor maintains acute leukemia by driving a MYB/EP300-dependent stemness program.HemaSphere · 2024Article
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- FLT3-targeted therapy restores GATA1 pathway function in NPM1/FLT3-ITD mutated acute myeloid leukaemia.EJHaem · 2023Article
- FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.Oncogene · 2023Article
- Var∣Decrypt: a novel and user-friendly tool to explore and prioritize variants in whole-exome sequencing data.Epigenetics & chromatin · 2023Article
- (R)-2-Hydroxyglutarate Inhibits KDM5 Histone Lysine Demethylases to Drive Transformation in IDH-Mutant Cancers.Cancer discovery · 2023Article
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- Erythroleukemia: Classification.EJHaem · 2023Article
- Autopsy findings of acute erythroid leukemia.Autopsy & case reports · 2023Article
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44 authors at 19 institutions in 12 countries.
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Abstract
Acute erythroleukemia (AEL or acute myeloid leukemia [AML]-M6) is a rare but aggressive hematologic malignancy. Previous studies showed that AEL leukemic cells often carry complex karyotypes and mutations in known AML-associated oncogenes. To better define the underlying molecular mechanisms driving the erythroid phenotype, we studied a series of 33 AEL samples representing 3 genetic AEL subgroups including TP53-mutated, epigenetic regulator-mutated (eg, DNMT3A, TET2, or IDH2), and undefined cases with low mutational burden. We established an erythroid vs myeloid transcriptome-based space in which, independently of the molecular subgroup, the majority of the AEL samples exhibited a unique mapping different from both non-M6 AML and myelodysplastic syndrome samples. Notably, >25% of AEL patients, including in the genetically undefined subgroup, showed aberrant expression of key transcriptional regulators, including SKI, ERG, and ETO2. Ectopic expression of these factors in murine erythroid progenitors blocked in vitro erythroid differentiation and led to immortalization associated with decreased chromatin accessibility at GATA1-binding sites and functional interference with GATA1 activity. In vivo models showed development of lethal erythroid, mixed erythroid/myeloid, or other malignancies depending on the cell population in which AEL-associated alterations were expressed. Collectively, our data indicate that AEL is a molecularly heterogeneous disease with an erythroid identity that results in part from the aberrant activity of key erythroid transcription factors in hematopoietic stem or progenitor cells.
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