ArticleBlood cancer discovery2022
Amplified EPOR/JAK2 Genes Define a Unique Subtype of Acute Erythroid Leukemia.
Article in Blood cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Complex Genomic Alterations in TP53-Mutated Myelodysplastic Syndrome and Acute Myeloid Leukemia Involving EPOR/JAK2 Amplification, ERG Copy Gains, and TCF3 Deletion.Genes, chromosomes & cancer · 2026Article
- Unraveling the role ofHemaSphere · 2026Review
- C-C motif chemokine receptor-like 2 promotes the interferon-γ signaling response in myeloid neoplasms with erythroid differentiation and mutatedHaematologica · 2026Article
- Article
- Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q.Blood cancer discovery · 2025Article
- Successful treatment of multi-hit TP53-mutated myelodysplastic syndromes with erythroid predominance using allogeneic stem cell transplantation and ruxolitinib.Annals of hematology · 2025Article
- The Molecular Pathology of Blood Cancer: A Comprehensive Review of Chromosome and Genetic Abnormalities and Their Clinical Utility.British journal of biomedical science · 2025Review
- Post-transplant transient abnormal myelopoiesis evolving from a GATA1 mutant clone in umbilical cord blood.Annals of hematology · 2024Article
- Article
- Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes.International journal of molecular sciences · 2024Review
- Erythroleukemia: Classification.EJHaem · 2023Article
- Article
- Article
- TP53-Mutated Myelodysplasia and Acute Myeloid Leukemia.Mediterranean journal of hematology and infectious diseases · 2023Review
- TP53-Mutated Myelodysplastic Syndrome and Acute Myeloid Leukemia: Biology, Current Therapy, and Future Directions.Cancer discovery · 2022Review
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Authors and funding
41 authors at 18 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute erythroid leukemia (AEL) is a unique subtype of acute myeloid leukemia characterized by prominent erythroid proliferation whose molecular basis is poorly understood. To elucidate the underlying mechanism of erythroid proliferation, we analyzed 121 AEL using whole-genome, whole-exome, and/or targeted-capture sequencing, together with transcriptome analysis of 21 AEL samples. Combining publicly available sequencing data, we found a high frequency of gains and amplifications involving EPOR/JAK2 in TP53-mutated cases, particularly those having >80% erythroblasts designated as pure erythroid leukemia (10/13). These cases were frequently accompanied by gains and amplifications of ERG/ETS2 and associated with a very poor prognosis, even compared with other TP53-mutated AEL. In addition to activation of the STAT5 pathway, a common feature across all AEL cases, these AEL cases exhibited enhanced cell proliferation and heme metabolism and often showed high sensitivity to ruxolitinib in vitro and in xenograft models, highlighting a potential role of JAK2 inhibition in therapeutics of AEL. SIGNIFICANCE: This study reveals the major role of gains, amplifications, and mutations of EPOR and JAK2 in the pathogenesis of pure erythroleukemia. Their frequent response to ruxolitinib in patient-derived xenograft and cell culture models highlights a possible therapeutic role of JAK2 inhibition for erythroleukemia with EPOR/JAK2-involving lesions. This article is highlighted in the In This Issue feature, p. 369.
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