ArticleLeukemia2024
Characterization of myeloproliferative neoplasms based on genetics only and prognostication of transformation to blast phase.
Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Clonal Metamorphosis: Deconstructing MPN Evolution with Single-Cell and Spatial Multi-Omics.Clinical and experimental medicine · 2026Review
- Genomic insights transform diagnosis, prognosis, and therapy in BCR::ABL1-negative myeloproliferative neoplasms.International journal of hematology · 2026Review
- A stem and progenitor cell-derived gene expression signature is prognostic for survival in myelofibrosis.Blood · 2026Article
- CDK6 inactivation counteracts CALR-mutant-induced MPN evolution and sensitizes MPN stem cells to interferon-α treatment.HemaSphere · 2026Article
- Parallel Evolution of Leukemic Clones in Myeloproliferative Neoplasms.Research square · 2025Article
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- [Clinical and molecular characteristics of myeloproliferative neoplasms patients with NFE2 gene mutations].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025Article
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- Article
- Predicting modelling for early diagnosis in early myeloproliferative neoplasms, not otherwise specified. Evidence from a machine learning study.Frontiers in oncology · 2025Article
- Analytical cohort study on splenomegaly and cytopenias in myeloproliferative disorders.Bioinformation · 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
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myeloproliferative neoplasms (MPN) are a heterogeneous group of clonal disorders characterized by aberrant hematopoietic proliferation and an intrinsic risk of progression to blast phase. The WHO classification 2022 identifies chronic myeloid leukemia and the BCR::ABL1 negative MPNs polycythemia vera, primary myelofibrosis and essential thrombocythemia as individual entities. However, overlaps, borderline findings or transitions between MPN subtypes occur and incomplete clinical data often complicates diagnosis. By conducting a thorough genetic analysis, we've developed a model that relies on 12 genetic markers to accurately stratify MPN patients. The model can be simplified into a decision tree for routine use. Comparing samples at chronic and blast phase revealed, that one third of patients lost their MPN driver-gene mutation, while mutations in splicing and chromatin modifying genes were stable, indicating a shared founder clone of chronic and blast phase with different driver mutations and therefore different progressing capacities. This was further supported by gain of typical de novo AML gene mutations, accompanied by gain of complex karyotypes and RAS pathway gene mutations. Our data suggest to perform a broader genetic screening at diagnosis and also at clinical progression, as driver mutations may change and the MPN-driver mutations present at diagnosis may disappear.
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