ArticleBlood2013
Acquired copy-neutral loss of heterozygosity of chromosome 1p as a molecular event associated with marrow fibrosis in MPL-mutated myeloproliferative neoplasms.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 92 citations in OpenAlex.
- Pacritinib and its use in the treatment of patients with myelofibrosis who have thrombocytopenia.Future oncology (London, England) · 2018Trial
- Glucose transport dependency defines a therapeutic vulnerability in JAK2V617F-driven myeloproliferative neoplasms.Cell communication and signaling : CCS · 2026Article
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- Physiological MplW514L expression in hematopoietic stem cell causes an essential thrombocythemia and progressive myelofibrosis.The Journal of clinical investigation · 2026Article
- Optical genome mapping in myelofibrosis: enhancing prognostic accuracy through high-resolution genomic profiling.Blood advances · 2026Article
- The molecular management of classic myeloproliferative neoplasm.Journal of the Egyptian National Cancer Institute · 2025Review
- Article
- Calreticulin-From the Endoplasmic Reticulum to the Plasma Membrane-Adventures of a Wandering Protein.Cancers · 2025Review
- Detecting Multiple Driver Mutations in a Patient with Essential Thrombocythemia.The American journal of case reports · 2024Article
- Myeloproliferative disorders and their effects on bone homeostasis: the role of megakaryocytes.Blood · 2022Review
- Molecular Pathogenesis of Myeloproliferative Neoplasms: From Molecular Landscape to Therapeutic Implications.International journal of molecular sciences · 2022Review
- Small molecule inhibition of deubiquitinating enzyme JOSD1 as a novel targeted therapy for leukemias with mutant JAK2.Leukemia · 2022Article
- Review
- The Genetic Basis of Primary Myelofibrosis and Its Clinical Relevance.International journal of molecular sciences · 2020Review
- Genomic characterization and prognostication applied to a Brazilian cohort of patients with myelofibrosis.International journal of hematology · 2020Article
- Review
- Different impact of calreticulin mutations on human hematopoiesis in myeloproliferative neoplasms.Oncogene · 2020Article
- Two activating mutations of MPL in triple-negative myeloproliferative neoplasms.Cancer medicine · 2019Article
- Unfolding the Role of Calreticulin in Myeloproliferative Neoplasm Pathogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Review
- Somatic mosaicisms of chromosome 1 at two different stages of ontogenetic development detected by Rh blood group discrepancies.Haematologica · 2019Article
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Authors and funding
21 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We studied mutations of MPL exon 10 in patients with essential thrombocythemia (ET) or primary myelofibrosis (PMF), first investigating a cohort of 892 consecutive patients. MPL mutation scanning was performed on granulocyte genomic DNA by using a high-resolution melt assay, and the mutant allele burden was evaluated by using deep sequencing. Somatic mutations of MPL, all but one involving codon W515, were detected in 26/661 (4%) patients with ET, 10/187 (5%) with PMF, and 7/44 (16%) patients with post-ET myelofibrosis. Comparison of JAK2 (V617F)-mutated and MPL-mutated patients showed only minor phenotypic differences. In an extended group of 62 MPL-mutated patients, the granulocyte mutant allele burden ranged from 1% to 95% and was significantly higher in patients with PMF or post-ET myelofibrosis compared with those with ET. Patients with higher mutation burdens had evidence of acquired copy-neutral loss of heterozygosity (CN-LOH) of chromosome 1p in granulocytes, consistent with a transition from heterozygosity to homozygosity for the MPL mutation in clonal cells. A significant association was found between MPL-mutant allele burden greater than 50% and marrow fibrosis. These observations suggest that acquired CN-LOH of chromosome 1p involving the MPL location may represent a molecular mechanism of fibrotic transformation in MPL-mutated myeloproliferative neoplasms.
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