ArticleHaematologica2014
Array comparative genomic hybridization and sequencing of 23 genes in 80 patients with myelofibrosis at chronic or acute phase.
Article in Haematologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Correlation of mutation profile and response in patients with myelofibrosis treated with ruxolitinib.Blood · 2015Trial
- Clonal Metamorphosis: Deconstructing MPN Evolution with Single-Cell and Spatial Multi-Omics.Clinical and experimental medicine · 2026Review
- Identification of M1 macrophage infiltration-related genes for immunotherapy in Her2-positive breast cancer based on bioinformatics analysis and machine learning.Scientific reports · 2025Article
- Screening of a Prognostic Gene Signature for Relapsed/Refractory Acute Myeloid Leukemia Based on Altered Circulating CircRNA Profiles.International journal of general medicine · 2024Article
- Epigenetic regulation by ASXL1 in myeloid malignancies.International journal of hematology · 2023Review
- The Prevalence ofCancers · 2021Review
- Genomic analysis of primary and secondary myelofibrosis redefines the prognostic impact of ASXL1 mutations: a FIM study.Blood advances · 2021Article
- RAS/CBL mutations predict resistance to JAK inhibitors in myelofibrosis and are associated with poor prognostic features.Blood advances · 2020Article
- European recommendations and quality assurance for cytogenomic analysis of haematological neoplasms.Leukemia · 2019Review
- Epigenomic profiling of myelofibrosis reveals widespread DNA methylation changes in enhancer elements andHaematologica · 2019Article
- Article
- Non-driver mutations in myeloproliferative neoplasm-associated myelofibrosis.Journal of hematology & oncology · 2017Article
- Genomic analysis of myeloproliferative neoplasms in chronic and acute phases.Haematologica · 2017Article
- Poly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Genetic-pathologic characterization of myeloproliferative neoplasms.Experimental & molecular medicine · 2016Article
- Molecular characterization of acute erythroid leukemia (M6-AML) using targeted next-generation sequencing.Leukemia · 2016Article
- Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis.Mediators of inflammation · 2015Review
- Mutational spectrum defines primary and secondary myelofibrosis.Haematologica · 2014Article
- Article
- Small RNAs with big implications: new insights into H/ACA snoRNA function and their role in human disease.Wiley interdisciplinary reviews. RNAReview
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13 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Myelofibrosis is a myeloproliferative neoplasm that occurs de novo (primary myelofibrosis) or results from the progression of polycythemia vera or essential thrombocytemia (hereafter designated as secondary myelofibrosis or post-polycythemia vera/ essential thrombocythemia myelofibrosis). To progress in the understanding of myelofibrosis and to find molecular prognostic markers we studied 104 samples of primary and secondary myelofibrosis at chronic (n=68) and acute phases (n=12) from 80 patients, by using array-comparative genomic hybridization and sequencing of 23 genes (ASXL1, BMI1, CBL, DNMT3A, EZH2, IDH1/2, JAK2, K/NRAS, LNK, MPL, NF1, PPP1R16B, PTPN11, RCOR1, SF3B1, SOCS2, SRSF2, SUZ12, TET2, TP53, TRPS1). We found copy number aberrations in 54% of samples, often involving genes with a known or potential role in leukemogenesis. We show that cases carrying a del(20q), del(17) or del(12p) evolve in acute myeloid leukemia (P=0.03). We found that 88% of the cases were mutated, mainly in signaling pathway (JAK2 69%, NF1 6%) and epigenetic genes (ASXL1 26%, TET2 14%, EZH2 8%). Overall survival was poor in patients with more than one mutation (P=0.001) and in patients with JAK2/ASXL1 mutations (P=0.02). Our study highlights the heterogeneity of myelofibrosis, and points to several interesting copy number aberrations and genes with diagnostic and prognostic impact.
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