ArticleHaematologica2012
ETV6-PDGFRB and FIP1L1-PDGFRA stimulate human hematopoietic progenitor cell proliferation and differentiation into eosinophils: the role of nuclear factor-κB.
Article in Haematologica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 53 citations in OpenAlex.
- Molecular Pathogenesis and Targeted Therapies for Myeloproliferative Hypereosinophilic Neoplasms.Current hematologic malignancy reports · 2026Review
- Rare Genetic and Uncommon Morphological Entities in Adults with Acute Myeloid Leukemia.Current oncology reports · 2025Review
- NetLnc: A Network-Based Computational Framework to Identify Immune Checkpoint-Related lncRNAs for Immunotherapy Response in Melanoma.International journal of molecular sciences · 2025Article
- Population-specific putative causal variants shape quantitative traits.Nature genetics · 2024Article
- Pan-cancer evaluation of regulated cell death to predict overall survival and immune checkpoint inhibitor response.NPJ precision oncology · 2024Article
- Approach to Acute Myeloid Leukemia with Increased Eosinophils and Basophils.Journal of clinical medicine · 2024Review
- Identifying immune checkpoint-related lncRNA biomarkers for immunotherapy response and prognosis in cancers.Scientific data · 2023Article
- Myeloid/Lymphoid Neoplasms withJournal of inflammation research · 2023Article
- LncRNA Hmrhl regulates expression of cancer related genes in chronic myelogenous leukemia through chromatin association.NAR cancer · 2021Article
- Molecular Pathogenesis and Treatment Perspectives for Hypereosinophilia and Hypereosinophilic Syndromes.International journal of molecular sciences · 2021Review
- Tumor-Infiltrating Immune-Related Long Non-Coding RNAs Indicate Prognoses and Response to PD-1 Blockade in Head and Neck Squamous Cell Carcinoma.Frontiers in immunology · 2021Article
- A novel fusion gene involving PDGFRB and GCC2 in a chronic eosinophilic leukemia patient harboring t(2;5)(q37;q31).Molecular genetics & genomic medicine · 2019Article
- PDGF-induced fibroblast growth requires monounsaturated fatty acid production by stearoyl-CoA desaturase.FEBS open bio · 2017Article
- Antitumor activity of S116836, a novel tyrosine kinase inhibitor, against imatinib-resistant FIP1L1-PDGFRα-expressing cells.Oncotarget · 2014Article
- IκB kinase activity drives fetal lung macrophage maturation along a non-M1/M2 paradigm.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Article
- The tyrosine phosphatase SHP2 is required for cell transformation by the receptor tyrosine kinase mutants FIP1L1-PDGFRα and PDGFRα D842V.Molecular oncology · 2014Article
- TRIP11-PDGFRB fusion in a patient with a therapy-related myeloid neoplasm with t(5;14)(q33;q32) after treatment for acute promyelocytic leukemia.Molecular cytogenetics · 2014Article
- Targeting the PDGF signaling pathway in tumor treatment.Cell communication and signaling : CCS · 2013Review
- STAT5 acetylation: Mechanisms and consequences for immunological control and leukemogenesis.JAK-STAT · 2013Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundETV6-PDGFRB (also called TEL-PDGFRB) and FIP1L1-PDGFRA are receptor-tyrosine kinase fusion genes that cause chronic myeloid malignancies associated with hypereosinophilia. The aim of this work was to gain insight into the mechanisms whereby fusion genes affect human hematopoietic cells and in particular the eosinophil lineage. DESIGN AND
methodsWe introduced ETV6-PDGFRB and FIP1L1-PDGFRA into human CD34(+) hematopoietic progenitor and stem cells isolated from umbilical cord blood.
resultsCells transduced with these oncogenes formed hematopoietic colonies even in the absence of cytokines. Both oncogenes also stimulated the proliferation of cells in liquid culture and their differentiation into eosinophils. This model thus recapitulated key features of the myeloid neoplasms induced by ETV6-PDGFRB and FIP1L1-PDGFRA. We next showed that both fusion genes activated the transcription factors STAT1, STAT3, STAT5 and nuclear factor-κB. Phosphatidylinositol-3 kinase inhibition blocked nuclear factor-κB activation in transduced progenitor cells and patients' cells. Nuclear factor-κB was also activated in the human FIP1L1-PDGFRA-positive leukemia cell line EOL1, the proliferation of which was blocked by bortezomib and the IκB kinase inhibitor BMS-345541. A mutant IκB that prevents nuclear translocation of nuclear factor-κB inhibited cell growth and the expression of eosinophil markers, such as the interleukin-5 receptor and eosinophil peroxidase, in progenitors transduced with ETV6-PDGFRB. In addition, several potential regulators of this process, including HES6, MYC and FOXO3 were identified using expression microarrays.
conclusionsWe show that human CD34(+) cells expressing PDGFR fusion oncogenes proliferate autonomously and differentiate towards the eosinophil lineage in a process that requires nuclear factor-κB. These results suggest new treatment possibilities for imatinib-resistant myeloid neoplasms associated with PDGFR mutations.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.