ArticleLeukemia2006
FLT3 is fused to ETV6 in a myeloproliferative disorder with hypereosinophilia and a t(12;13)(p13;q12) translocation.
Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 68 citations in OpenAlex.
- Targeted and epigenetic therapies for acute myeloid leukemia treatment.Discover oncology · 2025Review
- T cell phenotype and lack of eosinophilia are not uncommon in extramedullary myeloid/lymphoid neoplasms with ETV6::FLT3 fusion: a case report and review of the literature.Virchows Archiv : an international journal of pathology · 2024Review
- Characterisation of FLT3 alterations in childhood acute lymphoblastic leukaemia.British journal of cancer · 2024Article
- Prevalence ofFrontiers in pediatrics · 2024Article
- ACold Spring Harbor molecular case studies · 2023Review
- Myeloid/lymphoid neoplasms with FLT3 rearrangement.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- ETV6-FLT3-positive myeloid/lymphoid neoplasm with eosinophilia presenting in an infant: an entity distinct from JMML.Blood advances · 2021Article
- Sorafenib Induced Complete Cytogenetic and Molecular Response in a Chronic Eosinophilic Leukemia Case with t(12;13) Translocation.Clinical hematology international · 2020Article
- Two myeloid leukemia cases with rareCold Spring Harbor molecular case studies · 2018Article
- ETV6/FLT3 Fusion Is a Novel Client Protein of Hsp90.Oncology research · 2018Article
- A novel TRIP11-FLT3 fusion in a patient with a myeloid/lymphoid neoplasm with eosinophilia.Cancer genetics · 2017Article
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- Eosinophilia in Hematologic Disorders.Immunology and allergy clinics of North America · 2015Review
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- Direct binding of Grb2 has an important role in the development of myeloproliferative disease induced by ETV6/FLT3.Leukemia · 2013Article
- Molecular pathophysiology of myelodysplastic syndromes.Annual review of pathology · 2013Review
- ETV6-PDGFRB and FIP1L1-PDGFRA stimulate human hematopoietic progenitor cell proliferation and differentiation into eosinophils: the role of nuclear factor-κB.Haematologica · 2012Article
- Tyrosine kinase gene fusions in cancer: translating mechanisms into targeted therapies.Journal of cellular and molecular medicine · 2012Review
- Green tea epigallocatechin gallate exhibits anticancer effect in human pancreatic carcinoma cells via the inhibition of both focal adhesion kinase and insulin-like growth factor-I receptor.Journal of biomedicine & biotechnology · 2010Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The FMS-like tyrosine kinase 3 (FLT3) gene, belonging to the receptor tyrosine kinase (TK) subclass III family, plays an important role in normal hematopoiesis and is one of the most frequently mutated genes in hematologic malignancies as well as an attractive target for directed inhibition. Activating mutations of this gene, including internal tandem duplication in the juxtamembrane (JM) domain and point mutations in the TK domain, are found in approximately one-third of patients with acute myeloid leukemia and in a smaller subset of patients with acute lymphoblastic leukemia. We report here that FLT3 may contribute to leukemogenesis in a patient with myeloproliferative disorder and a t(12;13)(p13;q12) translocation through generating a fusion gene with the ETS variant gene 6 (ETV6) gene. ETV6 has been reported to fuse to various partner genes, including TK and transcription factors. Both ETV6/FLT3 and reciprocal FLT3/ETV6 transcripts were detected in the patient mRNA by reverse transcriptase-polymerase chain reaction. At the protein level, however, only ETV6/FLT3 products were expressed. Among them, one retains the helix-loop-helix (HLH) oligomerization domain of ETV6 and the JM as well as TK domain of FLT3. FLT3 receptor in leukemic cells might be inappropriately activated through dimerization by HLH domain of ETV6, which consequently interfered with proliferation and differentiation of hematopoietic cells.
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Registered trials
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.