ArticleLeukemia2005
The t(8;17)(p11;q23) in the 8p11 myeloproliferative syndrome fuses MYO18A to FGFR1.
Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 79 citations in OpenAlex.
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- MYO18A Expression is a Prognostic Factor for Progression-Free Survival in Grade 4 Adult gliomas. Preliminary Report.Oncology research · 2026Article
- Myeloid/lymphoid neoplasms with eosinophilia and FGFR1 rearrangement t(8;13)(p11;q12): A case report and literature review.Oncology letters · 2024Article
- Identification of a novel HOOK3-FGFR1 fusion gene involved in activation of the NF-kappaB pathway.Cancer cell international · 2022Article
- The 8p11 myeloproliferative syndrome: Genotypic and phenotypic classification and targeted therapy.Frontiers in oncology · 2022Review
- Multifaceted Function of Myosin-18, an Unconventional Class of the Myosin Superfamily.Frontiers in cell and developmental biology · 2021Review
- [Myeloid/lymphoid neoplasms with eosinophilia and FGFR1 rearrangement: 5 cases report and literatures review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Review
- GOLPH3: a Golgi phosphatidylinositol(4)phosphate effector that directs vesicle trafficking and drives cancer.Journal of lipid research · 2019Review
- [Clinical and molecular features of one case of 8p11 myeloproliferative syndrome with t(8;17) (p11; q24)].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2018Article
- Two myeloid leukemia cases with rareCold Spring Harbor molecular case studies · 2018Article
- MYO18A: An unusual myosin.Advances in biological regulation · 2018Review
- MultipleMolecular cytogenetics · 2017Article
- Non-muscle myosins in tumor progression, cancer cell invasion, and metastasis.Cytoskeleton (Hoboken, N.J.) · 2014Review
- The 8p12 myeloproliferative syndrome.Nigerian medical journal : journal of the Nigeria Medical Association · 2014Article
- Functional roles of fibroblast growth factor receptors (FGFRs) signaling in human cancers.Apoptosis : an international journal on programmed cell death · 2013Review
- Functional characterization of human myosin-18A and its interaction with F-actin and GOLPH3.The Journal of biological chemistry · 2013Article
- Centrosomal targeting of tyrosine kinase activity does not enhance oncogenicity in chronic myeloproliferative disorders.Leukemia · 2012Article
- JAK2 Inhibition: Reviewing a New Therapeutical Option in Myeloproliferative Neoplasms.Advances in hematology · 2012Article
- The kinase inhibitor TKI258 is active against the novel CUX1-FGFR1 fusion detected in a patient with T-lymphoblastic leukemia/lymphoma and t(7;8)(q22;p11).Haematologica · 2011Article
- Genomic alterations of primary tumor and blood in invasive ductal carcinoma of breast.World journal of surgical oncology · 2010Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 8p11 myeloproliferative syndrome (EMS) also known as stem cell leukemia-lymphoma syndrome (SCLL) is associated with translocations that disrupt FGFR1. The resultant fusion proteins are constitutively active tyrosine kinases, and different FGFR1 fusions are associated with subtly different disease phenotypes. We report here a patient with a t(8;17)(p11;q23) and an unusual myelodysplastic/myeloproliferative disease (MDS/MPD) characterized by thrombocytopenia due to markedly reduced size and numbers of megakaryocytes, with elevated numbers of monocytes, eosinophils and basophils. A novel mRNA fusion between exon 32 of the myosin XVIIIA gene (MYO18A) at chromosome band 17q11 and exon 9 of FGFR1 was identified. Partial characterization of the genomic breakpoints in combination of bubble-PCR with fluorescence in situ hybridization revealed that the t(8;17) arose from a three-way translocation with breaks at 8p11, 17q11 and 17q23. MYO18A-FGFR1 is structurally similar to other fusion tyrosine kinases and is likely to be the causative transforming lesion in this unusual MDS/MPD.
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