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http://purl.uniprot.org/citations/16930139http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16930139http://www.w3.org/2000/01/rdf-schema#comment"

Objectives

Friend leukemia integration-1 (Fli-1), a member of the Ets gene family of transcription factors, has been demonstrated to be a target of a leukaemia inducing virus in mice, and is known to be part of a fusion gene in Ewings' sarcoma in humans. Wild-type Fli-1 is involved in lineage commitment of megakaryocytes and myeloid progenitors through induction of Janus kinases (JAKs) following ligand binding to cytokine and growth factor receptors. Proliferation of atypical megakaryocytes is a predominant histopathological feature in Philadelphia chromosome negative chronic myeloproliferative disorders (Ph(-) CMPD) and a potential aberrant expression of Fli-1 has not been investigated so far.

Methods

Fli-1 expression was investigated by real-time RT-PCR and immunohistochemistry in bone marrow cells derived from Ph(-) CMPD (n = 80) and non-neoplastic haematopoiesis (n = 21) following determination of the JAK2 status.

Results

Fli-1 mRNA expression was significantly higher in Essential thrombocythaemia (ET) with JAK2 (V617F) compared with other Ph(-) CMPD and control (P < 0.001). By immunohistochemistry, Fli-1 protein could be detected in nuclei of atypical megakaryocytes in Ph(-) CMPD and, less accentuated, in non-neoplastic megakaryocytes. Fli-1 protein expression by myeloid progenitors was considerably heterogenous in Ph(-) CMPD independent of an underlying JAK2 (V617F) mutation and without notable differences to non-neoplastic haematopoiesis.

Conclusion

Fli-1 is rather constitutively expressed by bone marrow cells in Ph(-) CMPD independent of the underlying JAK2 status. The overall stronger labelling for Fli-1 in megakaryocytes in Ph(-) CMPD most likely reflects the degree of polyploidisation but aberrant activation of nuclear target genes can not be excluded."xsd:string
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http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/author"Hussein K."xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/author"Kreipe H."xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/author"Bock O."xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/author"Neusch M."xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/author"Wiese B."xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/author"Schlue J."xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/name"Eur J Haematol"xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/pages"463-470"xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/title"Transcription factor Fli-1 expression by bone marrow cells in chronic myeloproliferative disorders is independent of an underlying JAK2 (V617F) mutation."xsd:string
http://purl.uniprot.org/citations/16930139http://purl.uniprot.org/core/volume"77"xsd:string
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