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Establishment of a novel human myeloid leukaemia cell line (FKH‐1) with t(6;9)(p23;q34) and the expression of dek‐can chimaeric transcript
Author(s) -
Hamaguchi Hiroyuki,
Nagata Kaoru,
Yamamoto Katsuya,
Fujikawa Izumi,
Kobayashi Masaru,
Eguchi Mitsuoki
Publication year - 1998
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1998.00900.x
Subject(s) - myeloid , biology , cancer research , immunology , fusion transcript , chromosomal translocation , stem cell , cell culture , gene , microbiology and biotechnology , genetics
Translocation t(6;9)(p23;q34), resulting in a dek‐can gene fusion, is a recurrent chromosomal abnormality mainly associated with specific subtypes of acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS). Patients with this type of chromosomal change are usually young and their prognosis is poor. The role of fusion protein generated from dek‐can chimaeric transcript on the leukaemogenesis of t(6;9) AML or MDS is as yet unknown. We have established the first permanent cell line (FKH‐1) with t(6;9), derived from the peripheral blood of a patient with t(6;9) AML transformed from Philadelphia chromosome (Ph 1 )‐negative chronic myelocytic leukaemia (CML). The FKH‐1 expressed myelomonocytic markers and dek‐can chimaeric transcript. In the presence of 10 ng/ml recombinant human granulocyte colony‐stimulating factor (G‐CSF), the cells doubled every 54 h and showed multilineage myeloid differentiation, resulting in heterogenous morphologies such as macrophages, basophils, eosinophils and neutrophils. Thus, this cell line may be derived from a pluripotent myeloid stem cell and should be a useful tool for biomolecular studies on the pathogenesis of t(6;9) myeloid malignancies which have rarely been investigated because of the lack of continuously proliferating cells.

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