Abstract |
A novel cell line SKNO-1 was established from the bone marrow cells of a 22-year-old male suffering from acute myeloblastic leukaemia (AML) M2 with t(8;21) whose disease became resistant to chemotherapy after acquisition of 17 monosomy. SKNO-1 has been maintained for more than 36 months as a granulocyte-macrophage colony-stimulating factor ( GM-CSF) dependent line. Morphologically, SKNO-1 cells were myeloblasts somewhat matured. The cells grow in suspension with a doubling time of 48-72 h. The survival and growth of SKNO-1 cells was absolutely dependent on granulocyte-macrophage colony stimulating factor ( GM-CSF). SKNO-1 cells possessed t(8;21) and monosomy 17 which were observed in original leukaemic cells. We confirmed that the AML1 gene, located on chromosome 21, was rearranged and the AML1-MTG8 fusion transcript was expressed in SKNO-1 cells. Over-expression and mutation of the p53 gene were also detected in SKNO-1. It is likely that alterations of AML1 or MTG8 gene and p53 gene contribute to a disease progression in this case. Since t(8;21) translocation is a common chromosome abnormality in AML, and inactivation of the p53 gene may play a crucial role in disease progression in AML, SKNO-1 would be a useful tool for analysing the molecular mechanisms in myeloid leukaemogenesis.
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Authors | S Matozaki, T Nakagawa, R Kawaguchi, R Aozaki, M Tsutsumi, T Murayama, T Koizumi, R Nishimura, T Isobe, K Chihara |
Journal | British journal of haematology
(Br J Haematol)
Vol. 89
Issue 4
Pg. 805-11
(Apr 1995)
ISSN: 0007-1048 [Print] England |
PMID | 7772516
(Publication Type: Case Reports, Journal Article)
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Chemical References |
- DNA, Neoplasm
- Tumor Suppressor Protein p53
- Granulocyte-Macrophage Colony-Stimulating Factor
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Topics |
- Adult
- Blotting, Southern
- Cell Division
- Chromosomes, Human, Pair 17
- Chromosomes, Human, Pair 8
- DNA, Neoplasm
(analysis)
- Disease Progression
- Granulocyte-Macrophage Colony-Stimulating Factor
(pharmacology)
- Humans
- Karyotyping
- Leukemia, Myeloid, Acute
(genetics, pathology)
- Male
- Monosomy
- Translocation, Genetic
- Tumor Cells, Cultured
- Tumor Suppressor Protein p53
(genetics)
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