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Establishment of a myeloid leukaemic cell line (SKNO‐1) from a patient with t(8;21) who acquired monosomy 17 during disease progression
Author(s) -
Matozaki Sachiko,
Nakagawa Toshitaro,
Kawaguchi Ryuji,
Aozaki Ryoji,
Tsutsumi Masayoshi,
Murayama Tohru,
Koizumi Tamio,
Nishimura Ryuichiro,
Isobe Takashi,
Chihara Kazuo
Publication year - 1995
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 - 10.1111/j.1365-2141.1995.tb08418.x
Subject(s) - biology , monosomy , cancer research , myeloid , chromosomal translocation , chromosome abnormality , fusion gene , chromosome 7 (human) , bone marrow , granulocyte macrophage colony stimulating factor , immunology , karyotype , chromosome , gene , genetics , cytokine
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 maturated. 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.