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Establishment of a cell line with AML1‐MTG8 , TP53 , and TP73 abnormalities from acute myelogenous leukemia
Author(s) -
Inokuchi Koiti,
Hamaguchi Hiroyuki,
Taniwaki Masafumi,
Yamaguchi Hiroki,
Tanosaki Sakae,
Dan Kazuo
Publication year - 2001
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.1181
Subject(s) - biology , microbiology and biotechnology , chromosomal translocation , fluorescence in situ hybridization , clone (java method) , myeloid leukemia , leukemia , cancer research , gene , genetics , chromosome
Gene alterations accumulate during the progression of acute myelogenous leukemia (AML) to a malignant clone. Here, a new myeloid cell line, designated YSK‐21, with the balanced t(8;21)(q22;q22) and the unbalanced der(1)t(1;17)(p36;q21), was established. YSK‐21 grows well in a medium containing recombinant human granulocyte colony‐stimulating factor (rhG‐CSF), granulocyte‐macrophage colony‐stimulating factor (rhGM‐CSF), or interleukin‐3 (rhIL‐3). Molecular analysis using the reverse transcriptase‐polymerase chain reaction (RT‐PCR) and fluorescence in situ hybridization (FISH) revealed that t(8;21)(q22;q22) resulted in an AML1‐MTG8 fusion transcript. FISH and spectral karyotyping (SKY) in conjunction with G‐banding analysis revealed a der(1)t(1;17)(p36;q21) chromosomal translocation, which appeared in the clone developed from the original leukemic cells. Molecular analysis of the TP73 gene on 1p36 and the TP53 gene revealed a deletion of one‐allele in TP73 with partial demethylation of another allele in the initial clone of YSK, and a point mutation consisting of an A→T substitution in codon 288 of the TP53 gene in the developed clone of YSK‐21. YSK‐21 cells, expressing aberrant AML1‐MTG8, TP53, and TP73 protein molecules, may be useful for elucidating the pathophysiology of these aberrant proteins and for studying the der(1)t(1;17)(p36;q21) chromosomal translocation. © 2001 Wiley‐Liss, Inc.