A comparison of gene expression profiles between primary human AML cells and AML cell line

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Title
A comparison of gene expression profiles between primary human AML cells and AML cell line
Author(s)
J Lee; J Hwang; H S Kim; S Kim; Y H Kim; S Y Park; K S Kim; Z Y Ryoo; Kyu Tae Chang; S Lee
Bibliographic Citation
Genes & Genetic Systems, vol. 83, pp. 339-345
Publication Year
2008
Abstract
In acute myeloid leukemia (AML), hematologic malignancies are characterized by recurring chromosomal abnormalities. Chromosome translocation t(9;11)(p22;q23) is one of the most common genetic aberrations and results in the formation of the MLL-AF9 fusion gene that functions as a facilitator of cell growth directly. In order to study this type of AML, the cell lines with cytogenetically diagnosed t(9;11)(p22;q23), such as Mono Mac 6 (MM6), have been widely used. To examine whether there is any difference in gene expression between the primary human t(9;11) AML cells and MM6 cell line, genome-wide transcriptome analysis was performed on MM6 cell line using SAGE and the results were compared to the profile of primary human t(9;11) AML cells. 884 transcripts which were alternatively expressed between MM6 cells and primary human t(9;11) cells were identified through statistical analysis (P < 0.05) and 4-fold expression change. of these transcripts, 830 (94%) matched to known genes or EST were classified by functional categories (http://david.abcc. ncifcrf.gov/). The majority of alternatively expressed genes in MM6 were involved in biosynthetic and metabolic processes, but HRAS, a protein that is known to be associated with leukemogenesis, was expressed only in MM6 cells and several other genes involved in Erk1/Erk2 MAPK pathway were also over-expressed in MM6. Therefore, since MM6 cell line has a similar expression profile to primary human t(9;11) AML in general and expresses uniquely a strong Erk1/Erk2 MAPK pathway including HRAS, it can be used as a model for HRAS-positive t(9;11) AML.
Keyword
AMLGene expressionTranslocationSAGE
ISSN
1341-7568
Publisher
Genetics Soc Japan
DOI
http://dx.doi.org/10.1266/ggs.83.339
Type
Article
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1. Journal Articles > Journal Articles
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