Impact of trisomy 8 on expression of genes located on chromosome 8 in different AML subgroups

被引:32
作者
Schoch, Claudia
Kohlmann, Alexander
Dugas, Martin
Kern, Wolfgang
Schnittger, Susanne
Haferlach, Torsten
机构
[1] MLL, D-81377 Munich, Germany
[2] Roche Mol Syst, Pleasanton, CA USA
[3] Univ Munster, Dept Med Informat & Biomath, D-4400 Munster, Germany
关键词
D O I
10.1002/gcc.20380
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Trisomy 8 is the most frequently observed trisomy in acute myeloid leukemia (AML) occurring as a sole karyotype abnormality or in addition to other chromosome aberrations. It was the aim of this study to analyze the impact of trisomy 8 on the expression of genes located on chromosome 8 in distinct AML subgroups characterized by different chromosome abnormalities in addition to trisomy 8. Gene expression analyses were performed on a total of 567 AML cases comprising the following subgroups: +8 sole, +8 within a complex aberrant karyotype, +8 in addition to t(15; 17), inv(I 6), t(8;2 1), 11q23/MLL, or other abnormalities, AML with normal karyotype and the before mentioned subgroups without trisomy 8. A significant higher mean expression of genes located on chromosome 8 was observed in subgroups with +8 in comparison to their respective control groups. A varying number of significantly higher expressed genes was identified in all comparisons. No gene was significantly overexpressed in all comparisons, and no distinct gene expression pattern was identified allowing the identification of cases with trisomy 8. In conclusion, the gain of chromosome 8 leads to a higher expression of genes located on chromosome 8. However, no consistent pattern of genes was identified, which shows a higher expression in all AML subtypes with trisomy 8. These data suggest that trisomy 8 rather provides a platform for a higher expression of chromosome 8 genes which are individually up-regulated by the respective primary genetic abnormalities. Therefore, trisomy 8 in AML determines no specific disease characteristic but is a disease modulating secondary event. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045-2257/suppmat. (c) 2006 Wiley-Liss, Inc.
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页码:1164 / 1168
页数:5
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