Chromosomal breakpoints and changes in DNA copy number in refractory acute myeloid leukemia

被引:29
作者
ElRifai, W
Elonen, E
Larramendy, M
Ruutu, T
Knuutila, S
机构
[1] UNIV HELSINKI,HAARTMAN INST,DEPT MED GENET,FIN-00014 HELSINKI,FINLAND
[2] NATL RES CTR,DEPT HUMAN GENET,CAIRO,EGYPT
[3] UNIV HELSINKI,CENT HOSP,DEPT MED,FIN-00014 HELSINKI,FINLAND
[4] NATL UNIV LA PLATA,FAC CIENCIAS EXACTAS,LAB CITOGENET,RA-1900 LA PLATA,ARGENTINA
[5] NATL UNIV LA PLATA,FAC CIENCIAS EXACTAS,CATEDRA CITOL,RA-1900 LA PLATA,ARGENTINA
基金
芬兰科学院;
关键词
CGH; refractory AML; 5q; 7q; 12p;
D O I
10.1038/sj.leu.2400706
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Comparative genomic hybridization (CGH) was used to detect changes in DNA copy number in 25 cases of refractory acute myeloid leukemia (AML). CGH detected changes in DNA copy number in nine AML (36%). Losses (82%) were more frequent than gains (18%). No high-level amplifications were detected in any of the cases. Losses involved minimal overlapping regions at 5q14q32, 7q31.2q32 and 12p12. The most frequent gain was detected at 8q. CGH gave normal results in all cases with a normal karyotype or a translocation as the sole aberration. The absence of high-level DNA copy gains suggests that, in contrast to other malignancies, gene amplification is not an important mechanism for drug resistance in AML. In addition to 5q and 7q, known to be associated with disease refractoriness, 12p may be another region related to poor prognosis.
引用
收藏
页码:958 / 963
页数:6
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