MN1 overexpression is an important step in the development of inv(16) AML

被引：62
作者：
Carella, C.
Bonten, J.
Sirma, S.
Kranenburg, T. A.
Terranova, S.
Klein-Geltink, R.
Shurtleff, S.
Downing, J. R.
Zwarthoff, E. C.
Liu, P. P.
Grosveld, G. C.
机构：
[1] St Jude Childrens Res Hosp, Dept Genet & Tumor Cell Biol, Memphis, TN 38105 USA
[2] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA
[3] Josephine Nefkens Inst, Dept Pathol, Erasmus MC, Rotterdam, Netherlands
[4] NHGRI, NIH, Oncogenesis & Dev Sect, Bethesda, MD 20892 USA
来源：
LEUKEMIA | 2007年 / 21卷 / 08期
关键词：
AML; MN1; inv(16); CBF beta-SMMHC;
D O I：
10.1038/sj.leu.2404778
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
The gene encoding the transcriptional co-activator MN1 is the target of the reciprocal chromosome translocation (12;22) (p13;q12) in some patients with acute myeloid leukemia (AML). In addition, expression array analysis showed that MN1 was overexpressed in AML specified by inv(16), in some AML overexpressing ecotropic viral integration 1 site (EVI1) and in some AML without karyotypic abnormalities. Here we describe that mice receiving transplants of bone marrow (BM) overexpressing MN1 rapidly developed myeloproliferative disease (MPD). This BM also generated myeloid cell lines in culture. By mimicking the situation in human inv(16) AML, forced coexpression of MN1 and Cbf beta-SMMHC rapidly caused AML in mice. These findings identify MN1 as a highly effective hematopoietic oncogene and suggest that MN1 overexpression is an important cooperative event in human inv(16) AML.
引用
收藏
页码：1679 / 1690
页数：12
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