MN1 overexpression is an important step in the development of inv(16) AML
MN1 overexpression is an important step in the development of inv(16) AML
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DOI：
10.1038/sj.leu.2404778
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发表时间：
2007-08-01
期刊：
影响因子：
11.4
通讯作者：
Grosveld, G. C.
中科院分区：
文献类型：
--
作者：
Carella, C.;Bonten, J.;Grosveld, G. C.
编码转录共激活因子 MN1 的基因是某些急性髓系白血病 (AML) 患者染色体相互易位 (12;22) (p13;q12) 的靶标。此外，表达阵列分析显示，MN1在inv(16)指定的AML、一些过度表达亲嗜性病毒整合1位点(EVI1)的AML以及一些无核型异常的AML中过度表达。在这里，我们描述了接受过度表达 MN1 的骨髓 (BM) 移植的小鼠迅速发展为骨髓增生性疾病 (MPD)。该 BM 还在培养物中产生了骨髓细胞系。通过模仿人类 inv(16) AML 的情况，强制共表达 MN1 和 Cbf beta-SMMHC 迅速在小鼠中引起 AML。这些发现将 MN1 确定为一种高效的造血癌基因，并表明 MN1 过度表达是人类 inv(16) AML 中的重要协同事件。
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.