等离子体,单核细胞,中性粒细胞或血小板的增殖增加(1、3、4)。大约30%的被诊断为MD的患者最终患有急性髓样白血病(AML)(5)。eVI1首先被鉴定为具有逆转录病毒诱导的髓样恶质的小鼠中生态病毒整合的常见位点(6)。人类EVI1(MECOM)基因位于Chro-Mosome 3Q26上,EVI1的多种同工型在MECOM基因座(7)中编码。3q26染色体的重排,导致EVI1的上调,经常发生在包括MDS,AML和慢性髓样白血病(CML)在内的髓样恶性疾病中(8-10)。MDS,AML和CML具有INV(3)/T(3; 3)重排通常具有相似的病理特征,预后不良(8、11、12)。It was reported that chromosome rear- rangements cause overexpression of EVI1 due to relocation of enhancers, including GATA binding protein 2 (GATA2) enhancer in inv(3)/t(3;3) (q21q26) (13, 14) and MYC super-enhancer in t(3;8) (q26;q24) close to the EVI1 gene (15).EVI1过表达可能发生在没有3染色体重排的MDS患者中。EVI1上调