AML1是急性白血病中较常见的一种易位靶基因，除常见的t(8;21)即AML1-ETO融合方式外尚存在许多未知融合类型，发现并研究新的融合蛋白生物学功能对白血病诊断治疗具有十分重要的意义。前期研究中，我们通过自主设计的方法发现一种新的融合类型 t(1;21)(p32;q22)即AML1-PRP38A。本研究中我们将通过四环素诱导调控的慢病毒表达系统研究其对U937细胞增殖、分化、凋亡的影响以及诱导C57小鼠形成白血病的能力，比较其与AML1a、AML1-ETO9a、AML1-ETO生物学功能的异同；通过免疫共沉淀、蛋白飞行时间质谱等技术进一步研究其对正常AML1b蛋白的显性负调控作用及其C端CK2活化位点的生物学功能，探讨该融合蛋白致白血病的分子机制。此研究将有助于进一步揭示AML1基因相关白血病的发生机制，为开发具有我国自主知识产权的靶向药物、实现个体化治疗奠定理论基础。

AML1 gene is one of the more common translocation sites in patients with acute leukemia. In addition to common AML1-ETO generated by t (8;21) there are many unknown fusion types. It is of very important significance on diagnosis and treatment of leukemia to find those new fusion genes and figure out their biological features. In previous research, we had found and identified a novel fusion gene AML1-PRP38A, which is generated as a result of t(1;21)(q31;q22) using a self-designed method. In this study, we would identify the effect of fusion gene AML1-PRP38A on U937 cell proliferation, differentiation and apoptosis and the ability of inducing C57 mice to leukemia based on the lentiviral expression vector system induced by tetracycline, and compare its biological function with AML1a、AML1-ETO9a and AML1-ETO. Furthermore, we will research the dominant negative regulation function of AML1-PRP38A on the normal AML1b gene and the biology function of the C-terminal CK2 activity site through immunoprecipitate assay and matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry technology, exploring the molecular role of the fusion protein in human leukemogenesis. This will be helpful to further elucidate the pathogenesis of AML1 gene-related leukemia and to establish theoretical basis for developing targeted drug with proprietary intellectual property rights for individualized therapy.