Mouse models of NPM1-mutated acute myeloid leukemia: biological and clinical implications

净现值1 髓系白血病 生物 造血 白血病 核磷蛋白 髓样 癌症研究 干细胞 突变 免疫学 基因 遗传学 染色体 核型
作者
Paolo Sportoletti,Emanuela Varasano,Roberta Rossi,Annalisa Mupo,Enrico Tiacci,George S. Vassiliou,Maria Paola Martelli,Brunangelo Falini
出处
期刊:Leukemia [Springer Nature]
卷期号:29 (2): 269-278 被引量:40
标识
DOI:10.1038/leu.2014.257
摘要

Acute myeloid leukemia (AML) carrying nucleophosmin (NPM1) mutations displays distinct biological and clinical features that led to its inclusion as a provisional disease entity in the 2008 World Health Organization (WHO) classification of myeloid neoplasms. Studies of the molecular mechanisms underlying the pathogenesis of NPM1-mutated AML have benefited greatly from several mouse models of this leukemia developed over the past few years. Immunocompromised mice xenografted with NPM1-mutated AML served as the first valuable tool for defining the biology of the disease in vivo. Subsequently, genetically engineered mouse models of the NPM1 mutation, including transgenic and knock-in alleles, allowed the generation of mice with a constant genotype and a reproducible phenotype. These models have been critical for investigating the nature of the molecular effects of these mutations, defining the function of leukemic stem cells in NPM1-mutated AML, identifying chemoresistant preleukemic hemopoietic stem cells and unraveling the key molecular events that cooperate with NPM1 mutations to induce AML in vivo. Moreover, they can serve as a platform for the discovery and validation of new antileukemic drugs in vivo. Advances derived from the analysis of these mouse models promise to greatly accelerate the development of new molecularly targeted therapies for patients with NPM1-mutated AML.
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