Mouse Models of Frequently Mutated Genes in Acute Myeloid Leukemia

被引：4

作者：

Mohanty, Sagarajit ^{[1
]}

Heuser, Michael ^{[2
]}

机构：

[1] Mem Sloan Kettering Canc Ctr, Canc Biol & Genet, New York, NY 10065 USA

[2] Hannover Med Sch, Dept Hematol Hemostasis Oncol & Stem Cell Transpl, D-30625 Hannover, Germany

来源：

CANCERS | 2021年 / 13卷 / 24期

关键词：

AML; synergy; leukemia; mutations; transgenic mice; mouse models; HEMATOPOIETIC STEM-CELLS; WILMS-TUMOR GENE; KNOCK-IN MICE; ACUTE MYELOGENOUS LEUKEMIA; NUCLEOPHOSMIN NPMC(+) AML; C-KIT MUTATIONS; MYELOPROLIFERATIVE DISEASE; C/EBP-ALPHA; COHESIN COMPLEX; SELF-RENEWAL;

D O I：

10.3390/cancers13246192

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Acute myeloid leukemia is a clinically and biologically heterogeneous blood cancer with variable prognosis and response to conventional therapies. Comprehensive sequencing enabled the discovery of recurrent mutations and chromosomal aberrations in AML. Mouse models are essential to study the biological function of these genes and to identify relevant drug targets. This comprehensive review describes the evidence currently available from mouse models for the leukemogenic function of mutations in seven functional gene groups: cell signaling genes, epigenetic modifier genes, nucleophosmin 1 (NPM1), transcription factors, tumor suppressors, spliceosome genes, and cohesin complex genes. Additionally, we provide a synergy map of frequently cooperating mutations in AML development and correlate prognosis of these mutations with leukemogenicity in mouse models to better understand the co-dependence of mutations in AML.

引用

页数：30

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