Genetic alterations of m6A regulators predict poorer survival in acute myeloid leukemia

被引:175
作者
Kwok, Chau-To [1 ,2 ,3 ]
Marshall, Amy D. [1 ,3 ]
Rasko, John E. J. [1 ,3 ]
Wong, Justin J. L. [1 ,2 ,3 ]
机构
[1] Univ Sydney, Centenary Inst, Gene Stem Cell Therapy Program, Camperdown, NSW 2050, Australia
[2] Univ Sydney, Centenary Inst, Gene Regulat Canc Lab, Camperdown, NSW 2050, Australia
[3] Univ Sydney, Sydney Med Sch, Camperdown, NSW 2006, Australia
来源
JOURNAL OF HEMATOLOGY & ONCOLOGY | 2017年 / 10卷
基金
英国医学研究理事会;
关键词
RNA modification; m(6)A; Leukemia; Acute myeloid leukemia; TP53; mutation; MUTATIONS; GENOMICS;
D O I
10.1186/s13045-017-0410-6
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Methylation of N-6 adenosine (m(6)A) is known to be important for diverse biological processes including gene expression control, translation of protein, and messenger RNA (mRNA) splicing. However, its role in the development of human cancers is poorly understood. By analyzing datasets from the Cancer Genome Atlas Research Network (TCGA) acute myeloid leukemia (AML) study, we discover that mutations and/or copy number variations of m(6)A regulatory genes are strongly associated with the presence of TP53 mutations in AML patients. Further, our analyses reveal that alterations in m(6)A regulatory genes confer a worse survival in AML. Our work indicates that genetic alterations of m(6)A regulatory genes may cooperate with TP53 and/or its regulator/downstream targets in the pathogenesis and/or maintenance of AML.
引用
收藏
页数:6
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