Genetic alterations of m(6)A regulators predict poorer survival in acute myeloid leukemia

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. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13045-017-0410-6) contains supplementary material, which is available to authorized users.