Published on Feb. 2, 2017 in J Hematol Oncol volume 10(1).
PubMed ID: 28153030
Methylation of N adenosine (mA) 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 mA regulatory genes are strongly associated with the presence of TP53 mutations in AML patients. Further, our analyses reveal that alterations in mA regulatory genes confer a worse survival in AML. Our work indicates that genetic alterations of mA regulatory genes may cooperate with TP53 and/or its regulator/downstream targets in the pathogenesis and/or maintenance of AML.