Aberrant DNA methylation and its targeted therapy in acute myeloid leukemia.
- Author:
Xueying LI
1
;
Lixia ZHU
1
;
Xiujin YE
2
Author Information
1. Department of Hematology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
2. Department of Hematology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China. yxjsunny_yx@163.com.
- Publication Type:Journal Article
- MeSH:
DNA Methylation;
drug effects;
genetics;
physiology;
DNA Modification Methylases;
genetics;
physiology;
Drug Resistance, Neoplasm;
genetics;
Epigenesis, Genetic;
genetics;
physiology;
Humans;
Leukemia, Myeloid, Acute;
etiology;
genetics;
pathology;
Mutation;
genetics
- From:
Journal of Zhejiang University. Medical sciences
2016;45(4):387-394
- CountryChina
- Language:Chinese
-
Abstract:
The occurrence and development of acute myeloid leukemia (AML) is not only related to gene mutations, but also influenced by abnormal epigenetic regulation, in which DNA methylation is one of the most important mechanisms. Abnormal DNA methylation may lead to the activation of oncogene and the inactivation of tumor suppressor gene, resulting in the occurrence of leukemia. The mutations of DNA methylation enzymes associated with AML may have certain characteristics. The AML with recurrent cytogenetic abnormalities is also related to abnormal methylation. Some fusion genes can alter DNA methylation status to participate in the pathogenesis of leukemia. In addition, chemotherapy drug resistance in patients with AML is associated with the change of gene methylation status. Considering the reversibility of the epigenetic modification, targeted methylation therapy has become a hotspot of AML research.
