Effect of methylation inhibitor in the treatment of leukemia.
10.7534/j.issn.1009-2137.2013.02.059
- Author:
Zhen MENG
1
;
Jian-Min LUO
Author Information
1. Hengshui Harlson International Peace Hospital, Hebei Province, China.
- Publication Type:Journal Article
- MeSH:
DNA Methylation;
drug effects;
Humans;
Leukemia;
drug therapy;
metabolism;
Protein Tyrosine Phosphatase, Non-Receptor Type 6;
metabolism
- From:
Journal of Experimental Hematology
2013;21(2):536-538
- CountryChina
- Language:Chinese
-
Abstract:
More and more studies have found that the occurrence of tumors are directly related to the abnormal expression of oncogene and antioncogene. If the antioncogene is mutated or absent, the function of cells will be weakened and inactivated, the cells will be duplicated repeatedly out of control, then will induce occurrence and metastasis of tumor. For example, SHP-1 tyrosine phosphatase, as an antioncogene, is a key negative regulator in signaling transduction of haematopoietic cells. The decrease and silence of SHP-1 play an important role in tumorigenesis. If the oncogene in leukemia patients lost the effect of negative regulation of antioncogene, the oncogene would be expressed abnormally high, such as the oncogene c-kit (an important member of the class III in the tyrosine kinase receptor family) in many kinds of leukemia cells expresses actively. Studies have shown that the high methylation of promoter region would induce the inactivation of tumor suppressor and active expression of oncogene, therefore, the restoring normal methylation of promoter region will contribute to restoration of normal gene expression, thus achieving the purpose of gene therapy for leukemia. In this article, the methylation, methylation abnormality and leukemia, methylation suppressors and therapy of leukemia are briefly reviewed.
