Abnormality of p15(INK4b) gene and myelodysplastic syndrome.
- Author:
Zhen WANG
1
;
Yang-Qiu LI
Author Information
1. Institute of Hematology, Medical College of Jinan University, Guangzhou 510632, China.
- Publication Type:Journal Article
- MeSH:
Cell Cycle Proteins;
genetics;
Cyclin-Dependent Kinase Inhibitor p15;
Cyclin-Dependent Kinase Inhibitor p16;
genetics;
DNA Methylation;
Gene Deletion;
Genes, Tumor Suppressor;
Humans;
Mutation;
Myelodysplastic Syndromes;
etiology;
genetics;
therapy;
Tumor Suppressor Proteins
- From:
Journal of Experimental Hematology
2002;10(4):362-365
- CountryChina
- Language:Chinese
-
Abstract:
Among tumor suppressor genes, p15(INK4b) gene is gaining more attention for its important role in the progression of myelodyplastic syndrome (MDS). Serial studies demonstrated that highly frequent hypermethylation of p15(INK4b) gene, which is located at the 5'CpG island in the promoter region of exon 1 and is the main reason of inactivation of p15(INK4b) gene, occurs during the development of MDS towards AML. The assay of methylation-specific PCR (MSP) is sensitive to this pattern of methylation which is restricted to the MDS clone. Apoptosis mediated by cytokines such as Fas antigen and TGF-beta, and bHLH proteins is inhibited by the inactivation of p15(INK4b) gene. This may result in the evolution of MDS clone to AML. In as much as the close relationship between p15(INK4b) gene methylation and MDS, modulation of the methylation status of p15(INK4b) gene may be considered as a noval treatment modality for MDS.
