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Updated: May 11, 2026

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
Published on: August 5, 2022
[Effect of methylation inhibitor in the treatment of leukemia]
1Hengshui Harlson International Peace Hospital, Hebei Province, China.
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.
Insights
Tumor development is linked to abnormal oncogene and antioncogene expression. Restoring normal gene methylation patterns offers a potential gene therapy approach for leukemia by reactivating tumor suppressors.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Context:
- Tumorigenesis is associated with the dysregulation of oncogenes and antioncogenes.
- Antioncogenes, like SHP-1 tyrosine phosphatase, are crucial negative regulators in cell signaling.
- Leukemia development involves the abnormal expression of oncogenes, such as c-kit, due to loss of antioncogene regulation.
Purpose:
- To review the role of methylation in leukemia.
- To discuss methylation abnormalities and their impact on oncogene and antioncogene expression.
- To explore methylation suppressors and their therapeutic potential in leukemia treatment.
Summary:
- Abnormal gene expression of oncogenes and antioncogenes is a key factor in tumor formation.
- The inactivation of antioncogenes, such as SHP-1, and the overactivation of oncogenes like c-kit are implicated in leukemia.
- Aberrant methylation of promoter regions can silence tumor suppressors and activate oncogenes, suggesting that normalizing methylation is a viable therapeutic strategy.
Impact:
- Understanding methylation's role in leukemia can lead to novel diagnostic and therapeutic targets.
- Restoring normal methylation patterns may reverse oncogene activation and antioncogene silencing.
- This review highlights the potential of epigenetic therapy for leukemia by targeting DNA methylation.
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