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Updated: Jun 12, 2026
Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
Published on: June 16, 2017
Methylation status of DDIT3 gene in chronic myeloid leukemia
Ya-li Wang1, Jun Qian, Jiang Lin
1Department of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, PR China.
Background:
DNA-damage-inducible transcript 3 (DDIT3), a candidate tumor suppressor gene (TSG), has been found involved in the regulation of cellular growth and differentiation. The epigenetic changes of TSGs are recently recognized as an abnormal mechanism contributing to the development of chronic myeloid leukemia (CML). The aim of this study was to investigate the methylation status of DDIT3 gene in CML patients.
Methods:
The methylation status of DDIT3 promoter was detected in the bone marrow mononuclear cells from 53 patients with CML using methylation-specific PCR (MSP). The expression levels of DDIT3 and bcr/abl transcript were determined by real-time quantitative PCR (RQ-PCR). Clinical data of these patients were collected and analyzed.
Results:
The aberrant methylation of DDIT3 gene promoter was found in 35 of 53 (66%) CML cases. Correlation was not found between DDIT3 promoter hypermethylation and the age, sex, hemoglobin concentration, platelet counts, chromosomal abnormalities, bcr/abl transcript, and staging of CML patients (P > 0.05), but found between DDIT3 promoter hypermethylation and WBC counts of CML cases (R = 0.781, P < 0.001). The level of DDIT3 transcript in CML patients was significantly lower than that in controls (median 3.28 vs 19.69, P < 0.001), however, there was no difference in the level of DDIT3 transcript between methylation-positive CML cases (0.05-65.32, median 2.13) and methylation- negative CML cases (0.12-126.04, median 3.92) (P > 0.05).
Conclusion:
Our results demonstrate that aberrant methylation of DDIT3 occurs in CML frequently.
Insights
Aberrant methylation of the DNA-damage-inducible transcript 3 (DDIT3) gene occurs in 66% of chronic myeloid leukemia (CML) patients. This epigenetic change is linked to white blood cell counts but not other clinical factors in CML.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- DNA-damage-inducible transcript 3 (DDIT3) is a candidate tumor suppressor gene involved in cellular growth and differentiation.
- Epigenetic alterations, particularly gene methylation, are increasingly recognized as key mechanisms in the development of chronic myeloid leukemia (CML).
Purpose of the Study:
- To investigate the methylation status of the DDIT3 gene in patients diagnosed with chronic myeloid leukemia (CML).
Main Methods:
- Methylation-specific PCR (MSP) was employed to assess DDIT3 promoter methylation in bone marrow mononuclear cells from 53 CML patients.
- Real-time quantitative PCR (RQ-PCR) was used to determine DDIT3 and bcr/abl transcript expression levels.
- Clinical data from CML patients were collected and analyzed for correlations with methylation status.
Main Results:
- Aberrant DDIT3 promoter hypermethylation was detected in 66% (35/53) of CML cases.
- DDIT3 hypermethylation showed a significant positive correlation with white blood cell (WBC) counts (R = 0.781, P < 0.001) but not with other clinical parameters.
- DDIT3 transcript levels were significantly lower in CML patients compared to controls (median 3.28 vs 19.69, P < 0.001), with no significant difference between methylated and unmethylated CML cases.
Conclusions:
- Aberrant methylation of the DDIT3 gene promoter is a frequent epigenetic event in chronic myeloid leukemia (CML).
- The findings suggest a potential role for DDIT3 epigenetic dysregulation in CML pathogenesis, particularly in relation to WBC counts.
