ArticleMolecular genetics & genomic medicine2020
Aberrant DNA methylation of PTPRG as one possible mechanism of its under-expression in CML patients in the State of Qatar.
Article in Molecular genetics & genomic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Clinical applications of abnormal DNA methylation in chronic myeloid leukemia.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Gene Expression Landscape of Chronic Myeloid Leukemia K562 Cells Overexpressing the Tumor Suppressor Gene PTPRG.International journal of molecular sciences · 2022Article
- Current Views on the Interplay between Tyrosine Kinases and Phosphatases in Chronic Myeloid Leukemia.Cancers · 2021Review
- Predictive value of tyrosine phosphatase receptor gamma for the response to treatment tyrosine kinase inhibitors in chronic myeloid leukemia patients.Scientific reports · 2021Article
- The Role of the Tumor Suppressor Gene Protein Tyrosine Phosphatase Gamma in Cancer.Frontiers in cell and developmental biology · 2021Review
- Aberrant DNA methylation of PTPRG as one possible mechanism of its under-expression in CML patients in the State of Qatar.Molecular genetics & genomic medicine · 2020Article
- Protein Tyrosine Phosphatase Receptor Gamma as Potential Therapeutic Target for Chronic Myeloid Leukemia Patients.Cancer control : journal of the Moffitt Cancer CenterArticle
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16 authors at 9 institutions in 5 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundSeveral studies showed that aberrant DNA methylation is involved in leukemia and cancer pathogenesis. Protein tyrosine phosphatase receptor gamma (PTPRG) expression is a natural inhibitory mechanism that is downregulated in chronic myeloid leukemia (CML) disease. The mechanism behind its downregulation has not been fully elucidated yet.
aimThis study aimed to investigate the CpG methylation status at the PTPRG locus in CML patients.
methodsPeripheral blood samples from CML patients at time of diagnosis [no tyrosine kinase inhibitors (TKIs)] (n = 13), failure to (TKIs) treatment (n = 13) and healthy controls (n = 6) were collected. DNA was extracted and treated with bisulfite treatment, followed by PCR, sequencing of 25 CpG sites in the promoter region and 26 CpG sites in intron-1 region of PTPRG. The bisulfite sequencing technique was employed as a high-resolution method.
resultsCML groups (new diagnosed and failed treatment) showed significantly higher methylation levels in the promoter and intron-1 regions of PTPRG compared to the healthy group. There were also significant differences in methylation levels of CpG sites in the promoter and intron-1 regions amongst the groups.
conclusionAberrant methylation of PTPRG is potentially one of the possible mechanisms of PTPRG downregulation detected in CML.
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