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Methylation and Expression Status of The CpG-Island of SMG1 Promoter in Acute Myeloid Leukemia: A Follow-Up Study in Patients. | LitMetric

Objective: Aberrant alterations in DNA methylation are known as one of the hallmarks of oncogenesis and play a vital role in the progression of acute myeloid leukemia (AML). is a member of the Phosphoinositide 3-kinases family, acting as a tumor suppressor gene. The aim of this study was the evaluation of the expression level and methylation status of in AML.

Materials And Methods: In this follow-up study on AML patients admitted to Shariati Hospital, Tehran, Iran, the methylation status of [performed by methylation-specific polymerase chain reaction (PCR)] and its expression level (performed by qRT-PCR) were evaluated in three phases: newly diagnosed, under treatment and complete remission. The correlation of the methylation status of , its expression level, and clinical/paraclinical data was analyzed by SPSS ver.25.

Results: This study on 18 patients and five control individuals showed that the CpG-islands of the SMG1 promoter in newly diagnosed cases is hypomethylated compared to the normal group (P=0.002) The fold change of SMG1 expression levels in new cases is 0.464 ± 0.468, while the fold change of expression levels in under-treatment and in-remission patients is 0.973 ± 1.159 and 0.685 ± 0.885, respectively. In under-treatment patients, white blood cell (WBC) count decreases 114176.36 cell/μl with each unit of increase in fold change of SMG1 (P<0.0001), and Hb unit increases 2.062 g/dl with each unit of increase in fold change (P<0.0001). Also, in the remission phase, the Hb unit increases 1.395 g/dl with each unit increase in fold change (P=0.019).

Conclusion: The robust results of our study suggest that the methylation and expression of have a high impact on the pathogenesis of AML. Also, the methylation and expression of can play a prognostic role in AML.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9124448PMC
http://dx.doi.org/10.22074/cellj.2022.7798DOI Listing

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