Affiliations 

  • 1 Faculty of Medicine and Health Sciences, Universiti Sains Islam, Malaysia
  • 2 Haemato-Oncology Unit, Department of Internal Medicine, Universiti Sains Malaysia Hospital, Malaysia
  • 3 International Medical University, Universiti Sains Malaysia, USM Pinang, Malaysia
  • 4 Human Genome Centre, School of Medical Sciences, Universiti Sains Malaysia, USM Pinang, Malaysia
PMID: 29669505 DOI: 10.2174/1871529X18666180419101416

Abstract

BACKGROUND: In exploring the cause of Imatinib Mesylate (IM) resistance among Chronic Myeloid Leukemia (CML) patients who do not harbor BCR-ABL dependent mechanism, BCR-ABL independent pathways are the most probable pathways that should be explored. In BCR-ABL independent pathway, SOCS1 plays an important role as it helps in regulating optimal JAK/STAT activity.

OBJECTIVE: To identify the association of SOCS1 gene hypermethylation in mediating IM Resistance.

METHOD: The SOCS1 promoter methylation level of 92 BCR-ABL non mutated IM resistant CML patients, 83 IM good response CML patients and 5 normal samples from healthy individuals were measured using Methylation Specific-High Resolution Melt (MS-HRM) analysis.

RESULTS: Both primers used to amplify promoter region from -333 to -223 and from -332 to -188 showed less than 10% methylation in all CML and normal samples. Consequently, there was no significant difference in SOCS1 promoter methylation level between IM resistant and IM good response patients.

CONCLUSION: SOCS1 promoter methylation level is not suitable to be used as one of the biomarkers for predicting the possibility of acquiring resistance among CML patients treated with IM.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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