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
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
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.