Marjanu Hikmah Elias, Husin Azlan, Abdul Aziz Baba and Ravindran Ankathil* Pages 234 - 238 ( 5 )
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.
Chronic myeloid leukemia, imatinib mesylate, methylation, high resolution melt analysis, cytokine signaling tumour.
Faculty of Medicine and Health Sciences, Universiti Sains Islam, Haemato-Oncology Unit, Department of Internal Medicine, Universiti Sains Malaysia Hospital, International Medical University, Universiti Sains Malaysia, USM Pinang, Human Genome Centre, School of Medical Sciences, Universiti Sains Malaysia, USM Pinang