Elias M.H.Azlan H.Baba A.A.Ankathil R.2024-05-282024-05-2820181871529X10.2174/1871529X186661804191014162-s2.0-85055076182https://www.scopus.com/inward/record.uri?eid=2-s2.0-85055076182&doi=10.2174%2f1871529X18666180419101416&partnerID=40&md5=5075fbe793fffe3ebcfab489bea84757https://oarep.usim.edu.my/handle/123456789/934629669505Background: 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. � 2018 Bentham Science Publishers.en-USChronic myeloid leukemiaCytokine signaling tumourHigh resolution melt analysisImatinib mesylateMethylationArticle234238183