- Volume 15 Issue 11
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Silencing of Suppressor of Cytokine Signaling-3 due to Methylation Results in Phosphorylation of STAT3 in Imatinib Resistant BCR-ABL Positive Chronic Myeloid Leukemia Cells
- Al-Jamal, Hamid AN (Department of Haematology, School of Medical Sciences, Universiti Sains Malaysia) ;
- Jusoh, Siti Asmaa Mat (Department of Haematology, School of Medical Sciences, Universiti Sains Malaysia) ;
- Yong, Ang Cheng (Department of Haematology, School of Medical Sciences, Universiti Sains Malaysia) ;
- Asan, Jamaruddin Mat (Department of Immunology, School of Medical Sciences, Universiti Sains Malaysia) ;
- Hassan, Rosline (Department of Haematology, School of Medical Sciences, Universiti Sains Malaysia) ;
- Johan, Muhammad Farid (Department of Haematology, School of Medical Sciences, Universiti Sains Malaysia)
- Published : 2014.06.15
Background: Silencing due to methylation of suppressor of cytokine signaling-3 (SOCS-3), a negative regulator gene for the JAK/STAT signaling pathway has been reported to play important roles in leukemogenesis. Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets the BCR-ABL protein and induces hematological remission in patients with chronic myeloid leukemia (CML). Unfortunately, the majority of CML patients treated with imatinib develop resistance under prolonged therapy. We here investigated the methylation profile of SOCS-3 gene and its downstream effects in a BCR-ABL positive CML cells resistant to imatinib. Materials and Methods: BCR-ABL positive CML cells resistant to imatinib (K562-R) were developed by overexposure of K562 cell lines to the drug. Cytotoxicity was determined by MTS assays and
Supported by : Universiti Sains Malaysia
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