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Different Protein Expression between Human Eosinophilic Leukemia Cells, EoL-1 and Imatinib-resistant EoL-1 Cells, EoL-1-IR
Biomed Sci Letters 2018;24:426-429
Published online December 31, 2018;
© 2018 The Korean Society For Biomedical Laboratory Sciences.

Kee-Hyung Sung1,2,*, In-Sik Kim1,3,** and Ji-Sook Lee4,†,**

1Department of Senior Healthcare, BK21 Plus Program, Graduate School, Eulji University, Daejeon 34824, Korea
2Department of Laboratory Medicine, Seoul National University Bundang Hospital, Seongnam, Gyeonggi-do, 13620, Korea
3Department of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon 34824, Korea
4Department of Clinical Laboratory Science, Wonkwang Health Science University, Iksan 54538, Korea
Correspondence to: *Researcher, **Professor.
Ji-Sook Lee. Department of Clinical Laboratory Science, Wonkwang Health Science University, Iksan 54538, Korea.
Tel: +82-63-840-1216, Fax: +82-63-840-1219, e-mail:
Received September 14, 2018; Revised November 7, 2018; Accepted November 12, 2018.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Chronic eosinophilic leukemia (CEL) is characterized by eosinophilia and organ damage. Imatinib is widely used for treating CEL, chronic myeloid leukemia (CML) and acute myeloid leukemia (AML). Unfortunately, the cancer cells gain resistance against the drug after prolonged molecular-targeted therapies. Imatinib-resistant EoL-1 (EoL-1-IR) cells were produced from chronic eosinophilic leukemia cells (EoL-1) after treatment with imatinib for a long duration. Two-dimensional electrophoresis (2-DE) analysis revealed numerous protein variations in the EoL-1 and EoL-1-IR sub-types. Compared to the EoL-1 cells, expression levels of TIP49, RBBP7, α-enolase, adenosine deaminase, C protein, galactokinase, eukaryotic translation initiation factor, IFN-γ, and human protein homologous to DROER were increased, whereas core I protein, proteasome subunit p42, heterogeneous ribonuclear particle protein, chain B, and nucleoside diphosphate were decreased in the EoL-1-IR cells. Taken together, these results contribute to understanding the pathogenic mechanism of drug-resistant diseases.
Keywords : Chronic eosinophilic leukemia, Imatinib, Drug resistance