Blood Res 2019; 54(2): 102-107
Enhanced polo-like kinase 1 expression in myelodysplastic syndromes
Kyoung Il Min1, Silvia Park1, Seung-Hwan Shin2, Yong-Rim Kwon3, Hye-Joung Kim3, Yoo Jin Kim3,4
1Division of Hematology, Department of Internal Medicine, Seoul St. Mary’s Hematology Hospital, 2Department of Hematology, Yeoido St. Mary’s Hospital, 3Laboratory of Hematological Disease and Immunology, 4Leukemia Research Institute, College of Medicine, The Catholic University of Korea, Seoul, Korea
Correspondence to: Yoo Jin Kim, M.D., Ph.D.
Division of Hematology, Department of Internal Medicine, Seoul St. Mary’s Hematology Hospital, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Korea
Received: November 9, 2018; Revised: November 22, 2018; Accepted: November 25, 2018; Published online: June 30, 2019.
© The Korean Journal of Hematology. All rights reserved.

cc 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.
Cancer is characterized by uncontrolled cellular proliferation, and Polo-like kinase 1 (PLK1), a key regulator of the cell cycle, is overexpressed in many cancers, including acute leukemia and lymphoma. However, the dynamics of PLK1 transcription in myelodysplastic syndromes (MDS) are unknown. This study aimed to investigate the transcript dynamics of PLK1 and determine its role in the pathophysiology of MDS.
PLK1 mRNA obtained from the bone marrow samples of 67 patients with MDS, 16 patients with secondary acute myeloid leukemia (sAML), and 10 healthy controls were analyzed using quantitative real-time PCR and compared according to various clinical parameters.
The median PLK1 expression levels differed slightly, but not significantly, between MDS and sAML patients [661.21 (range, 29.38‒8,987.31) vs. 1,462.05 (32.22‒5,734.09), respectively], but were significantly higher (P<0.001) than the levels in the healthy controls [19.0 (1.60‒49.90)]. Further analyses of PLK1 levels according to the WHO classification of MDS, prognostic risk groups, karyotype risk groups, marrow blast percentage, and depth of cytopenia did not reveal any significant associations. In patients progressing to sAML, PLK1 expression levels differed significantly according to the presence or absence of resistance to hypomethylation treatment (2,470.58 vs. 415.98, P=0.03).
PLK1 is upregulated in MDS patients; however, its role in the pathophysiology of MDS is unclear. Gene upregulation in cases with pharmacotherapeutic resistance warrants further investigation.
Keywords: Myelodysplastic syndromes, Polo-like kinase 1, Protein-serine-threonine kinases, DNA methylation, Gene expression


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