Blood Res  
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
1Seoul St. Mary’s Hematology Hospital, 2 Department 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.
Seoul St. Mary’s Hematology Hospital, College of Medicine, The Catholic University of Korea, 222 BanpoDaero, Seocho-Gu, Seoul 06591, Korea
E-mail: yoojink@catholic.ac.kr
Published online: April 11, 2019.
© The Korean Journal of Hematology. All rights reserved.

Abstract
Background: 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. PLK1 is upregulated in 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.
Methods: 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.
Results: 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 [2.10 (0.40–49.90)]. 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).
Conclusions: 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.


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