Evidence map›Paper›PMID 41530586›Full record

ArticleDiscover oncology2026

Abnormal PLK2 expression is associated with specific subtypes and may help risk stratification in acute myeloid leukemia.

Qin Chen, Zijun Xu, Tingting Du, Wei Zhao, Dongming Yao, Haoxi Ni

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Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Qin ChenLaboratory Center, Affiliated People's Hospital of Jiangsu University, Zhenjiang, People's Republic of China. 1049572816@qq.com.
Zijun XuLaboratory Center, Affiliated People's Hospital of Jiangsu University, Zhenjiang, People's Republic of China.
Tingting DuInstitute of Hematology, Jiangsu University, Zhenjiang, People's Republic of China.
Wei ZhaoInstitute of Hematology, Jiangsu University, Zhenjiang, People's Republic of China.
Dongming YaoInstitute of Hematology, Jiangsu University, Zhenjiang, People's Republic of China.
Haoxi NiLaboratory Center, Affiliated People's Hospital of Jiangsu University, Zhenjiang, People's Republic of China.

Funding

the Research Fund Project of Zhenjiang First People's Hospital Y2022010the Research Fund Project of Zhenjiang First People's Hospital Y2023007-Sthe Research Fund Project of Zhenjiang First People's Hospital YP2023001the Social Development Foundation of Zhenjiang SH2023022the Social Development Foundation of Zhenjiang SH2024001the Social Development Foundation of Zhenjiang SH2024031the Youth Medical Talents Project of "Ke Jiao Qiang Wei" project of Jiangsu province QNRC2016449the Zhenjiang Clinical Research Center of Hematology SS2018009
6 · The paper itself

Abstract

Abnormal expression of polo-like kinase 2 (PLK2) has been identified in various cancers and is correlated with disease progression, chemoresistance, prognosis, and recurrence. However, the clinical significance of abnormal PLK2 expression in acute myeloid leukemia (AML) has not been explored fully. The present investigation explored the PLK2 expression status and clinical significance in AML. PLK2 mRNA transcript was significantly higher in AML patients than in controls determined by public database analysis and real-time quantitative PCR validation. The clinical significance of PLK2 expression was assessed in AML cohorts from The Cancer Genome Atlas, the Gene Expression Omnibus and our hospital. The results of ROC curve analysis suggested that PLK2 transcript levels could be a potential indicator for AML diagnosis both in total AML and cytogenetically normal AML patients. Abnormal PLK2 expression was associated with specific subtypes in AML. High PLK2 expression was more common in FAB-M5 subtype and less frequent in favorable karyotypic/molecular risks. Patients with high PLK2 expression had a higher incidence of NPM1/DNMT3A mutations but a lower frequency of TP53/CEBPA mutations. PLK2 overexpression was an adverse prognostic indicator of overall survival for AML patients. Furthermore, patients with high PLK2 expression may profit more from transplantation than those without, suggesting PLK2 expression may have potential to help hypothesis-generating for HSCT decision support in AML. Additionally, PLK2 expression was strongly negatively correlated with PLK2 methylation both in AML patients, primary and demethylation-treated AML cells, indicating PLK2 expression is regulated by its promoter methylation. Bioinformatics analysis demonstrated high PLK2 expression was positively associated with oncogenes such as FAM163A, CTNND2, DAAM2, PITX1, POU1F1, mir-196a and negatively associated with tumor suppressors such as EMX2, PADI3, CDO1, SHOX2 and mir-508. In conclusion, the research elaborates on the expression profile and the clinical significance of PLK2 gene in AML, suggesting PLK2 expression may help risk stratification and hypothesis-generating for HSCT decision support.

Indexed as

Acute myeloid leukemiaExpressionMethylationPLK2Prognosis

Identifiers

PMID41530586
PMCPMC12886605

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.