ReviewOncogene2005
Polo-like kinases and oncogenesis.
Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
186 citing papers in PubMed, 1 synthesis or guideline pooled it, 369 citations in OpenAlex.
- Patients with chronically diseased livers have lower incidence of colorectal liver metastases: a meta-analysis.PloS one · 2014Pooled it
- Trial
- Treatment of higher risk myelodysplastic syndrome patients unresponsive to hypomethylating agents with ON 01910.Na.Leukemia research · 2012Trial
- A Bilingual Computational Workflow for Identifying Potential PLK1 Inhibitors in American Sign Language and English.Journal of visualized experiments : JoVE · 2026Article
- The Role of Protein Kinases in the Management of Oncological Diseases by Acting on Ferroptotic Pathways.International journal of molecular sciences · 2026Review
- Bora bridges Aurora-A activation and substrate recognition of PLK1.EMBO reports · 2026Article
- Polo-like kinase 1-inhibitor co-complex structures via the surface-entropy reduction approach and a DARPin-assisted approach.Acta crystallographica. Section D, Structural biology · 2025Article
- High-throughput virtual screening, identification andJournal of enzyme inhibition and medicinal chemistry · 2025Article
- Thymoquinone-conjugated liposomes improve cytotoxic and proapoptotic effects against hepatocellular cancer by altering the EGFR/ERK/MEK signaling axis.Discover oncology · 2025Article
- Design, synthesis, and biological evaluation of 5-chlorine-2-amino-pyrimidine derivatives as potent PLK4 inhibitors.RSC medicinal chemistry · 2025Article
- Structural regulation of PLK1 activity: implications for cell cycle function and drug discovery.Cancer gene therapy · 2025Review
- Pharmacological inhibition of PLK1/PRC1 triggers mitotic catastrophe and sensitizes lung cancers to chemotherapy.Cell death & disease · 2025Article
- Cyclin C promotes development and progression of B-cell acute lymphoblastic leukemia by counteracting p53-mediated stress responses.Haematologica · 2025Article
- CYR61 Acts as an Intracellular Microtubule-Associated Protein and Coordinates Mitotic Progression via PLK1-FBW7 Pathway.International journal of biological sciences · 2024Article
- Design, synthesis, and biological evaluation of novel pyrimidin-2-amine derivatives as potent PLK4 inhibitors.RSC medicinal chemistry · 2023Article
- Article
- PLK1 and PARP positively correlate in Middle Eastern breast cancer and their combined inhibition overcomes PARP inhibitor resistance in triple negative breast cancer.Frontiers in oncology · 2023Article
- Escape from G1 arrest during acute MEK inhibition drives the acquisition of drug resistance.NAR cancer · 2022Article
- In vivo delivery of CRISPR-Cas9 genome editing components for therapeutic applications.Biomaterials · 2022Review
- Sequential Targeting of PLK1 and PARP1 Reverses the Resistance to PARP Inhibitors and Enhances Platin-Based Chemotherapy in BRCA-Deficient High-Grade Serous Ovarian Cancer with KRAS Amplification.International journal of molecular sciences · 2022Article
126 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo-like kinases (Plks) play pivotal roles in the regulation of cell cycle progression. Plk1, the best characterized family member among mammalian Plks, strongly promotes the progression of cells through mitosis. Furthermore, Plk1 is found to be overexpressed in a variety of human tumors and its expression correlates with cellular proliferation and prognosis of tumor patients. Although all Plks share two conserved elements, the N-terminal Ser/Thr kinase domain and a highly homologues C-terminal region termed the polo-box motif, their functions diverge considerably. While Plk1 is inhibited by different checkpoint pathways, Plk2 and Plk3 are activated by the spindle checkpoint or the DNA damage checkpoint. Thus, Plk2 and Plk3 seem to inhibit oncogenic transformation. Deregulation of Plk1 activity contributes to genetic instability, which in turn leads to oncogenic transformation. In contrast, Plk2 and Plk3 are involved in checkpoint-mediated cell cycle arrest to ensure genetic stability, thereby inhibiting the accumulation of genetic defects. In this review, we shall discuss the roles of Plks in oncogenesis and Plk1 as a target for therapeutic intervention against cancer.
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What OpenQuestion holds
Registered trials
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.