ReviewCancers2020
The CINs of Polo-Like Kinase 1 in Cancer.
Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Identification of Natural Flavonoids Targeting PLK-1 as Potential Anti-Metastatic Agents: A Computational Approach.International journal of molecular sciences · 2026Article
- Discovery of Small Molecule Inhibitors against Polo-Like Kinase 1 Targeting Breast Cancer.Anti-cancer agents in medicinal chemistry · 2026Article
- The kinesin motor Kif9 regulates centriolar satellite positioning during interphase.Current biology : CB · 2025Article
- Identification of targetable vulnerabilities of PLK1-overexpressing cancers by synthetic dosage lethality.Cell genomics · 2025Article
- TheLife (Basel, Switzerland) · 2025Article
- SKA1 promotes oncogenic properties in oral dysplasia and oral squamous cell carcinoma, and augments resistance to radiotherapy.Molecular oncology · 2025Article
- Neoblast-like stem cells of Fasciola hepatica.PLoS pathogens · 2024Article
- DLGAP5 promotes lung adenocarcinoma growth via upregulating PLK1 and serves as a therapeutic target.Journal of translational medicine · 2024Article
- Leveraging the Fragment Molecular Orbital Method to Explore the PLK1 Kinase Binding Site and Polo-Box Domain for Potent Small-Molecule Drug Design.International journal of molecular sciences · 2023Article
- The Role of Polo-Like Kinase 1 in Regulating the Forkhead Box Family Transcription Factors.Cells · 2023Review
- Polo-Like Kinase 1 Regulates Chromosomal Instability and Paclitaxel Resistance in Breast Cancer Cells.Journal of breast cancer · 2022Article
- Mitotic spindle formation in the absence of Polo kinase.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Prognostic Biomarkers in Uveal Melanoma: The Status Quo, Recent Advances and Future Directions.Cancers · 2021Review
- Chromosomal Instability in Acute Myeloid Leukemia.Cancers · 2021Review
- Review
- Integrated Transcriptome Analysis Reveals the Impact of Photodynamic Therapy on Cerebrovascular Endothelial Cells.Frontiers in oncology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Polo-like kinase 1 (PLK1) is overexpressed near ubiquitously across all cancer types and dysregulation of this enzyme is closely tied to increased chromosomal instability and tumor heterogeneity. PLK1 is a mitotic kinase with a critical role in maintaining chromosomal integrity through its function in processes ranging from the mitotic checkpoint, centrosome biogenesis, bipolar spindle formation, chromosome segregation, DNA replication licensing, DNA damage repair, and cytokinesis. The relation between dysregulated PLK1 and chromosomal instability (CIN) makes it an attractive target for cancer therapy. However, clinical trials with PLK1 inhibitors as cancer drugs have generally displayed poor responses or adverse side-effects. This is in part because targeting CIN regulators, including PLK1, can elevate CIN to lethal levels in normal cells, affecting normal physiology. Nevertheless, aiming at related genetic interactions, such as synthetic dosage lethal (SDL) interactions of PLK1 instead of PLK1 itself, can help to avoid the detrimental side effects associated with increased levels of CIN. Since PLK1 overexpression contributes to tumor heterogeneity, targeting SDL interactions may also provide an effective strategy to suppressing this malignant phenotype in a personalized fashion.
Indexed as
Identifiers
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.