ArticleBMC cancer2016
Polo-like Kinase 1 as a potential therapeutic target in Diffuse Intrinsic Pontine Glioma.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Reirradiation for diffuse intrinsic pontine glioma: a systematic review and meta-analysis.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2019Pooled it
- Radiotherapy and radio-sensitization in H3CNS neuroscience & therapeutics · 2023Review
- Pediatric Diffuse Midline Gliomas: An Unfinished Puzzle.Diagnostics (Basel, Switzerland) · 2022Review
- AURKA and PLK1 inhibition selectively and synergistically block cell cycle progression in diffuse midline glioma.iScience · 2022Article
- The Intricate Epigenetic and Transcriptional Alterations in Pediatric High-Grade Gliomas: Targeting the Crosstalk as the Oncogenic Achilles' Heel.Biomedicines · 2022Review
- Review
- Calcyphosine promotes the proliferation of glioma cells and serves as a potential therapeutic target.The Journal of pathology · 2021Article
- Combinatorial Effect of PLK1 Inhibition with Temozolomide and Radiation in Glioblastoma.Cancers · 2021Article
- Review
- Radiosensitization in Pediatric High-Grade Glioma: Targets, Resistance and Developments.Frontiers in oncology · 2021Review
- Circular RNA ZNF609 promotes the malignant progression of glioma by regulating miR-1224-3p/PLK1 signaling.Journal of Cancer · 2021Article
- Review
- Article
- Proneural and mesenchymal glioma stem cells display major differences in splicing and lncRNA profiles.NPJ genomic medicine · 2020Article
- Radiosensitization of Non-Small Cell Lung Cancer Cells by the Plk1 Inhibitor Volasertib Is Dependent on the p53 Status.Cancers · 2019Article
- Long noncoding RNA ENST00000413528 sponges microRNA-593-5p to modulate human glioma growth via polo-like kinase 1.CNS neuroscience & therapeutics · 2019Article
- Identification of FDA-Approved Oncology Drugs with Selective Potency in High-Risk Childhood Ependymoma.Molecular cancer therapeutics · 2018Article
- Article
- The clinical and prognostic value of polo-like kinase 1 in lung squamous cell carcinoma patients: immunohistochemical analysis.Bioscience reports · 2017Article
- The GSK461364 PLK1 inhibitor exhibits strong antitumoral activity in preclinical neuroblastoma models.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDiffuse intrinsic pontine gliomas (DIPGs) are highly aggressive, fatal, childhood tumors that arise in the brainstem. DIPGs have no effective treatment, and their location and diffuse nature render them inoperable. Radiation therapy remains the only standard of care for this devastating disease. New therapeutic targets are needed to develop novel therapy for DIPG.
methodsWe examined the expression of PLK1 mRNA in DIPG tumor samples through microarray analysis and found it to be up regulated versus normal pons. Using the DIPG tumor cells, we inhibited PLK1 using a clinically relevant specific inhibitor BI 6727 and evaluated the effects on, proliferation, apoptosis, induction of DNA damage and radio sensitization of the DIPG tumor cells.
resultsTreatment of DIPG cell lines with BI 6727, a new generation, highly selective inhibitor of PLK1, resulted in decreased cell proliferation and a marked increase in cellular apoptosis. Cell cycle analysis showed a significant arrest in G2-M phase and a substantial increase in cell death. Treatment also resulted in an increased γH2AX expression, indicating induction of DNA damage. PLK1 inhibition resulted in radiosensitization of DIPG cells.
conclusionThese findings suggest that targeting PLK1 with small-molecule inhibitors, in combination with radiation therapy, will hold a novel strategy in the treatment of DIPG that warrants further investigation.
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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.