ArticleBrain pathology (Zurich, Switzerland)2013
Aurora kinase B is a potential therapeutic target in pediatric diffuse intrinsic pontine glioma.
Article in Brain pathology (Zurich, Switzerland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
20 citing papers in PubMed, 37 citations in OpenAlex.
- Development of a selectively AURKB targeting peptide degradation drug with artificial intelligence-assisted design for the treatment of acute lymphoblastic leukemia.Journal of advanced research · 2026Article
- AURKB affects the proliferation of clear cell renal cell carcinoma by regulating fatty acid metabolism.Discover oncology · 2025Article
- Radiotherapy and radio-sensitization in H3CNS neuroscience & therapeutics · 2023Review
- AURKA and PLK1 inhibition selectively and synergistically block cell cycle progression in diffuse midline glioma.iScience · 2022Article
- Reversing tozasertib resistance in glioma through inhibition of pyruvate dehydrogenase kinases.Molecular oncology · 2022Article
- Deploying Kinase Inhibitors to Study Pediatric Gliomas.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Diffuse intrinsic pontine glioma: current insights and future directions.Chinese neurosurgical journal · 2021Review
- Review
- RecQL4-Aurora B kinase axis is essential for cellular proliferation, cell cycle progression, and mitotic integrity.Oncogenesis · 2018Article
- Functional analysis of KIF20A, a potential immunotherapeutic target for glioma.Journal of neuro-oncology · 2017Article
- Polo-like Kinase 1 as a potential therapeutic target in Diffuse Intrinsic Pontine Glioma.BMC cancer · 2016Article
- Pediatric brainstem gliomas: new understanding leads to potential new treatments for two very different tumors.Current oncology reports · 2015Review
- Radiotherapy followed by aurora kinase inhibition targets tumor-propagating cells in human glioblastoma.Molecular cancer therapeutics · 2015Article
- Article
- Diffuse intrinsic pontine glioma: a reassessment.Journal of neuro-oncology · 2014Review
- Molecular profiling of childhood cancer: Biomarkers and novel therapies.BBA clinical · 2014Review
- Genomic analysis of diffuse intrinsic pontine gliomas identifies three molecular subgroups and recurrent activating ACVR1 mutations.Nature genetics · 2014Article
- Management of diffuse pontine gliomas in children: recent developments.Paediatric drugs · 2013Review
- Gliomas in children.Current treatment options in neurology · 2013Article
- Overcoming translational barriers in H3K27-altered diffuse midline glioma: Increasing the drug-tumor residence time.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Pediatric high-grade astrocytomas (HGAs) account for 15-20% of all pediatric central nervous system tumors. These neoplasms predominantly involve the supratentorial hemispheres or the pons--diffuse intrinsic pontine gliomas (DIPG). Assumptions that pediatric HGAs are biologically similar to adult HGAs have recently been challenged, and the development of effective therapeutic modalities for DIPG and supratentorial HGA hinges on a better understanding of their biological properties. Here, 20 pediatric HGAs (9 DIPGs and 11 supratentorial HGAs) were subject to gene expression profiling following approval by the research ethics board at our institution. Many of these tumors showed expression signatures composed of genes that promote G1/S and G2/M cell cycle progression. In particular, Aurora kinase B (AURKB) was consistently and highly overexpressed in 6/9 DIPGs and 8/11 HGAs. Array data were validated using quantitative real-time PCR and immunohistochemistry, as well as cross-validation of our data set with previously published series. Inhibition of Aurora B activity in DIPG and in pediatric HGA cell lines resulted in growth arrest accompanied by morphological changes, cell cycle aberrations, nuclear fractionation and polyploidy as well as a reduction in colony formation. Our data highlight Aurora B as a potential therapeutic target in DIPG.
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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.