ArticleCancer research2014
Aurora-A inhibition offers a novel therapy effective against intracranial glioblastoma.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed.
- CBX6-CA9 axis: An epigenetic-metabolic vulnerability in glioblastoma.Molecular therapy. Oncology · 2026Article
- Chromatin-associated α-satellite RNA maintains chromosome stability by reestablishing SAF-A in the mitotic cell cycle.Nucleic acids research · 2025Article
- Article
- vNARs as Neutralizing Intracellular Therapeutic Agents: Glioblastoma as a Target.Antibodies (Basel, Switzerland) · 2024Review
- Targeting senescence as an anticancer therapy.Molecular oncology · 2022Review
- Article
- Aurora-A kinase is differentially expressed in the nucleus and cytoplasm in normal Müllerian epithelium and benign, borderline and malignant serous ovarian neoplasms.Diagnostic pathology · 2021Article
- Aurora kinase A inhibition reverses the Warburg effect and elicits unique metabolic vulnerabilities in glioblastoma.Nature communications · 2021Article
- Exploiting the Complexities of Glioblastoma Stem Cells: Insights for Cancer Initiation and Therapeutic Targeting.International journal of molecular sciences · 2020Review
- The therapeutic potential of Aurora kinases targeting in glioblastoma: from preclinical research to translational oncology.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Therapeutic Rationale to Target Highly Expressed Aurora kinase A Conferring Poor Prognosis in Cholangiocarcinoma.Journal of Cancer · 2020Article
- Activation of Aurora A kinase increases YAP stability via blockage of autophagy.Cell death & disease · 2019Article
- Cytotoxic synergy between alisertib and carboplatin versus alisertib and irinotecan are inversely dependent on MGMT levels in glioblastoma cells.Journal of neuro-oncology · 2019Article
- Elevated signature of a gene module coexpressed with CDC20 marks genomic instability in glioma.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Aurora A plays a dual role in migration and survival of human glioblastoma cells according to the CXCL12 concentration.Oncogene · 2019Article
- OncogenicOncotarget · 2018Article
- Tumour treating fields in a combinational therapeutic approach.Oncotarget · 2018Review
- G2/M inhibitors as pharmacotherapeutic opportunities for glioblastoma: the old, the new, and the future.Cancer biology & medicine · 2018Article
- An Aurora kinase inhibitor, AMG900, inhibits glioblastoma cell proliferation by disrupting mitotic progression.Cancer medicine · 2018Article
- Concurrent Inhibition of Neurosphere and Monolayer Cells of Pediatric Glioblastoma by Aurora A Inhibitor MLN8237 Predicted Survival Extension in PDOX Models.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Glioblastoma remains a devastating disease for which novel therapies are urgently needed. Here, we report that the Aurora-A kinase inhibitor alisertib exhibits potent efficacy against glioblastoma neurosphere tumor stem-like cells in vitro and in vivo. Many glioblastoma neurosphere cells treated with alisertib for short periods undergo apoptosis, although some regain proliferative activity upon drug removal. Extended treatment, however, results in complete and irreversible loss of tumor cell proliferation. Moreover, alisertib caused glioblastoma neurosphere cells to partially differentiate and enter senescence. These effects were also observed in glioma cells treated with the Aurora-A inhibitor TC-A2317 or anti-Aurora-A siRNA. Furthermore, alisertib extended median survival of mice bearing intracranial human glioblastoma neurosphere tumor xenografts. Alisertib exerted similar effects on glioblastoma neurosphere cells in vivo and resulted in markedly reduced activated phosphoThr288Aurora-A and increased abnormal mitoses and cellular ploidy, consistent with on-target activity. Our results offer preclinical proof-of-concept for alisertib as a new therapeutic for glioma treatment.
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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.