ArticleExperimental cell research2009
Short and long-term tumor cell responses to Aurora kinase inhibitors.
Article in Experimental cell research, 2009. 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.
- Reversing tozasertib resistance in glioma through inhibition of pyruvate dehydrogenase kinases.Molecular oncology · 2022Article
- Microtubule-associated proteins promote microtubule generation in the absence of γ-tubulin in human colon cancer cells.The Journal of cell biology · 2021Article
- RNA Interference-Mediated Aurora Kinase A Gene Silencing Inhibits Human Glioma Cells Proliferation and Tumor Growth in Mice.Journal of Cancer · 2021Article
- Analysis of the role of GSK3 in the mitotic checkpoint.Scientific reports · 2018Article
- Targeting bromodomain and extraterminal proteins in breast cancer.Pharmacological research · 2018Review
- Ku70 Serine 155 mediates Aurora B inhibition and activation of the DNA damage response.Scientific reports · 2016Article
- Bromodomain and Extraterminal Protein Inhibition Blocks Growth of Triple-negative Breast Cancers through the Suppression of Aurora Kinases.The Journal of biological chemistry · 2016Article
- Borealin dimerization mediates optimal CPC checkpoint function by enhancing localization to centromeres and kinetochores.Nature communications · 2015Article
- Induction of p21CIP1 protein and cell cycle arrest after inhibition of Aurora B kinase is attributed to aneuploidy and reactive oxygen species.The Journal of biological chemistry · 2014Article
- Mitosis as an anti-cancer drug target.Chromosoma · 2013Review
- A role for p38 in transcriptional elongation of p21 (CIP1) in response to Aurora B inhibition.Cell cycle (Georgetown, Tex.) · 2013Article
- Ras-driven transcriptome analysis identifies aurora kinase A as a potential malignant peripheral nerve sheath tumor therapeutic target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Sensitivity of BRCA2 mutated human cell lines to Aurora kinase inhibition.Investigational new drugs · 2012Article
- Regulation of sororin by Cdk1-mediated phosphorylation.Journal of cell science · 2011Article
- Dynamin inhibitors induce caspase-mediated apoptosis following cytokinesis failure in human cancer cells and this is blocked by Bcl-2 overexpression.Molecular cancer · 2011Article
- VX680/MK-0457, a potent and selective Aurora kinase inhibitor, targets both tumor and endothelial cells in clear cell renal cell carcinoma.American journal of translational research · 2010Article
- Activity of the Aurora kinase inhibitor VX-680 against Bcr/Abl-positive acute lymphoblastic leukemias.Molecular cancer therapeutics · 2010Article
- Role of senescence and mitotic catastrophe in cancer therapy.Cell division · 2010Article
- Discovery and exploitation of inhibitor-resistant aurora and polo kinase mutants for the analysis of mitotic networks.The Journal of biological chemistry · 2009Article
- Aurora kinase inhibitors as anticancer molecules.Biochimica et biophysica actaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Aurora kinases are essential for mitosis and are candidate targets of novel chemotherapeutic agents. The inhibitors ZM447439, MK-0457 (VX-680) as well as Hesperadin have been used to dissect the roles of Aurora kinases in the cell cycle and have been tested clinically for the treatment of cancer. Here we have carried out a detailed kinetic analysis of two isogenic cell lines differing in p53 function and have compared the effects of ZM447439 and VE-465 (related to MK-0457). We find that p53 is needed for efficient cell cycle arrest when Aurora kinases are inhibited by either ZM447439 or VE-465. However, the p53-induced cell cycle block is neither immediate nor absolute. ZM447439 induced the localized accumulation of gammaH2A.X indicating that p53 induction by this drug occurs in response to DNA damage. Our analysis of the long-term effects of ZM447439 indicates that cells can evade killing by the drug, but not via a classical drug-resistance mechanism. Several mechanisms to explain how cells may evade killing by Aurora kinase inhibitors are described.
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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.