Evidence map›Paper›PMID 20863917›Full record

ReviewBiochimica et biophysica acta

Aurora kinase inhibitors as anticancer molecules.

Hiroshi Katayama, Subrata Sen

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
6.7field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
  2. Article
  3. The Supression of Migration and Metastasis via Inhibition of Vascular Endothelial Growth Factor in Pancreatic Adenocarcinoma Cells Applied Danusertib.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Treatment of RB-deficient retinoblastoma with Aurora-A kinase inhibitor.The Kaohsiung journal of medical sciences · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Biotransformation Pathways and Metabolite Profiles of Oral [Drug metabolism and disposition: the biological fate of chemicals · 2020
    Article
  20. Article

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Hiroshi KatayamaDepartment of Molecular Pathology, Unit 951, The University of Texas M.D. Anderson Cancer Center, 7435 Fannin, Houston, TX 77054, USA.
Subrata Sen
Center for Translational Molecular Medicine · NLThe University of Texas MD Anderson Cancer Center · US

Funding

Novel human oncogene STK15/BTAK/Aurora 2R01CA089716 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SEN, SUBRATA · 2001 to 2012
$2.3M
NCI NIH HHS R01 CA089716NCI NIH HHS R01CA089716
6 · The paper itself

Abstract

Aurora kinase family of serine/threonine kinases are important regulators of mitosis that are frequently over expressed in human cancers and have been implicated in oncogenic transformation including development of chromosomal instability in cancer cells. In humans, among the three members of the kinase family, Aurora-A, -B and -C, only Aurora-A and -B are expressed at detectable levels in all somatic cells undergoing mitotic cell division and have been characterized in greater detail for their involvement in cellular pathways relevant to the development of cancer associated phenotypes. Aurora-A and -B are being investigated as potential targets for anticancer therapy. Development of inhibitors against Aurora kinases as anticancer molecules gained attention because of the facts that aberrant expression of these kinases leads to chromosomal instability and derangement of multiple tumor suppressor and oncoprotein regulated pathways. Preclinical studies and early phase I and II clinical trials of multiple Aurora kinase inhibitors as targeted anticancer drugs have provided encouraging results. This article discusses functional involvement of Aurora kinase-A and -B in the regulation of cancer relevant cellular phenotypes together with findings on some of the better characterized Aurora kinase inhibitors in modulating the functional interactions of Aurora kinases. Future possibilities about developing next generation Aurora kinase inhibitors and their clinical utility as anticancer therapeutic drugs are also discussed.

Indexed as

AnimalsAntineoplastic AgentsAurora Kinase AAurora KinasesCell Transformation, NeoplasticChromosomal InstabilityClinical Trials, Phase I as TopicClinical Trials, Phase II as TopicDrug Screening Assays, AntitumorGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansMitosisNeoplasmsProtein Kinase InhibitorsProtein Serine-Threonine KinasesAntineoplastic AgentsAURKA protein, humanAurora Kinase AAurora KinasesProtein Kinase InhibitorsProtein Serine-Threonine Kinases

Identifiers

PMID20863917
PMCPMC4501772
OpenAlexW2037988871

What OpenQuestion holds

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Registered trials

None linked

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.