Evidence map›Paper›PMID 26779440›Full record

ReviewFrontiers in oncology2015

Aurora-A Kinase as a Promising Therapeutic Target in Cancer.

Antonino B D'Assoro, Tufia Haddad, Evanthia Galanis

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.8field-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

61 citing papers in PubMed, 124 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
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  5. Review
  6. Selective Aurora A-TPX2 Interaction Inhibitors HaveJournal of medicinal chemistry · 2024
    Article
  7. Article
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  10. Review
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  14. Review
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  18. Review
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1 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

3 authors at 2 institutions in 1 country.

Antonino B D'AssoroDepartment of Medical Oncology, Mayo Clinic College of Medicine, Rochester, MN, USA; Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Tufia HaddadDepartment of Medical Oncology, Mayo Clinic College of Medicine , Rochester, MN , USA.
Evanthia GalanisDepartment of Medical Oncology, Mayo Clinic College of Medicine, Rochester, MN, USA; Department of Molecular Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

The Role of CHFR in Tumorigenesis and Paclitaxel-Sensitivity in Breast CancerP50CA116201 · NCI · MAYO CLINIC ROCHESTER · PI PETER C LUCAS · 2005 to 2026
$49.9M
6 · The paper itself

Abstract

Mammalian Aurora family of serine/threonine kinases are master regulators of mitotic progression and are frequently overexpressed in human cancers. Among the three members of the Aurora kinase family (Aurora-A, -B, and -C), Aurora-A and Aurora-B are expressed at detectable levels in somatic cells undergoing mitotic cell division. Aberrant Aurora-A kinase activity has been implicated in oncogenic transformation through the development of chromosomal instability and tumor cell heterogeneity. Recent studies also reveal a novel non-mitotic role of Aurora-A activity in promoting tumor progression through activation of epithelial-mesenchymal transition reprograming resulting in the genesis of tumor-initiating cells. Therefore, Aurora-A kinase represents an attractive target for cancer therapeutics, and the development of small molecule inhibitors of Aurora-A oncogenic activity may improve the clinical outcomes of cancer patients. In the present review, we will discuss mitotic and non-mitotic functions of Aurora-A activity in oncogenic transformation and tumor progression. We will also review the current clinical studies, evaluating small molecule inhibitors of Aurora-A activity and their efficacy in the management of cancer patients.

Indexed as

cancercell cyclemitotic kinasetargeted therapytumor progression

Identifiers

PMID26779440
PMCPMC4701905
OpenAlexW2266287744

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.