Evidence map›Paper›PMID 21943074›Full record

ArticleBMC cancer2011

Aurora kinases are expressed in medullary thyroid carcinoma (MTC) and their inhibition suppresses in vitro growth and tumorigenicity of the MTC derived cell line TT.

Enke Baldini, Yannick Arlot-Bonnemains, Salvatore Sorrenti, Caterina Mian, Maria R Pelizzo, Enrico De Antoni, Silvio Palermo, Stefania Morrone, Susi Barollo, Angela Nesca and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Acetate Metabolism in Thyroid Cancer Progression.International journal of molecular sciences · 2026
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  14. A new aurora in anaplastic thyroid cancer therapy.International journal of endocrinology · 2014
    Review
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  16. Maternally recruited Aurora C kinase is more stable than Aurora B to support mouse oocyte maturation and early development.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
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

13 authors at 5 institutions in 2 countries.

Enke BaldiniDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Yannick Arlot-Bonnemains
Salvatore Sorrenti
Caterina Mian
Maria R Pelizzo
Enrico De Antoni
Silvio Palermo
Stefania Morrone
Susi Barollo
Angela Nesca
Costanzo G Moretti
Massimino D'Armiento
Salvatore Ulisse
Sapienza University of Rome · ITUniversity of Padua · ITInstitut de génétique et de développement de Rennes · FRIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Aurora kinase family members, Aurora-A, -B and -C, are involved in the regulation of mitosis, and alterations in their expression are associated with cell malignant transformation. To date no information on the expression of these proteins in medullary thyroid carcinoma (MTC) are available. We here investigated the expression of the Aurora kinases in human MTC tissues and their potential use as therapeutic targets.

methodsThe expression of the Aurora kinases in 26 MTC tissues at different TNM stages was analyzed at the mRNA level by quantitative RT-PCR. We then evaluated the effects of the Aurora kinase inhibitor MK-0457 on the MTC derived TT cell line proliferation, apoptosis, soft agar colony formation, cell cycle and ploidy.

resultsThe results showed the absence of correlation between tumor tissue levels of any Aurora kinase and tumor stage indicating the lack of prognostic value for these proteins. Treatment with MK-0457 inhibited TT cell proliferation in a time- and dose-dependent manner with IC50 = 49.8 ± 6.6 nM, as well as Aurora kinases phosphorylation of substrates relevant to the mitotic progression. Time-lapse experiments demonstrated that MK-0457-treated cells entered mitosis but were unable to complete it. Cytofluorimetric analysis confirmed that MK-0457 induced accumulation of cells with ≥ 4N DNA content without inducing apoptosis. Finally, MK-0457 prevented the capability of the TT cells to form colonies in soft agar.

conclusionsWe demonstrate that Aurora kinases inhibition hampered growth and tumorigenicity of TT cells, suggesting its potential therapeutic value for MTC treatment.

Indexed as

AdultAgedAurora KinasesCarcinoma, NeuroendocrineCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHistonesHumansIntracellular SpaceMaleMiddle AgedMutationNeoplasm StagingPhosphorylationAurora KinasesHistonesProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-retRET protein, human

Identifiers

PMID21943074
PMCPMC3199016
OpenAlexW2075005660

What OpenQuestion holds

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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.