Evidence map›Paper›PMID 19671766›Full record

ArticleMolecular cancer therapeutics2009

Aurora A is a negative prognostic factor and a new therapeutic target in human neuroblastoma.

Xiaoying Shang, Susan M Burlingame, M Fatih Okcu, Ningling Ge, Heidi V Russell, Rachel A Egler, Rodney D David, Sanjeev A Vasudevan, Jianhua Yang, Jed G Nuchtern

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 94 citations in OpenAlex.

  1. Phase II Trial of Alisertib in Combination with Irinotecan and Temozolomide for Patients with Relapsed or Refractory Neuroblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
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  11. Crystal structure of a covalently linked Aurora-A-MYCN complex.Acta crystallographica. Section D, Structural biology · 2023
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  19. Molecular Mechanisms ofFrontiers in oncology · 2020
    Review
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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

10 authors at 2 institutions in 1 country.

Xiaoying ShangTexas Children's Cancer Center, Michael E DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas 77030, USA.
Susan M Burlingame
M Fatih Okcu
Ningling Ge
Heidi V Russell
Rachel A Egler
Rodney D David
Sanjeev A Vasudevan
Jianhua Yang
Jed G Nuchtern
Children's Cancer Center · USBaylor College of Medicine · US

Funding

Analysis of a Novel Secreted Protein in NeuroblastomaR21CA106513 · NCI · BAYLOR COLLEGE OF MEDICINE · PI YANG, JIANHUA · 2005 to 2006
$254k
NCI NIH HHS 1R21CA106513-01A2NCI NIH HHS R21 CA106513
6 · The paper itself

Abstract

We studied expression of the Aurora A gene and its clinical significance in a cohort of neuroblastoma patients. In addition, we investigated the antitumor activity of MLN8054, a novel small-molecule inhibitor of Aurora A kinase, on cultured NB cell lines in vitro. Aurora A mRNA expression was assessed by quantitative real-time PCR in tumor tissue specimens from 67 patients at diagnosis and in 9 human neuroblastoma cell lines. Western blot assays for Aurora A protein were done on tumor tissue of 53 patients. The results were correlated with various prognostic factors of neuroblastoma. Aurora A mRNA and protein expression were identified in 9 of 9 neuroblastoma cell lines. Overexpression of Aurora A mRNA in neuroblastoma tumor tissue is associated with high risk (P = 0.019), high-stage (International Neuroblastoma Staging System III and IV) tumors (P = 0.007), unfavorable histology (P = 0.007), MYCN amplification (P = 0.017), disease relapse (P = 0.019), and decreased progression-free survival (P < 0.0001) but not correlated with the age at diagnosis (P = 0.877). Similarly, Aurora A protein expression also significantly correlated with high risk (P = 0.011), high stage (P = 0.0028), unfavorable histology (P = 0.0006), MYCN amplification (P = 0.0029), and disease relapse (P = 0.044). Small interfering RNA-mediated knockdown of the endogenous Aurora A gene causes a proliferation defect and enhances chemosensitivity in human neuroblastoma cell lines. In support of these observations, the Aurora A kinase inhibitor, MLN8054, markedly inhibited growth of cultured neuroblastoma cell lines through an apoptosis-dependent pathway. Overexpression of Aurora A is associated with disease progression in neuroblastoma. Inhibition of this kinase is a promising modality for neuroblastoma treatment.

Indexed as

Antineoplastic AgentsApoptosisAurora KinasesBenzazepinesCell Line, TumorCell ProliferationCohort StudiesHumansNeuroblastomaPrognosisProtein Serine-Threonine KinasesRNA, MessengerAntineoplastic AgentsAurora KinasesBenzazepinesMLN8054Protein Serine-Threonine KinasesRNA, Messenger

Identifiers

PMID19671766
PMCPMC3966113
OpenAlexW2122742535

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Registered trials

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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.