Evidence map›Paper›PMID 16222316›Full record

ArticleBritish journal of cancer2005

Overexpression of aurora B kinase (AURKB) in primary non-small cell lung carcinoma is frequent, generally driven from one allele, and correlates with the level of genetic instability.

S L Smith, N L Bowers, D C Betticher, O Gautschi, D Ratschiller, P R Hoban, R Booton, M F Santibáñez-Koref, J Heighway

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 11% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Double-checking chromosome segregation.The Journal of cell biology · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Aurora B kinase: a potential drug target for cancer therapy.Journal of cancer research and clinical oncology · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

4 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

9 authors at 5 institutions in 2 countries.

S L Smith1Gene Function Group, Roy Castle Lung Cancer Programme, University of Liverpool Cancer Research Centre, 200 London Road, Liverpool L3 9TA, UK.
N L Bowers
D C Betticher
O Gautschi
D Ratschiller
P R Hoban
R Booton
M F Santibáñez-Koref
J Heighway
University of Bern · CHUniversity of Liverpool · GBCentre for Life · GBKeele University · GBThe Christie Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aurora kinases are key regulators of chromosome segregation during mitosis. We have previously shown by microarray analysis of primary lung carcinomas and matched normal tissue that AURKB (22 out of 37) and AURKA (15 out of 37) transcripts are frequently over-represented in these tumours. We now confirm these observations in a second series of 44 carcinomas and also show that aurora B kinase protein levels are raised in the tumours compared to normal tissue. Elevated levels of expression in tumours are not a consequence of high-level amplification of the AURKB gene. Using a coding sequence polymorphism we show that in most cases (seven out of nine) tumour expression is predominantly driven from one AURKB allele. Given the function of aurora B kinase, we examined whether there was an association between expression levels and genetic instability. We defined two groups of high and low AURKB expression. Using a panel of 10 microsatellite markers, we found that the group showing the higher level of expression had a higher frequency of allelic imbalance (P=0.0012). Analysis of a number of other genes that are strongly and specifically expressed in tumour over normal lung, including SERPINB5, TERT and PRAME, showed marked allelic expression imbalances in the tumour tissue in the context of balanced or only marginally imbalanced relative allelic copy numbers. Our data support a model of early carcinogenesis wherein defects in the process of inactivation of lung stem-cell associated genes during differentiation, contributes to the development of carcinogenesis.

Indexed as

Allelic ImbalanceGene Expression Regulation, EnzymologicAntigens, NeoplasmAurora Kinase AAurora Kinase BAurora KinasesBiomarkers, TumorBlotting, WesternCarcinoma, Non-Small-Cell LungCatalytic DomainDNA-Binding ProteinsEpithelial CellsGenes, Tumor SuppressorHumansLung NeoplasmsMicrosatellite RepeatsAntigens, NeoplasmAURKA protein, humanAURKB protein, humanAurora Kinase AAurora Kinase BAurora KinasesBiomarkers, TumorDNA-Binding ProteinsPRAME protein, humanProtein Serine-Threonine KinasesSerine Proteinase InhibitorsSERPIN-B5SerpinsTelomeraseTERT protein, human

Identifiers

PMID16222316
PMCPMC2361619
OpenAlexW2042783729

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.