Evidence map›Paper›PMID 18071362›Full record

ArticleBritish journal of cancer2008

Frequent deletion of the CDKN2A locus in chordoma: analysis of chromosomal imbalances using array comparative genomic hybridisation.

K H Hallor, J Staaf, G Jönsson, M Heidenblad, F Vult von Steyern, H C F Bauer, M Ijszenga, P C W Hogendoorn, N Mandahl, K Szuhai and 1 more

Open access · hybridAbstract readComparative Study
In one paragraph

Article in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Chordoma: Genetics and Contemporary Management.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Molecular features and vulnerabilities of recurrent chordomas.Journal of experimental & clinical cancer research : CR · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Deficiency ofOncoTargets and therapy · 2020
    Article
  18. Review
  19. Article
  20. 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

11 authors at 3 institutions in 2 countries.

K H HallorDepartment of Clinical Genetics, Lund University Hospital, Lund SE-221 85, Sweden. Karolin.Hansen_Hallor@med.lu.se
J Staaf
G Jönsson
M Heidenblad
F Vult von Steyern
H C F Bauer
M Ijszenga
P C W Hogendoorn
N Mandahl
K Szuhai
F Mertens
Lund University · SELeiden University Medical Center · NLKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The initiating somatic genetic events in chordoma development have not yet been identified. Most cytogenetically investigated chordomas have displayed near-diploid or moderately hypodiploid karyotypes, with several numerical and structural rearrangements. However, no consistent structural chromosome aberration has been reported. This is the first array-based study characterising DNA copy number changes in chordoma. Array comparative genomic hybridisation (aCGH) identified copy number alterations in all samples and imbalances affecting 5 or more out of the 21 investigated tumours were seen on all chromosomes. In general, deletions were more common than gains and no high-level amplification was found, supporting previous findings of primarily losses of large chromosomal regions as an important mechanism in chordoma development. Although small imbalances were commonly found, the vast majority of these were detected in single cases; no small deletion affecting all tumours could be discerned. However, the CDKN2A and CDKN2B loci in 9p21 were homo- or heterozygously lost in 70% of the tumours, a finding corroborated by fluorescence in situ hybridisation, suggesting that inactivation of these genes constitute an important step in chordoma development.

Indexed as

Chromosome AberrationsGene DeletionGenes, p16Nucleic Acid HybridizationOligonucleotide Array Sequence AnalysisAdultAgedAged, 80 and overChordomaChromosomes, Human, Pair 9Cyclin-Dependent Kinase Inhibitor p15FemaleGene DosageHumansIn Situ Hybridization, FluorescenceMaleCDKN2B protein, humanCyclin-Dependent Kinase Inhibitor p15

Identifiers

PMID18071362
PMCPMC2361468
OpenAlexW2000611245

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.