Evidence map›Paper›PMID 23019410›Full record

ArticleNeoplasia (New York, N.Y.)2012

High-resolution whole-genome analysis of skull base chordomas implicates FHIT loss in chordoma pathogenesis.

Roberto Jose Diaz, Mustafa Guduk, Rocco Romagnuolo, Christian A Smith, Paul Northcott, David Shih, Fitim Berisha, Adrienne Flanagan, David G Munoz, Michael D Cusimano and 2 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  3. Article
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  7. Frontiers in oncology · 2022
    Article
  8. Article
  9. Deficiency ofOncoTargets and therapy · 2020
    Article
  10. Article
  11. The molecular aspects of chordoma.Neurosurgical review · 2016
    Review
  12. Review
  13. Epigenetic deregulations in chordoma.Cell proliferation · 2015
    Review
  14. Article
  15. Article
  16. Molecular profiling of chordoma.International journal of oncology · 2014
    Article
  17. Article
  18. Article
  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

12 authors at 6 institutions in 3 countries.

Roberto Jose DiazArthur and Sonia Labatt Brain Tumor Research Centre, The Hospital for Sick Children, Toronto, Ontario, Canada.
Mustafa Guduk
Rocco Romagnuolo
Christian A Smith
Paul Northcott
David Shih
Fitim Berisha
Adrienne Flanagan
David G Munoz
Michael D Cusimano
M Necmettin Pamir
James T Rutka
SickKids Foundation · CAAcıbadem University · TRHospital for Sick Children · CARoyal National Orthopaedic Hospital · GBSt. Michael's Hospital · CAUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Chordoma is a rare tumor arising in the sacrum, clivus, or vertebrae. It is often not completely resectable and shows a high incidence of recurrence and progression with shortened patient survival and impaired quality of life. Chemotherapeutic options are limited to investigational therapies at present. Therefore, adjuvant therapy for control of tumor recurrence and progression is of great interest, especially in skull base lesions where complete tumor resection is often not possible because of the proximity of cranial nerves. To understand the extent of genetic instability and associated chromosomal and gene losses or gains in skull base chordoma, we undertook whole-genome single-nucleotide polymorphism microarray analysis of flash frozen surgical chordoma specimens, 21 from the clivus and 1 from C1 to C2 vertebrae. We confirm the presence of a deletion at 9p involving CDKN2A, CDKN2B, and MTAP but at a much lower rate (22%) than previously reported for sacral chordoma. At a similar frequency (21%), we found aneuploidy of chromosome 3. Tissue microarray immunohistochemistry demonstrated absent or reduced fragile histidine triad (FHIT) protein expression in 98% of sacral chordomas and 67%of skull base chordomas. Our data suggest that chromosome 3 aneuploidy and epigenetic regulation of FHIT contribute to loss of the FHIT tumor suppressor in chordoma. The finding that FHIT is lost in a majority of chordomas provides new insight into chordoma pathogenesis and points to a potential new therapeutic target for this challenging neoplasm.

Indexed as

Acid Anhydride HydrolasesAdolescentAdultAgedAged, 80 and overBis(5'-adenosyl)triphosphataseCell Transformation, NeoplasticChildChordomaDNA Copy Number VariationsFemaleGenome-Wide Association StudyHumansMaleMiddle AgedNeoplasm ProteinsAcid Anhydride HydrolasesBis(5'-adenosyl)triphosphataseNeoplasm Proteins

Identifiers

PMID23019410
PMCPMC3459274
OpenAlexW1564861257

What OpenQuestion holds

Textmetadata
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.