Evidence map›Paper›PMID 19147536›Full record

ArticleMolecular cancer research : MCR2009

Loss-of-function fibroblast growth factor receptor-2 mutations in melanoma.

Michael G Gartside, Huaibin Chen, Omar A Ibrahimi, Sara A Byron, Amy V Curtis, Candice L Wellens, Ana Bengston, Laura M Yudt, Anna V Eliseenkova, Jinghong Ma and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.0field-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

60 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Gray-Horse Melanoma-A Wolf in Sheep's Clothing.International journal of molecular sciences · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Cancer discovery · 2021
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. FGF Family: From Drug Development to Clinical Application.International journal of molecular sciences · 2018
    Review
  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

20 authors at 6 institutions in 2 countries.

Michael G GartsideDivision of Cancer and Cell Biology, Translational Genomics Research Institute, Phoenix, AZ 85004, USA.
Huaibin Chen
Omar A Ibrahimi
Sara A Byron
Amy V Curtis
Candice L Wellens
Ana Bengston
Laura M Yudt
Anna V Eliseenkova
Jinghong Ma
John A Curtin
Pilar Hyder
Ursula L Harper
Erica Riedesel
Graham J Mann
Jeffrey M Trent
Boris C Bastian
Paul S Meltzer
Moosa Mohammadi
Pamela M Pollock
New York University · USNational Cancer Institute · USTranslational Genomics Research Institute · USUniversity of California, San Francisco · USCenter for Cancer Research · USWestmead Institute · AU

Funding

MEDICAL SCIENTIST TRAININGT32GM007308 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PHILIPS, MARK REID · 1985 to 2019
$23.2M
Cancer Genomics Technology DevelopmentZIABC011091 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MELTZER, PAUL S. · 2009 to 2025
$16.9M
MECHANISMS OF FGF RECEPTOR REGULATION AND SIGNALINGR01DE013686 · NIDCR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MOHAMMADI, MOOSA · 2000 to 2020
$12.3M
Biomarker Discovery for the Classification of MelanomaR01CA131524 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BASTIAN, BORIS C. · 2008 to 2012
$1.9M
NCI NIH HHS R01 CA131524NIDCR NIH HHS 2R01 DE 13686-08NIDCR NIH HHS R01 DE013686NIGMS NIH HHS T32 GM007308
6 · The paper itself

Abstract

We report that 10% of melanoma tumors and cell lines harbor mutations in the fibroblast growth factor receptor 2 (FGFR2) gene. These novel mutations include three truncating mutations and 20 missense mutations occurring at evolutionary conserved residues in FGFR2 as well as among all four FGFRs. The mutation spectrum is characteristic of those induced by UV radiation. Mapping of these mutations onto the known crystal structures of FGFR2 followed by in vitro and in vivo studies show that these mutations result in receptor loss of function through several distinct mechanisms, including loss of ligand binding affinity, impaired receptor dimerization, destabilization of the extracellular domains, and reduced kinase activity. To our knowledge, this is the first demonstration of loss-of-function mutations in a class IV receptor tyrosine kinase in cancer. Taken into account with our recent discovery of activating FGFR2 mutations in endometrial cancer, we suggest that FGFR2 may join the list of genes that play context-dependent opposing roles in cancer.

Indexed as

MutationPolymorphism, Single NucleotideCell DivisionCell Line, TumorConserved SequenceHumansMelanomaModels, MolecularProtein ConformationReceptor, Fibroblast Growth Factor, Type 2Skin NeoplasmsFGFR2 protein, humanReceptor, Fibroblast Growth Factor, Type 2

Identifiers

PMID19147536
PMCPMC4233648
OpenAlexW2108939654

What OpenQuestion holds

Textmetadata
LicenceTDM
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.