Evidence map›Paper›PMID 11114733›Full record

ArticleOncogene2000

Somatic mutations of fibroblast growth factor receptor 3 (FGFR3) are uncommon in carcinomas of the uterine cervix.

R Wu, D Connolly, C Ngelangel, F X Bosch, N Muñoz, K R Cho

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. The Conundrum of Genetic "Drivers" in Benign Conditions.Journal of the National Cancer Institute · 2016
    Review
  6. FGFR3-TACC3: A novel gene fusion in cervical cancer.Gynecologic oncology reports · 2015
    Article
  7. Article
  8. Functional roles of fibroblast growth factor receptors (FGFRs) signaling in human cancers.Apoptosis : an international journal on programmed cell death · 2013
    Review
  9. Mutational Status of FGFR3 in Oral Squamous Cell Carcinoma.Journal of dentistry (Tehran, Iran) · 2012
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. 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

6 authors at 5 institutions in 4 countries.

R WuDepartment of Pathology, The University of Michigan Medical School, Ann Arbor 48109, USA.
D Connolly
C Ngelangel
F X Bosch
N Muñoz
K R Cho
University of Michigan–Ann Arbor · USCentre International de Recherche sur le Cancer · FRInstitut Català d'Oncologia · ESRegional West Medical Center · USUniversity of the Philippines Manila · PH

Funding

MOLECULAR PATHOGENESIS OF CERVICAL CANCERR29CA064466 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHO, KATHLEEN R. · 1995 to 1999
–
NCI NIH HHS CA64466
6 · The paper itself

Abstract

Germline mutations of the gene encoding human fibroblast growth factor receptor 3 (FGFR3) have been shown to be responsible for several related autosomal dominant forms of syndromic craniosynostosis and short limb dwarfism. Somatic activating mutations of FGFR3 were recently reported to occur in three of 12 (25%) uterine cervical carcinomas and nine of 26 (35%) bladder carcinomas, suggesting that constitutive activation of FGFR3 may be an important mechanism underlying the development and/or progression of these common epithelial malignancies. In order to investigate further a possible role for FGFR3 mutations in cervical carcinogenesis, we performed sequence-based mutational analysis of FGFR3 in 51 primary cervical carcinomas and seven cervical carcinoma-derived cell lines. The regions analysed (exons 7, 10, 13, 15, and 19) encompassed all previously described FGFR3 mutations. A single nucleotide substitution at codon 249, predicting a serine to cysteine amino acid substitution (S249C) in the FGFR3 extracellular domain, was identified in one primary tumor. Only wild type FGFR3 alleles were identified in the remaining tumors and cell lines. The S249C mutation is the only FGFR3 mutation described to date in cervical carcinomas. These findings suggest that while activating mutations of FGFR3 occur in cervical cancer, they may not be as common as initially reported.

Indexed as

Mutation, MissenseProtein-Tyrosine KinasesBlotting, NorthernCarcinomaDNA Mutational AnalysisFemaleGerm-Line MutationHumansMiddle AgedReceptor, Fibroblast Growth Factor, Type 3Receptors, Fibroblast Growth FactorRNA, MessengerTumor Cells, CulturedUterine Cervical NeoplasmsFGFR3 protein, humanProtein-Tyrosine KinasesReceptor, Fibroblast Growth Factor, Type 3Receptors, Fibroblast Growth FactorRNA, Messenger

Identifiers

PMID11114733
OpenAlexW2327902685

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.