Evidence map›Paper›PMID 19250537›Full record

ArticleBMC cancer2009

Loss of heterozygosity of TRIM3 in malignant gliomas.

Jean-Louis Boulay, Urs Stiefel, Elisabeth Taylor, Béatrice Dolder, Adrian Merlo, Frank Hirth

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Diploidy confers genomic instability inbioRxiv : the preprint server for biology · 2025
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  4. Advances in the antitumor mechanisms of tripartite motif-containing protein 3.Journal of cancer research and clinical oncology · 2024
    Review
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  13. Review
  14. Modeling Neurodegenerative Disorders inInternational journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Exosomal TRIM3 is a novel marker and therapy target for gastric cancer.Journal of experimental & clinical cancer research : CR · 2018
    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

6 authors at 3 institutions in 2 countries.

Jean-Louis BoulayDepartment of Biomedicine, University Hospital, Basel, Switzerland. Jean-Louis.Boulay@unibas.ch
Urs Stiefel
Elisabeth Taylor
Béatrice Dolder
Adrian Merlo
Frank Hirth
University Hospital of Basel · CHKing's College London · GBUniversity of Basel · CH

Funding

Medical Research Council G0701498
6 · The paper itself

Abstract

backgroundMalignant gliomas are frequent primary brain tumors associated with poor prognosis and very limited response to conventional chemo- and radio-therapies. Besides sharing common growth features with other types of solid tumors, gliomas are highly invasive into adjacent brain tissue, which renders them particularly aggressive and their surgical resection inefficient. Therefore, insights into glioma formation are of fundamental interest in order to provide novel molecular targets for diagnostic purposes and potential anti-cancer drugs. Human Tripartite motif protein 3 (TRIM3) encodes a structural homolog of Drosophila brain tumor (brat) implicated in progenitor cell proliferation control and cancer stem cell suppression. TRIM3 is located within the loss of allelic heterozygosity (LOH) hotspot of chromosome segment 11p15.5, indicating a potential role in tumor suppression.

methodsHere we analyze 70 primary human gliomas of all types and grades and report somatic deletion mapping as well as single nucleotide polymorphism analysis together with quantitative real-time PCR of chromosome segment 11p15.5.

resultsOur analysis identifies LOH in 17 cases (24%) of primary human glioma which defines a common 130 kb-wide interval within the TRIM3 locus as a minimal area of loss. We further detect altered genomic dosage of TRIM3 in two glioma cases with LOH at 11p15.5, indicating homozygous deletions of TRIM3.

conclusionLoss of heterozygosity of chromosome segment 11p15.5 in malignant gliomas suggests TRIM3 as a candidate brain tumor suppressor gene.

Indexed as

Loss of HeterozygosityBrain NeoplasmsCarrier ProteinsChromosome MappingChromosomes, Human, Pair 11Gene DosageGenes, Tumor SuppressorGliomaHumansPolymerase Chain ReactionPolymorphism, Single NucleotideSequence Tagged SitesCarrier ProteinsTRIM3 protein, human

Identifiers

PMID19250537
PMCPMC2653542
OpenAlexW2018698422

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.