Evidence map›Paper›PMID 21734802›Full record

ArticleWorld journal of gastroenterology2011

Genomic imbalances in esophageal carcinoma cell lines involve Wnt pathway genes.

Jacqueline Brown, Hannelie Bothma, Robin Veale, Pascale Willem

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Roles and regulation of δ-catenin in tumorigenesis and neuronal diseases.Frontiers in cell and developmental biology · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. LRP1B: A Giant Lost in Cancer Translation.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Oncogenic function of SCCRO5/DCUN1D5 requires its Neddylation E3 activity and nuclear localization.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    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

4 authors at 1 institution in 1 country.

Jacqueline BrownNational Health Laboratory Services and University of the Witwatersrand, York Rd, Parktown Johannesburg 2193, South Africa. jacqueline.brown@nhls.ac.za
Hannelie Bothma
Robin Veale
Pascale Willem
National Health Laboratory Service · ZA

Funding

Medical Research Council
6 · The paper itself

Abstract

aimTo identify molecular markers shared across South African esophageal squamous cell carcinoma (ESCC) cell lines using cytogenetics, fluorescence in situ hybridization (FISH) and single nucleotide polymorphism (SNP) array copy number analysis.

methodsWe used conventional cytogenetics, FISH, and multicolor FISH to characterize the chromosomal rearrangements of five ESCC cell lines established in South Africa. The whole genome copy number profile was established from 250K SNP arrays, and data was analyzed with the CNAT 4.0 and GISTIC software.

resultsWe detected common translocation breakpoints involving chromosomes 1p11-12 and 3p11.2, the latter correlated with the deletion, or interruption of the EPHA3 gene. The most significant amplifications involved the following chromosomal regions and genes: 11q13.3 (CCND1, FGF3, FGF4, FGF19, MYEOV), 8q24.21(C-MYC, FAM84B), 11q22.1-q22.3 (BIRC2, BIRC3), 5p15.2 (CTNND2), 3q11.2-q12.2 (MINA) and 18p11.32 (TYMS, YES1). The significant deletions included 1p31.2-p31.1 (CTH, GADD45α, DIRAS3), 2q22.1 (LRP1B), 3p12.1-p14.2 (FHIT), 4q22.1-q32.1 (CASP6, SMAD1), 8p23.2-q11.1 (BNIP3L) and 18q21.1-q21.2 (SMAD4, DCC). The 3p11.2 translocation breakpoint was shared across four cell lines, supporting a role for genes involved at this site, in particular, the EPHA3 gene which has previously been reported to be deleted in ESCC.

conclusionThe finding that a significant number of genes that were amplified (FGF3, FGF4, FGF19, CCND1 and C-MYC) or deleted (SFRP2 gene) are involved in the Wnt and fibroblast growth factor signaling pathways, suggests that these pathways may be activated in these cell lines.

Indexed as

Biomarkers, TumorCarcinoma, Squamous CellCell Line, TumorChromosome AberrationsChromosomes, Human, Pair 1Chromosomes, Human, Pair 3Cytogenetic AnalysisEsophageal NeoplasmsFibroblast Growth FactorsHumansIn Situ Hybridization, FluorescenceKaryotypingPolymorphism, Single NucleotideSignal TransductionWnt ProteinsBiomarkers, TumorFibroblast Growth FactorsWnt ProteinsCancerEsophagusFluorescent in situ hybridizationSingle nucleotide polymorphism arrays

Identifiers

PMID21734802
PMCPMC3129505
OpenAlexW2099236143

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.