Evidence map›Paper›PMID 24503940›Full record

ArticlePloS one2014

Resolving tumor heterogeneity: genes involved in chordoma cell development identified by low-template analysis of morphologically distinct cells.

Amin El-Heliebi, Thomas Kroneis, Karin Wagner, Katharina Meditz, Dagmar Kolb, Julia Feichtinger, Gerhard G Thallinger, Franz Quehenberger, Bernadette Liegl-Atzwanger, Beate Rinner

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Frontiers in oncology · 2022
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The molecular aspects of chordoma.Neurosurgical review · 2016
    Review
  8. Article
  9. 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

10 authors at 2 institutions in 1 country.

Amin El-HeliebiInstitute of Pathology, Medical University of Graz, Graz, Austria.
Thomas KroneisInstitute of Cell Biology, Histology & Embryology, Medical University of Graz, Graz, Austria.
Karin WagnerCenter for Medical Research, Medical University of Graz, Graz, Austria.
Katharina MeditzCenter for Medical Research, Medical University of Graz, Graz, Austria.
Dagmar KolbInstitute of Cell Biology, Histology & Embryology, Medical University of Graz, Graz, Austria ; Center for Medical Research, Medical University of Graz, Graz, Austria.
Julia FeichtingerInstitute for Genomics and Bioinformatics, Graz University of Technology, Graz, Austria ; Core Facility Bioinformatics, Austrian Centre of Industrial Biotechnology, Graz, Austria.
Gerhard G ThallingerInstitute for Genomics and Bioinformatics, Graz University of Technology, Graz, Austria ; Core Facility Bioinformatics, Austrian Centre of Industrial Biotechnology, Graz, Austria.
Franz QuehenbergerInstitute for Medical Informatics, Statistics and Documentation, Medical University of Graz, Graz, Austria.
Bernadette Liegl-AtzwangerInstitute of Pathology, Medical University of Graz, Graz, Austria.
Beate RinnerCenter for Medical Research, Medical University of Graz, Graz, Austria.
Medical University of Graz · ATGraz University of Technology · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The classical sacrococcygeal chordoma tumor presents with a typical morphology of lobulated myxoid tumor tissue with cords, strands and nests of tumor cells. The population of cells consists of small non-vacuolated cells, intermediate cells with a wide range of vacuolization and large heavily vacuolated (physaliferous) cells. To date analysis was only performed on bulk tumor mass because of its rare incidence, lack of suited model systems and technical limitations thereby neglecting its heterogeneous composition. We intended to clarify whether the observed cell types are derived from genetically distinct clones or represent different phenotypes. Furthermore, we aimed at elucidating the differences between small non-vacuolated and large physaliferous cells on the genomic and transcriptomic level. Phenotype-specific analyses of small non-vacuolated and large physaliferous cells in two independent chordoma cell lines yielded four candidate genes involved in chordoma cell development. UCHL3, coding for an ubiquitin hydrolase, was found to be over-expressed in the large physaliferous cell phenotype of MUG-Chor1 (18.7-fold) and U-CH1 (3.7-fold) cells. The mannosyltransferase ALG11 (695-fold) and the phosphatase subunit PPP2CB (18.6-fold) were found to be up-regulated in large physaliferous MUG-Chor1 cells showing a similar trend in U-CH1 cells. TMEM144, an orphan 10-transmembrane family receptor, yielded contradictory data as cDNA microarray analysis showed up- but RT-qPCR data down-regulation in large physaliferous MUG-Chor1 cells. Isolation of few but morphologically identical cells allowed us to overcome the limitations of bulk analysis in chordoma research. We identified the different chordoma cell phenotypes to be part of a developmental process and discovered new genes linked to chordoma cell development representing potential targets for further research in chordoma tumor biology.

Indexed as

Cell Line, TumorCell Transformation, NeoplasticChordomaComparative Genomic HybridizationFemaleGene Expression ProfilingHumansImmunohistochemistryMiddle AgedPhenotype

Identifiers

PMID24503940
PMCPMC3913634
OpenAlexW2093421736

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.