Evidence map›Paper›PMID 25393000›Full record

ArticlePloS one2014

Normal and functional TP53 in genetically stable myxoid/round cell liposarcoma.

Anders Ståhlberg, Christina Kåbjörn Gustafsson, Katarina Engtröm, Christer Thomsen, Soheila Dolatabadi, Emma Jonasson, Chieh-Yuan Li, David Ruff, Shiaw-Min Chen, Pierre Åman

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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Myxoid Liposarcomas: Systemic Treatment Options.Current treatment options in oncology · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
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  15. 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 2 countries.

Anders StåhlbergSahlgrenska Cancer Center, Department of Pathology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Christina Kåbjörn GustafssonSahlgrenska Cancer Center, Department of Pathology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Katarina EngtrömDepartment of Oncology, Institute of Medical Sciences, University of Gothenburg, Gothenburg, Sweden.
Christer ThomsenSahlgrenska Cancer Center, Department of Pathology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Soheila DolatabadiSahlgrenska Cancer Center, Department of Pathology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Emma JonassonSahlgrenska Cancer Center, Department of Pathology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Chieh-Yuan LiGenetic, Medical and Applied Sciences division, Life Science Group, Thermo Fisher Scientific, South San Francisco, CA, United States of America.
David RuffGenetic, Medical and Applied Sciences division, Life Science Group, Thermo Fisher Scientific, South San Francisco, CA, United States of America.
Shiaw-Min ChenGenetic, Medical and Applied Sciences division, Life Science Group, Thermo Fisher Scientific, South San Francisco, CA, United States of America.
Pierre ÅmanSahlgrenska Cancer Center, Department of Pathology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
University of Gothenburg · SEThermo Fisher Scientific (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myxoid/round-cell liposarcoma (MLS/RCLS) is characterized by either the fusion gene FUS-DDIT3 or the less commonly occurring EWSR1-DDIT3 and most cases carry few or no additional cytogenetic changes. There are conflicting reports concerning the status and role of TP53 in MLS/RCLS. Here we analysed four MLS/RCLS derived cell lines for TP53 mutations, expression and function. Three SV40 transformed cell lines expressed normal TP53 proteins. Irradiation caused normal posttranslational modifications of TP53 and induced P21 expression in two of these cell lines. Transfection experiments showed that the FUS-DDIT3 fusion protein had no effects on irradiation induced TP53 responses. Ion Torrent AmpliSeq screening, using the Cancer Hotspot panel, showed no dysfunctional or disease associated alleles/mutations. In conclusion, our results suggest that most MLS/RCLS cases carry functional TP53 genes and this is consistent with the low numbers of secondary mutations observed in this tumor entity.

Indexed as

MutationCell Line, TransformedCell Line, TumorCyclin-Dependent Kinase Inhibitor p21Genomic InstabilityHumansLiposarcoma, MyxoidTumor Suppressor Protein p53CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25393000
PMCPMC4231113
OpenAlexW2079386541

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.