Evidence map›Paper›PMID 20501624›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2010

Control of tumorigenesis and chemoresistance by the DEK oncogene.

Erica Riveiro-Falkenbach, María S Soengas

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

48 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. A DEK domain-containing protein GhDEK2D mediatedPlant signaling & behavior · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Role of the DEK oncogene in the development of squamous cell carcinoma.International journal of clinical oncology · 2020
    Review
  18. 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

2 authors at 1 institution in 1 country.

Erica Riveiro-FalkenbachCentro Nacional de Investigaciones Oncológicas (Spanish National Cancer Research Centre), Madrid, Spain.
María S Soengas
Spanish National Cancer Research Centre · ES

Funding

Apoptosis in Melanoma Progression and ChemoresistanceR01CA107237 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SOENGAS, MARIA S · 2004 to 2008
$1.3M
The Unfolded Protein Response in Melanoma Progression and ChemoresistanceR01CA125017 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SOENGAS, MARIA S · 2008 to 2012
$1.0M
NCI NIH HHS CA125017NCI NIH HHS R01 CA107237NCI NIH HHS R01 CA125017
6 · The paper itself

Abstract

Slight modifications of chromatin dynamics can translate into small- and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and accessibility are tightly dependent on chromatin architecture. Consequently, it is perhaps not surprising that factors controlling chromatin organization are frequently deregulated (directly or indirectly) in cancer cells. DEK is emerging as a novel class of DNA topology modulators that can be both targets and effectors of protumorigenic events. The locus containing DEK at chromosome 6p22.3 is amplified or reorganized in multiple cancer types. In addition, DEK can be subject to a variety of tumor-associated transcriptional and post-translational modifications. In turn, DEK can favor cell transformation, at least in part by inhibiting cell differentiation and premature senescence. More recently, DEK has also been linked to the resistance of malignant cells to apoptotic inducers. Interestingly, a fraction of DEK can also bind RNA and affect alternative splicing, further illustrating the pleiotropic roles that this protein may exert in cancer cells. Here we will summarize the current literature about the regulation and function(s) of DEK as a proto-oncogene. In addition, the translational relevance of DEK as a putative diagnostic marker and candidate for drug development will be discussed.

Indexed as

Drug Resistance, NeoplasmGene Expression RegulationCell Transformation, NeoplasticChromatinChromosomal Proteins, Non-HistoneDrug Delivery SystemsHumansNeoplasmsOncogene ProteinsPoly-ADP-Ribose Binding ProteinsProtein Processing, Post-TranslationalProto-Oncogene MasProto-OncogenesChromatinChromosomal Proteins, Non-HistoneDEK protein, humanMAS1 protein, humanOncogene ProteinsPoly-ADP-Ribose Binding ProteinsProto-Oncogene Mas

Identifiers

PMID20501624
PMCPMC2931273
OpenAlexW2121490986

What OpenQuestion holds

Textmetadata
LicenceTDM
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.