Evidence map›Paper›PMID 26425120›Full record

ReviewJournal of oncology2015

Dissecting the Potential Interplay of DEK Functions in Inflammation and Cancer.

Nicholas A Pease, Trisha Wise-Draper, Lisa Privette Vinnedge

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Potential ofMolecular and clinical oncology · 2022
    Article
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  15. Article
  16. Article
  17. Article
  18. Observational
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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

3 authors at 2 institutions in 1 country.

Nicholas A PeaseDivision of Oncology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Trisha Wise-DraperDepartment of Internal Medicine, Division of Hematology/Oncology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Lisa Privette VinnedgeDivision of Oncology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati Medical Center · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
KL2 Training ProgramKL2TR001426 · NCATS · UNIVERSITY OF CINCINNATI · PI ZELLER, MARGARET H · 2015 to 2024
$6.8M
NCATS NIH HHS UL1 TR001425
6 · The paper itself

Abstract

There is a long-standing correlation between inflammation, inflammatory cell signaling pathways, and tumor formation. Understanding the mechanisms behind inflammation-driven tumorigenesis is of great research and clinical importance. Although not entirely understood, these mechanisms include a complex interaction between the immune system and the damaged epithelium that is mediated by an array of molecular signals of inflammation-including reactive oxygen species (ROS), cytokines, and NFκB signaling-that are also oncogenic. Here, we discuss the association of the unique DEK protein with these processes. Specifically, we address the role of DEK in chronic inflammation via viral infections and autoimmune diseases, the overexpression and oncogenic activity of DEK in cancers, and DEK-mediated regulation of NFκB signaling. Combined, evidence suggests that DEK may play a complex, multidimensional role in chronic inflammation and subsequent tumorigenesis.

Identifiers

PMID26425120
PMCPMC4575739
OpenAlexW1575480098

What OpenQuestion holds

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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.