Evidence map›Paper›PMID 23071688›Full record

ArticlePloS one2012

The DEK oncogene is a target of steroid hormone receptor signaling in breast cancer.

Lisa M Privette Vinnedge, Shuk-Mei Ho, Kathryn A Wikenheiser-Brokamp, Susanne I Wells

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Aqueous Humor Markers in Retinoblastoma, a Review.Translational vision science & technology · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

4 authors at 3 institutions in 1 country.

Lisa M Privette VinnedgeCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States of America.
Shuk-Mei Ho
Kathryn A Wikenheiser-Brokamp
Susanne I Wells
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · USUniversity of Cincinnati Medical Center · US

Funding

Role and Regulaton of the Human DEK Proto-OncogeneR01CA116316 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI WELLS, SUSANNE I · 2006 to 2016
$2.9M
Training program in hematologic and oncologic diseasesT32HL091805 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2008 to 2012
$835k
The role of DEK in breast cancer development and therapyF32CA139931 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI PRIVETTE VINNEDGE, LISA M. · 2009 to 2010
$98k
NCI NIH HHS CA116316NCI NIH HHS F32 CA139931NCI NIH HHS F32CA139931NCI NIH HHS R01 CA116316NHLBI NIH HHS T32 HL091805NHLBI NIH HHS T32HL091805
6 · The paper itself

Abstract

Expression of estrogen and progesterone hormone receptors indicates a favorable prognosis due to the successful use of hormonal therapies such as tamoxifen and aromatase inhibitors. Unfortunately, 15-20% of patients will experience breast cancer recurrence despite continued use of tamoxifen. Drug resistance to hormonal therapies is of great clinical concern so it is imperative to identify novel molecular factors that contribute to tumorigenesis in hormone receptor positive cancers and/or mediate drug sensitivity. The hope is that targeted therapies, in combination with hormonal therapies, will improve survival and prevent recurrence. We have previously shown that the DEK oncogene, which is a chromatin remodeling protein, supports breast cancer cell proliferation, invasion and the maintenance of the breast cancer stem cell population. In this report, we demonstrate that DEK expression is associated with positive hormone receptor status in primary breast cancers and is up-regulated in vitro following exposure to the hormones estrogen, progesterone, and androgen. Chromatin immunoprecipitation experiments identify DEK as a novel estrogen receptor α (ERα) target gene whose expression promotes estrogen-induced proliferation. Finally, we report for the first time that DEK depletion enhances tamoxifen-induced cell death in ER+ breast cancer cell lines. Together, our data suggest that DEK promotes the pathogenesis of ER+ breast cancer and that the targeted inhibition of DEK may enhance the efficacy of conventional hormone therapies.

Indexed as

Base SequenceBreast NeoplasmsCell DeathCell Line, TumorCell ProliferationChromatin ImmunoprecipitationChromosomal Proteins, Non-HistoneEstradiolEstrogen AntagonistsEstrogen Receptor alphaEstrogensFemaleGene Expression Regulation, NeoplasticHumansMolecular Sequence DataOncogene ProteinsChromosomal Proteins, Non-HistoneDEK protein, humanESR1 protein, humanEstradiolEstrogen AntagonistsEstrogen Receptor alphaEstrogensOncogene ProteinsPoly-ADP-Ribose Binding ProteinsProgesteroneReceptors, AndrogenReceptors, SteroidTamoxifen

Identifiers

PMID23071688
PMCPMC3468546
OpenAlexW2067721598

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.