Evidence map›Paper›PMID 24157551›Full record

ArticleCancer biology & therapy2013

ETV1 positively regulates transcription of tumor suppressor ARF.

Evan Zynda, Mark W Jackson, Partho Bhattacharya, Eugene S Kandel

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Molecular Mechanism ofJournal of pharmaceutical sciences and pharmacology · 2015
    Article
  3. Article
  4. 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 2 institutions in 1 country.

Evan ZyndaDepartment of Cell Stress Biology; Roswell Park Cancer Institute; Buffalo, NY USA.
Mark W JacksonDepartment of Pathology; Case Western Reserve University; Cleveland, OH USA.
Partho BhattacharyaDepartment of Cell Stress Biology; Roswell Park Cancer Institute; Buffalo, NY USA.
Eugene S KandelDepartment of Cell Stress Biology; Roswell Park Cancer Institute; Buffalo, NY USA.
Roswell Park Comprehensive Cancer Center · USCase Western Reserve University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ETV1 (ETS variant 1) is a transcription factor from the ETS family and an oncogene in several types of human malignancies. Paradoxically, a predicted inactivating mutation in ETV1 was previously found in a clone of HT1080 cells with reduced activity of p53. We report that elevated expression of ETV1 makes p53-null tumor cells hypersensitive to restoration of said tumor suppressor. Furthermore, elevated levels of either wild-type ETV1 or its truncated derivative, dETV1, which mimics the product of an oncogenic rearrangement in certain tumors, results in increased expression of mRNA for p14ARF, a known activator of p53. Accordingly, expression of a luciferase reporter, which is driven by a putative ARF promoter, was elevated by concomitant expression of either ETV1 or dETV1. Our observations point to yet another example of a tumor suppressor gene being activated by a potentially oncogenic signal. A better understanding of the mechanisms that allow a cell to bypass such safeguards is needed in order to predict and prevent the development of an oncogene-tolerant state during cancer evolution.

Indexed as

Cell Line, TumorDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticTranscription FactorsTranscription, GeneticTumor Suppressor Protein p14ARFTumor Suppressor Protein p53DNA-Binding ProteinsETV1 protein, humanTranscription FactorsTumor Suppressor Protein p14ARFTumor Suppressor Protein p53ETV1oncogenic transformationp14ARFp53tumor suppression

Identifiers

PMID24157551
PMCPMC3912040
OpenAlexW1986884756

What OpenQuestion holds

Textmetadata
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.