Evidence map›Paper›PMID 25232244›Full record

ReviewWorld journal of gastroenterology2014

Nuclear receptors and pathogenesis of pancreatic cancer.

Simone Polvani, Mirko Tarocchi, Sara Tempesti, Andrea Galli

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Exploring the Therapeutic Potential ofCurrent pharmaceutical design · 2025
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  15. CCR7 regulates Twist to induce the epithelial-mesenchymal transition in pancreatic ductal adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. 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 1 institution in 1 country.

Simone PolvaniSimone Polvani, Mirko Tarocchi, Sara Tempesti, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.
Mirko TarocchiSimone Polvani, Mirko Tarocchi, Sara Tempesti, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.
Sara TempestiSimone Polvani, Mirko Tarocchi, Sara Tempesti, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.
Andrea GalliSimone Polvani, Mirko Tarocchi, Sara Tempesti, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with a median overall survival time of 5 mo and the five years survival less than 5%, a rate essentially unchanged over the course of the years. A well defined progression model of accumulation of genetic alterations ranging from single point mutations to gross chromosomal abnormalities has been introduced to describe the origin of this disease. However, due to the its subtle nature and concurring events PDAC cure remains elusive. Nuclear receptors (NR) are members of a large superfamily of evolutionarily conserved ligand-regulated DNA-binding transcription factors functionally involved in important cellular functions ranging from regulation of metabolism, to growth and development. Given the nature of their ligands, NR are very tempting drug targets and their pharmacological modulation has been widely exploited for the treatment of metabolic and inflammatory diseases. There are now clear evidences that both classical ligand-activated and orphan NR are involved in the pathogenesis of PDAC from its very early stages; nonetheless many aspects of their role are not fully understood. The purpose of this review is to highlight the striking connections that link peroxisome proliferator activated receptors, retinoic acid receptors, retinoid X receptor, androgen receptor, estrogen receptors and the orphan NR Nur, chicken ovalbumin upstream promoter transcription factor II and the liver receptor homologue-1 receptor to PDAC development, connections that could lead to the identification of novel therapies for this disease.

Indexed as

AnimalsBiomarkers, TumorCarcinoma, Pancreatic DuctalHumansPancreatic NeoplasmsPrognosisReceptors, Cytoplasmic and NuclearSignal TransductionBiomarkers, TumorReceptors, Cytoplasmic and NuclearCOUP-TFIINuclear receptorsNuclear receptors 2F2Nuclear receptors 4A2Orphan nuclear receptorPancreatic cancerPancreatic intraepithelial neoplasiaPeroxisome proliferator activated receptorRetinoid X receptorTesticular receptor 3

Identifiers

PMID25232244
PMCPMC4161795
OpenAlexW1968888940

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.