Evidence map›Paper›PMID 24178582›Full record

ReviewToxicologic pathology2014

Pathogenesis of pancreatic cancer: lessons from animal models.

L Charles Murtaugh

Open access · bronzeAbstract readReview
In one paragraph

Review in Toxicologic pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
2.5field-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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Novel Acinar Metaplastic States Uncovered in Exocrine Pancreas Disease.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  4. Review
  5. Review
  6. Kras mutation rate precisely orchestrates ductal derived pancreatic intraepithelial neoplasia and pancreatic cancer.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  7. Nanomedicine for Imaging and Therapy of Pancreatic Adenocarcinoma.Frontiers in bioengineering and biotechnology · 2019
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Regeneration and repair of the exocrine pancreas.Annual review of physiology · 2015
    Review
  16. Article
  17. Macromolecular therapeutics.Journal of controlled release : official journal of the Controlled Release Society · 2014
    Review
  18. Obesity and cancer pathogenesis.Annals of the New York Academy of Sciences · 2014
    Review
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

1 author at 1 institution in 1 country.

L Charles Murtaugh1Department of Human Genetics, University of Utah, Salt Lake City, Utah, USA.
University of Utah · US

Funding

An epigenetic switch controlling pancreatic cancer susceptibilityR21CA179453 · NCI · UNIVERSITY OF UTAH · PI MURTAUGH, LEWIS C · 2013 to 2014
$370k
NCI NIH HHS 1-R21-CA179453NCI NIH HHS R21 CA179453
6 · The paper itself

Abstract

The past several decades have seen great effort devoted to mimicking the key features of pancreatic ductal adenocarcinoma (PDAC) in animals and have produced 2 robust models of this deadly cancer. Carcinogen-treated Syrian hamsters develop PDAC with genetic lesions, which reproduce those of human, including activation of the Kras oncogene, and early studies in this species validated nongenetic risk factors for PDAC including pancreatitis, obesity, and diabetes. More recently, PDAC research has been invigorated by the development of genetically engineered mouse models based on tissue-specific Kras activation and deletion of tumor suppressor genes. Surprisingly, mouse PDAC appears to arise from exocrine acinar rather than ductal cells, via a process of phenotypic reprogramming that is accelerated by inflammation. Studies in both models have uncovered molecular mechanisms by which inflammation promotes and sustains PDAC and identified targets for chemoprevention to suppress PDAC in high-risk individuals. The mouse model, in particular, has also been instrumental in developing new approaches to early detection as well as treatment of advanced disease. Together, animal models enable diverse approaches to basic and preclinical research on pancreatic cancer, the results of which will accelerate progress against this currently intractable cancer.

Indexed as

Disease Models, AnimalAnimalsCarcinoma, Pancreatic DuctalCricetinaeHumansMicePancreatic NeoplasmsProto-Oncogene Proteins p21(ras)Risk FactorsProto-Oncogene Proteins p21(ras)animal modelsgastrointestinal systemgenetically engineered mice.pancreatic cancer

Identifiers

PMID24178582
PMCPMC3926968
OpenAlexW2106597511

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.