Evidence map›Paper›PMID 23506980›Full record

ReviewMolecular oncology2013

Genetically engineered mouse models of pancreatic adenocarcinoma.

Carmen Guerra, Mariano Barbacid

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

100 citing papers in PubMed, 177 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. KRAS: the Achilles' heel of pancreas cancer biology.The Journal of clinical investigation · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
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  11. Review
  12. Article
  13. Article
  14. Farnesoid X receptor activation inhibits pancreatic carcinogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2023
    Article
  15. Heparin Prowess: Favorable Vascular-Immune Reprogramming in Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  16. Uncovering Tumor-Promoting Roles of Activin A in Pancreatic Ductal Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  17. Clinical and Molecular Attributes and Evaluation of Pancreatic Cystic Neoplasm.Biochimica et biophysica acta. Reviews on cancer · 2023
    Review
  18. Review
  19. Review
  20. Review

40 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Carmen GuerraMolecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO), Melchor Fernandez Almagro 3, E-28029 Madrid, Spain. mcguerra@cnio.es
Mariano Barbacid
Spanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal types of human cancer for which there are no effective therapies. Deep sequencing of PDAC tumors has revealed the presence of a high number of mutations (>50) that affect at least a dozen key signaling pathways. This scenario highlights the urgent need to develop experimental models that faithfully reproduce the natural history of these human tumors in order to understand their biology and to design therapeutic approaches that might effectively interfere with their multiple mutated pathways. Over the last decade, several models, primarily based on the genetic activation of resident KRas oncogenes knocked-in within the endogenous KRas locus have been generated. These models faithfully reproduce the histological lesions that characterize human pancreatic tumors. Decoration of these models with additional mutations, primarily involving tumor suppressor loci known to be also mutated in human PDAC tumors, results in accelerated tumor progression and in the induction of invasive and metastatic malignancies. Mouse PDACs also display a desmoplastic stroma and inflammatory responses that closely resemble those observed in human patients. Interestingly, adult mice appear to be resistant to PDAC development unless the animals undergo pancreatic damage, mainly in the form of acute, chronic or even temporary pancreatitis. In this review, we describe the most representative models available to date and how their detailed characterization is allowing us to understand their cellular origin as well as the events involved in tumor progression. Moreover, their molecular dissection is starting to unveil novel therapeutic strategies that could be translated to the clinic in the very near future.

Indexed as

Disease Models, AnimalGenetic EngineeringAdenocarcinomaAnimalsHumansMiceNeoplastic Stem CellsPancreatic NeoplasmsSignal Transduction

Identifiers

PMID23506980
PMCPMC5528418
OpenAlexW1974351257

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.