Evidence map›Paper›PMID 25024603›Full record

ReviewWorld journal of gastroenterology2014

Pancreatic cancer organotypics: High throughput, preclinical models for pharmacological agent evaluation.

Stacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Pseudopterosin andBioengineering (Basel, Switzerland) · 2020
    Article
  9. Review
  10. Article
  11. Review
  12. Organotypic Modeling of the Tumor Landscape.Frontiers in cell and developmental biology · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  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

8 authors at 1 institution in 1 country.

Stacey J ColemanStacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher, Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Jennifer WattStacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher, Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Prabhu ArumugamStacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher, Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Leonardo SolainiStacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher, Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Elisabeta CarapucaStacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher, Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Mohammed GhallabStacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher, Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Richard P GroseStacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher, Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Hemant M KocherStacey J Coleman, Jennifer Watt, Prabhu Arumugam, Leonardo Solaini, Elisabeta Carapuca, Mohammed Ghallab, Richard P Grose, Hemant M Kocher, Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Queen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer carries a terrible prognosis, as the fourth most common cause of cancer death in the Western world. There is clearly a need for new therapies to treat this disease. One of the reasons no effective treatment has been developed in the past decade may in part, be explained by the diverse influences exerted by the tumour microenvironment. The tumour stroma cross-talk in pancreatic cancer can influence chemotherapy delivery and response rate. Thus, appropriate preclinical in vitro models which can bridge simple 2D in vitro cell based assays and complex in vivo models are required to understand the biology of pancreatic cancer. Here we discuss the evolution of 3D organotypic models, which recapitulare the morphological and functional features of pancreatic ductal adenocarcinoma (PDAC). Organotypic cultures are a valid high throughput preclinical in vitro model that maybe a useful tool to help establish new therapies for PDAC. A huge advantage of the organotypic model system is that any component of the model can be easily modulated in a short time-frame. This allows new therapies that can target the cancer, the stromal compartment or both to be tested in a model that mirrors the in vivo situation. A major challenge for the future is to expand the cellular composition of the organotypic model to further develop a system that mimics the PDAC environment more precisely. We discuss how this challenge is being met to increase our understanding of this terrible disease and develop novel therapies that can improve the prognosis for patients.

Indexed as

High-Throughput Screening AssaysAnimalsAntineoplastic AgentsCell CommunicationCell Line, TumorCoculture TechniquesDrug Screening Assays, AntitumorEpithelial CellsHumansPancreatic NeoplasmsStromal CellsTime FactorsTumor MicroenvironmentAntineoplastic Agents3D organotypic modelPancreatic cancerPancreatic stellate cellPreclinical modelsStroma

Identifiers

PMID25024603
PMCPMC4093698
OpenAlexW2016459836

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.