Evidence map›Paper›PMID 32552827›Full record

ArticleCell communication and signaling : CCS2020

Identification of a novel IL-5 signaling pathway in chronic pancreatitis and crosstalk with pancreatic tumor cells.

Sarah B Gitto, Jordan M Beardsley, Sai Preethi Nakkina, Jeremiah L Oyer, Kathryn A Cline, Sally A Litherland, Alicja J Copik, Amr S Khaled, Na'im Fanaian, J Pablo Arnoletti and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Review
  9. Role of Interleukins in Pancreatic Cancer: A Literature Review.Journal of gastrointestinal cancer · 2024
    Review
  10. Review
  11. Interleukins: pathophysiological role in acute pancreatitis.Archives of medical science : AMS · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
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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

11 authors at 4 institutions in 1 country.

Sarah B GittoBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Blvd., Orlando, FL, 32827, USA.
Jordan M BeardsleyBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Blvd., Orlando, FL, 32827, USA.
Sai Preethi NakkinaBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Blvd., Orlando, FL, 32827, USA.
Jeremiah L OyerBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Blvd., Orlando, FL, 32827, USA.
Kathryn A ClineBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Blvd., Orlando, FL, 32827, USA.
Sally A LitherlandAdventHealth Cancer Institute, Orlando, FL, 32804, USA.
Alicja J CopikBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Blvd., Orlando, FL, 32827, USA.
Amr S KhaledOrlando Veteran's Affairs Medical Center, Orlando, FL, 32827, USA.
Na'im FanaianAdventHealth Lab, Orlando, FL, 32804, USA.
J Pablo ArnolettiAdventHealth Cancer Institute and Institute for Surgical Advancement, Orlando, FL, 32804, USA.
Deborah A AltomareBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 6900 Lake Nona Blvd., Orlando, FL, 32827, USA. Deborah.Altomare@ucf.edu.ORCID 0000-0002-7014-0397
University of Central Florida · USFlorida Hospital Cancer Institute · USAdventHealth Orlando · USOrlando VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhile inflammation is associated with pancreatic cancer, the underlying mechanisms leading to cancer initiation are still being delineated. Eosinophils may promote or inhibit tumor growth, although the specific role in pancreatic cancer has yet to be determined. Eosinophil-supporting cytokine interleukin-5 and receptor are likely to have a role, but the significance in the pancreatic cancer microenvironment is unknown.

methodsGenetically engineered Akt1

resultsCompound Akt1

conclusionsChronic inflammation induces increased pancreatic cancer progression and immune cells such as eosinophils are attracted to areas of fibrosis. Results suggest that IL-5 in the pancreatic compartment stimulates increased IL-5Rα on ductal tumor cells to increase pancreatic tumor motility. Collectively, IL-5/IL-5Rα signaling in the mouse and human pancreatic tumors microenvironment is a novel mechanism to facilitate tumor progression. Additional file 1: Video Abstract.

Indexed as

Signal TransductionAcinar CellsAnimalsCarcinogenesisCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementHumansImmunity, InnateInflammationInterleukin-5LeukocytesMiceModels, BiologicalPancreatic NeoplasmsPancreatitis, ChronicInterleukin-5Receptors, Interleukin-5STAT5 Transcription FactorEosinophilsIL-5IL-5RPancreatic ductal adenocarcinomaPancreatitis

Identifiers

PMID32552827
PMCPMC7302008
OpenAlexW3036833184

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.