Evidence map›Paper›PMID 31540511›Full record

ArticleCells2019

Interleukin 21 Receptor/Ligand Interaction Is Linked to Disease Progression in Pancreatic Cancer.

Alica Linnebacher, Philipp Mayer, Nicole Marnet, Frank Bergmann, Esther Herpel, Steffie Revia, Libo Yin, Li Liu, Thilo Hackert, Thomas Giese and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Interleukin 15 (IL15)-based near-infrared photoimmunotherapy.Cancer immunology, immunotherapy : CII · 2025
    Article
  2. Review
  3. Epigenetics · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. TargetingFrontiers in immunology · 2021
    Article
  8. Article
  9. Review
  10. The Immune Microenvironment in Pancreatic Cancer.International journal of molecular sciences · 2020
    Review
  11. Article
  12. 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

12 authors at 3 institutions in 1 country.

Alica LinnebacherInstitute of Pathology, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Philipp MayerClinic for Diagnostic and Interventional Radiology, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Nicole MarnetInstitute of Pathology, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Frank BergmannInstitute of Pathology, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Esther HerpelInstitute of Pathology, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Steffie ReviaHelmholtz-University Group "Cell Plasticity and Epigenetic Remodeling", German Cancer Research Center (DKFZ) and Institute of Pathology, University Hospital, 69120 Heidelberg, Germany.
Libo YinMolecular OncoSurgery Group, Department of General, Visceral, and Transplantation Surgery, University of Heidelberg and German Cancer Research Center, 69120 Heidelberg, Germany.
Li LiuMolecular OncoSurgery Group, Department of General, Visceral, and Transplantation Surgery, University of Heidelberg and German Cancer Research Center, 69120 Heidelberg, Germany.
Thilo HackertDepartment of General, Visceral, and Transplantation Surgery, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Thomas GieseInstitute of Immunology, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Ingrid HerrMolecular OncoSurgery Group, Department of General, Visceral, and Transplantation Surgery, University of Heidelberg and German Cancer Research Center, 69120 Heidelberg, Germany.
Matthias M GaidaInstitute of Pathology, University Hospital Heidelberg, 69120 Heidelberg, Germany. matthias.gaida@unimedizin-mainz.de.
Heidelberg University · DEGerman Cancer Research Center · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) displays a marked fibro-inflammatory microenvironment in which infiltrated immune cells fail to eliminate the tumor cells and often-rather paradoxically-promote tumor progression. Of special interest are tumor-promoting T cells that assume a Th17-like phenotype because their presence in PDAC tissue is associated with a poor prognosis. In that context, the role of IL-21, a major cytokine released by Th17-like cells, was assessed. In all tissue samples (n = 264) IL-21

Indexed as

Disease ProgressionAnimalsCarcinoma, Pancreatic DuctalCell ProliferationChickensHumansInterleukin-21InterleukinsLigandsPancreatic NeoplasmsReceptors, Interleukin-21Tumor Cells, CulturedInterleukin-21InterleukinsLigandsReceptors, Interleukin-21Blimp-1IL-21invasionpancreatic cancerTh17tumor microenvironment

Identifiers

PMID31540511
PMCPMC6770770
OpenAlexW2998829477

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.