Evidence map›Paper›PMID 32174917›Full record

ArticleFrontiers in immunology2020

Blockade of Stromal Gas6 Alters Cancer Cell Plasticity, Activates NK Cells, and Inhibits Pancreatic Cancer Metastasis.

Lucy Ireland, Teifion Luckett, Michael C Schmid, Ainhoa Mielgo

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Navigating TAM receptor dynamics in tumour immunotherapy.Cancer immunology, immunotherapy : CII · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. NK cells direct the perspective approaches to cancer immunotherapy.Medical oncology (Northwood, London, England) · 2023
    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

4 authors at 1 institution in 1 country.

Lucy IrelandDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
Teifion LuckettDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
Michael C SchmidDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
Ainhoa MielgoDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.
University of Liverpool · GB

Funding

Cancer Research UK 25607Medical Research Council MR/L000512/1Wellcome Trust 102521/Z/13/Z
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDA) is one of the deadliest cancers due to its aggressive and metastatic nature. PDA is characterized by a rich tumor stroma with abundant macrophages, fibroblasts, and collagen deposition that can represent up to 90% of the tumor mass. Activation of the tyrosine kinase receptor AXL and expression of its ligand growth arrest-specific protein 6 (Gas6) correlate with a poor prognosis and increased metastasis in pancreatic cancer patients. Gas6 is a multifunctional protein that can be secreted by several cell types and regulates multiple processes, including cancer cell plasticity, angiogenesis, and immune cell functions. However, the role of Gas6 in pancreatic cancer metastasis has not been fully investigated. In these studies we find that, in pancreatic tumors, Gas6 is mainly produced by tumor associated macrophages (TAMs) and cancer associated fibroblasts (CAFs) and that pharmacological blockade of Gas6 signaling partially reverses epithelial-to-mesenchymal transition (EMT) of tumor cells and supports NK cell activation, thereby inhibiting pancreatic cancer metastasis. Our data suggest that Gas6 simultaneously acts on both the tumor cells and the NK cells to support pancreatic cancer metastasis. This study supports the rationale for targeting Gas6 in pancreatic cancer and use of NK cells as a potential biomarker for response to anti-Gas6 therapy.

Indexed as

Lymphocyte ActivationAnimalsAxl Receptor Tyrosine KinaseCancer-Associated FibroblastsCarcinoma, Pancreatic DuctalCell Line, TumorCell PlasticityCollagenEpithelial-Mesenchymal TransitionFemaleGrowth Arrest-Specific Protein 6HumansIntercellular Signaling Peptides and ProteinsKiller Cells, NaturalMiceMice, Inbred C57BLAxl Receptor Tyrosine KinaseCollagenGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesfibroblastsGas6macrophagesmetastasisNK cellspancreatic cancer

Identifiers

PMID32174917
PMCPMC7056881
OpenAlexW3008112408

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.