Evidence map›Paper›PMID 31227713›Full record

ArticleNature communications2019

IL-33-mediated mast cell activation promotes gastric cancer through macrophage mobilization.

Moritz F Eissmann, Christine Dijkstra, Andrew Jarnicki, Toby Phesse, Jamina Brunnberg, Ashleigh R Poh, Nima Etemadi, Evelyn Tsantikos, Stefan Thiem, Nicholas D Huntington and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed
–field-weighted citation impact
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

156 citing papers in PubMed.

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  12. Deciphering the Role of Mast Cells in HPV-Related Cancers.International journal of molecular sciences · 2025
    Review
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96 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

17 authors.

Moritz F EissmannCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.
Christine DijkstraCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.
Andrew JarnickiDepartment of Pharmacology and Therapeutics, University of Melbourne, Melbourne, VIC, 3010, Australia.
Toby PhesseCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.ORCID http://orcid.org/0000-0001-9568-4916
Jamina BrunnbergCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.
Ashleigh R PohCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.
Nima EtemadiCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.ORCID http://orcid.org/0000-0002-7137-1373
Evelyn TsantikosDepartment of Immunology and Pathology, Monash University, Melbourne, VIC, 3004, Australia.
Stefan ThiemCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.
Nicholas D HuntingtonMolecular Immunology Division, The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Melbourne, VIC, 3052, Australia.
Margaret L HibbsDepartment of Immunology and Pathology, Monash University, Melbourne, VIC, 3004, Australia.
Alex BoussioutasDepartment of Medicine, University of Melbourne, Melbourne, VIC, 3050, Australia.
Michele A GrimbaldestonCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, 5000, Australia.
Michael BuchertCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.
Robert J J O'DonoghueCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.
Frederick MassonCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia.
Matthias ErnstCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia. Matthias.ernst@onjcri.org.au.ORCID http://orcid.org/0000-0002-6399-1177

Funding

Cancer Council Victoria 1160708Department of Health | National Health and Medical Research Council (NHMRC) 1067244Department of Health | National Health and Medical Research Council (NHMRC) 1069024Department of Health | National Health and Medical Research Council (NHMRC) 1092788Medical Research Council MR/R026424/1
6 · The paper itself

Abstract

The contribution of mast cells in the microenvironment of solid malignancies remains controversial. Here we functionally assess the impact of tumor-adjacent, submucosal mast cell accumulation in murine and human intestinal-type gastric cancer. We find that genetic ablation or therapeutic inactivation of mast cells suppresses accumulation of tumor-associated macrophages, reduces tumor cell proliferation and angiogenesis, and diminishes tumor burden. Mast cells are activated by interleukin (IL)-33, an alarmin produced by the tumor epithelium in response to the inflammatory cytokine IL-11, which is required for the growth of gastric cancers in mice. Accordingly, ablation of the cognate IL-33 receptor St2 limits tumor growth, and reduces mast cell-dependent production and release of the macrophage-attracting factors Csf2, Ccl3, and Il6. Conversely, genetic or therapeutic macrophage depletion reduces tumor burden without affecting mast cell abundance. Therefore, tumor-derived IL-33 sustains a mast cell and macrophage-dependent signaling cascade that is amenable for the treatment of gastric cancer.

Indexed as

AminopyridinesAnimalsCell DegranulationCromolyn SodiumDisease Models, AnimalEpitheliumFemaleGastric MucosaHumansInterleukin-1 Receptor-Like 1 ProteinInterleukin-33MacrophagesMaleMast CellsMiceMice, TransgenicAminopyridinesCromolyn SodiumIL1RL1 protein, humanIl1rl1 protein, mouseIL33 protein, humanIl33 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33pexidartinibPyrroles

Identifiers

PMID31227713
PMCPMC6588585

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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.