Evidence map›Paper›PMID 29907597›Full record

ArticleEMBO molecular medicine2018

Myeloid p38α signaling promotes intestinal IGF-1 production and inflammation-associated tumorigenesis.

Catrin Youssif, Monica Cubillos-Rojas, Mònica Comalada, Elisabeth Llonch, Cristian Perna, Nabil Djouder, Angel R Nebreda

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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, 30 citations in OpenAlex.

  1. AScience signaling · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. P38 kinase in gastrointestinal cancers.Cancer gene therapy · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Gut · 2021
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Requirement for epithelial p38α in KRAS-driven lung tumor progression.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. Article
  20. 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

7 authors at 4 institutions in 1 country.

Catrin YoussifInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology, Barcelona, Spain.
Monica Cubillos-RojasInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology, Barcelona, Spain.
Mònica ComaladaInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology, Barcelona, Spain.
Elisabeth LlonchInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology, Barcelona, Spain.
Cristian PernaHospital Universitario Ramón y Cajal, IRYCIS, Madrid, Spain.
Nabil DjouderCentro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain.
Angel R NebredaInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology, Barcelona, Spain angel.nebreda@irbbarcelona.org.ORCID 0000-0002-7631-4060
Institute for Research in Biomedicine · ESInstitució Catalana de Recerca i Estudis Avançats · ESInstituto Ramón y Cajal de Investigación Sanitaria · ESSpanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The protein kinase p38α plays a key role in cell homeostasis, and p38α signaling in intestinal epithelial cells protects against colitis-induced tumorigenesis. However, little is known on the contribution of p38α signaling in intestinal stromal cells. Here, we show that myeloid cell-specific downregulation of p38α protects mice against inflammation-associated colon tumorigenesis. The reduced tumorigenesis correlates with impaired detection in the colon of crucial chemokines for immune cell recruitment. We identify insulin-like growth factor-1 (IGF-1) as a novel mediator of the p38α pathway in macrophages. Moreover, using genetic and pharmacological approaches, we confirm the implication of IGF-1 produced by myeloid cells in colon inflammation and tumorigenesis. We also show a correlation between IGF-1 pathway activation and the infiltration of myeloid cells with active p38α in colon samples from patients with ulcerative colitis or colon cancer. Altogether, our results uncover an important role for myeloid IGF-1 downstream of p38α in colitis-associated tumorigenesis and suggest the interest in evaluating IGF-1 therapies for inflammation-associated intestinal diseases, taking into consideration IGF-1 signaling and immune cell infiltration in patient biopsies.

Indexed as

AnimalsCarcinogenesisChemokinesColitisColonic NeoplasmsDown-RegulationFemaleHumansInsulin-Like Growth Factor IIntestinal MucosaIntestinesMaleMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 14Myeloid CellsChemokinesinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IMitogen-Activated Protein Kinase 14colon tumorigenesisIGF‐1intestinal inflammationmacrophagep38 MAPK

Identifiers

PMID29907597
PMCPMC6034132
OpenAlexW2808558566

What OpenQuestion holds

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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.