Evidence map›Paper›PMID 26942052›Full record

ArticleOncoimmunology

Interleukin-1 is required for cancer eradication mediated by tumor-specific Th1 cells.

Ole Audun Werner Haabeth, Kristina Berg Lorvik, Hideo Yagita, Bjarne Bogen, Alexandre Corthay

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
2.8field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Second-line chemoimmunotherapy with nivolumab and paclitaxel in immune-related biomarker-enriched advanced gastric cancer: a multicenter phase Ib/II study.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024
    Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Two inflammation-related genes model could predict risk in prognosis of patients with lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  8. RSC chemical biology · 2025
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Targeting inflammation as cancer therapy.Journal of hematology & oncology · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Article

7 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

5 authors at 2 institutions in 2 countries.

Ole Audun Werner HaabethCentre for Immune Regulation; University of Oslo and Oslo University Hospital Rikshospitalet ; Oslo, Norway.
Kristina Berg LorvikCentre for Immune Regulation; University of Oslo and Oslo University Hospital Rikshospitalet ; Oslo, Norway.
Hideo YagitaDepartment of Immunology; Juntendo University School of Medicine ; Tokyo, Japan.
Bjarne BogenCentre for Immune Regulation; University of Oslo and Oslo University Hospital Rikshospitalet; Oslo, Norway; K.G. Jebsen Centre for Influenza Vaccine Research; University of Oslo; Oslo, Norway.
Alexandre CorthayCentre for Immune Regulation; University of Oslo and Oslo University Hospital Rikshospitalet ; Oslo, Norway.
Oslo University Hospital · NOJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of inflammation in cancer is controversial as both tumor-promoting and tumor-suppressive aspects of inflammation have been reported. In particular, it has been shown that pro-inflammatory cytokines, like interleukin-1α (IL-1α), IL-1β, IL-6, and tumor necrosis factor α (TNFα), may either promote or suppress cancer. However, the cellular and molecular basis underlying these opposing outcomes remains enigmatic. Using mouse models for myeloma and lymphoma, we have recently reported that inflammation driven by tumor-specific T helper 1 (Th1) cells conferred protection against B-cell cancer and that interferon-γ (IFN-γ) was essential for this process. Here, we have investigated the contribution of several inflammatory mediators. Myeloma eradication by Th1 cells was not affected by inhibition of TNF-α, TNF-related weak inducer of apoptosis (TWEAK), or TNF-related apoptosis-inducing ligand (TRAIL). In contrast, cancer elimination by tumor-specific Th1 cells was severely impaired by the

Indexed as

and IL33cancer immunosurveillanceCD4+ T cellsIFN-γIL-1RAIL-1αIL-1βIL-21IL-27inflammationmacrophagesTh1

Identifiers

PMID26942052
PMCPMC4760324
OpenAlexW2234981442

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.