Evidence map›Paper›PMID 33264572›Full record

ReviewAnnual review of pathology2021

Opposing Roles of Type I Interferons in Cancer Immunity.

Giselle M Boukhaled, Shane Harding, David G Brooks

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 2% 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

127 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Mitochondrial double-stranded RNA fuels pancreatic cancer growth via RIG-I/TLR3 inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Article
  13. Type I interferons induced upon respiratory viral infection impair lung metastatic initiation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  14. Review
  15. Article
  16. TNF-⍺-mediated myeloid-instructed CD14Cell reports. Medicine · 2026
    Article
  17. Article
  18. Review
  19. Review
  20. Review

67 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

3 authors at 2 institutions in 1 country.

Giselle M BoukhaledPrincess Margaret Cancer Centre, University Health Network Toronto, Ontario M5G 2M9, Canada; email: dbrooks@uhnresearch.ca.
Shane HardingPrincess Margaret Cancer Centre, University Health Network Toronto, Ontario M5G 2M9, Canada; email: dbrooks@uhnresearch.ca.
David G BrooksPrincess Margaret Cancer Centre, University Health Network Toronto, Ontario M5G 2M9, Canada; email: dbrooks@uhnresearch.ca.
University Health Network · CAUniversity of Toronto · CA

Funding

Mechanisms of Viral PersistenceR01AI085043 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BROOKS, DAVID G · 2010 to 2023
$4.5M
CIHR 165926CIHR FDN148386NIAID NIH HHS R01 AI085043
6 · The paper itself

Abstract

The immune system is tasked with identifying malignant cells to eliminate or prevent cancer spread. This involves a complex orchestration of many immune cell types that together recognize different aspects of tumor transformation and growth. In response, tumors have developed mechanisms to circumvent immune attack. Type I interferons (IFN-Is) are a class of proinflammatory cytokines produced in response to viruses and other environmental stressors. IFN-Is are also emerging as essential drivers of antitumor immunity, potently stimulating the ability of immune cells to eliminate tumor cells. However, a more complicated role for IFN-Is has arisen, as prolonged stimulation can promote feedback inhibitory mechanisms that contribute to immune exhaustion and other deleterious effects that directly or indirectly permit cancer cells to escape immune clearance. We review the fundamental and opposing functions of IFN-Is that modulate tumor growth and impact immune function and ultimately how these functions can be harnessed for the design of new cancer therapies.

Indexed as

AnimalsHumansInterferon Type INeoplasmsTumor EscapeInterferon Type Icancer immunologyhallmarks of cancerIFN-IIFN-stimulated geneimmunotherapyISGtype I interferon

Identifiers

PMID33264572
PMCPMC8063563
OpenAlexW3107190126

What OpenQuestion holds

Textmetadata
LicenceTDM
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.