Evidence map›Paper›PMID 33449132›Full record

ArticleCancer immunology, immunotherapy : CII2021

Loss of type I IFN responsiveness impairs natural killer cell antitumor activity in breast cancer.

Damien J Zanker, Katie L Owen, Nikola Baschuk, Alex J Spurling, Belinda S Parker

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Designing nucleic acid-based therapeutics for cancer treatment: Updates on the state of the art.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Review
  2. Review
  3. Review
  4. PD-L1 restrains PD-1Cell reports · 2024
    Article
  5. Article
  6. Review
  7. Plasticity of NK cells in Cancer.Frontiers in immunology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. TheFrontiers in oncology · 2021
    Article
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 3 institutions in 1 country.

Damien J Zanker *Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, 3000, Australia.ORCID http://orcid.org/0000-0003-1163-9902
Katie L Owen *Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, 3000, Australia.ORCID http://orcid.org/0000-0002-9580-214X
Nikola BaschukMurdoch Children's Research Institute, Parkville, VIC, 3052, Australia.
Alex J SpurlingCancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, 3000, Australia.
Belinda S ParkerCancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, VIC, 3000, Australia. belinda.parker@petermac.org.ORCID http://orcid.org/0000-0002-8333-1926
The University of Melbourne · AUMurdoch Children's Research Institute · AUPeter MacCallum Cancer Centre · AU

Funding

Cancer Council Victoria 1127757
6 · The paper itself

Abstract

Competent type I IFN signaling is the lynchpin of most immune surveillance mechanisms and has recently proven critical to the efficacy of several anticancer agents. Expression of the type I IFN receptor, IFNAR, underpins type I IFN responsiveness in all cells and facilitates the activation and cytotoxic potential of lymphocytes, while loss of IFNAR on lymphocytes has previously been associated with tumor progression and poor patient survival. This study underscores the importance of intact type I IFN signaling to NK cells in the regulation of tumorigenesis and metastasis, whereby ablation of NK cell IFNAR1 impairs antitumor activity and tumor clearance. Using a preclinical model of triple negative breast cancer, we identified that intact IFNAR on NK cells is required for an effective response to type I IFN-inducing immunotherapeutics that may be mediated by pathways associated with NK cell degranulation. Taken together, these data provide a rationale for considering the IFNAR status on NK cells when devising therapeutic strategies aimed at inducing systemic type I IFN signaling in breast cancer.

Indexed as

AnimalsBreast NeoplasmsCarcinogenesisCell Line, TumorFemaleInterferon Type IKiller Cells, NaturalLymphocyte ActivationLymphocytesMiceMice, Inbred C57BLReceptor, Interferon alpha-betaSignal TransductionInterferon Type IReceptor, Interferon alpha-betaAntitumor immunityBreast cancerImmunotherapyNatural killer cellsType I interferon

Identifiers

PMID33449132
PMCPMC10992771
OpenAlexW3120368463

What OpenQuestion holds

Textmetadata
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.