Evidence map›Paper›PMID 28233863›Full record

ArticleNature communications2017

IFN-γ is required for cytotoxic T cell-dependent cancer genome immunoediting.

Kazuyoshi Takeda, Masafumi Nakayama, Yoshihiro Hayakawa, Yuko Kojima, Hiroaki Ikeda, Naoko Imai, Kouetsu Ogasawara, Ko Okumura, David M Thomas, Mark J Smyth

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
6.5field-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

99 citing papers in PubMed, 144 citations in OpenAlex.

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39 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 7 institutions in 2 countries.

Kazuyoshi TakedaDivision of Cell Biology, Biomedical Research Center, Graduate School of Medicine, Juntendo University, Bunkyo-ku, Tokyo 113-8421, Japan.
Masafumi NakayamaFrontier Research Institute for Interdisciplinary Sciences, Tohoku University, Sendai 980-8578, Japan.
Yoshihiro HayakawaCancer Immunology Program, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, 3002 Victoria, Australia.
Yuko KojimaLaboratory of Morphology and Image Analysis, Biomedical Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Hiroaki IkedaDepartment of Immuno-Gene Therapy, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Naoko ImaiDepartment of Immuno-Gene Therapy, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Kouetsu OgasawaraDepartment of Immunobiology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai 980-8575, Japan.
Ko OkumuraDepartment of Biofunctional Micribiota, Graduate School of Medicine, Juntendo University, Bunkyo-ku, Tokyo 113-8421, Japan.
David M ThomasCancer Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia.
Mark J SmythCancer Immunology Program, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, 3002 Victoria, Australia.
Juntendo University · JPMie University · JPTohoku University · JPGarvan Institute of Medical Research · AUPeter MacCallum Cancer Centre · AUUniversity of Queensland · AUUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic evolution that occurs during cancer progression enables tumour heterogeneity, thereby fostering tumour adaptation, therapeutic resistance and metastatic potential. Immune responses are known to select (immunoedit) tumour cells displaying immunoevasive properties. Here we address the role of IFN-γ in mediating the immunoediting process. We observe that, in several mouse tumour models such as HA-expressing 4T1 mammary carcinoma cells, OVA-expressing EG7 lymphoma cells and CMS5 MCA-induced fibrosarcoma cells naturally expressing mutated extracellular signal-regulated kinase (ERK) antigen, the action of antigen-specific cytotoxic T cell (CTL) in vivo results in the emergence of resistant cancer cell clones only in the presence of IFN-γ within the tumour microenvironment. Moreover, we show that exposure of tumours to IFN-γ-producing antigen-specific CTLs in vivo results in copy-number alterations (CNAs) associated with DNA damage response and modulation of DNA editing/repair gene expression. These results suggest that enhanced genetic instability might be one of the mechanisms by which CTLs and IFN-γ immunoedits tumours, altering their immune resistance as a result of genetic evolution.

Indexed as

AnimalsAntigens, NeoplasmDisease ProgressionDNA DamageDNA RepairEvolution, MolecularExtracellular Signal-Regulated MAP KinasesFemaleGene Expression Regulation, NeoplasticGenomic InstabilityHumansImmune ToleranceInterferon-gammaMiceMice, Inbred BALB CMice, Inbred C57BLAntigens, NeoplasmExtracellular Signal-Regulated MAP KinasesInterferon-gamma

Identifiers

PMID28233863
PMCPMC5333095
OpenAlexW2590027393

What OpenQuestion holds

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LicenceCC BY
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.