Evidence map›Paper›PMID 30143537›Full record

ArticleCancer immunology research2018

Restoration of Endogenous Retrovirus Infectivity Impacts Mouse Cancer Models.

Eleonora Ottina, Prisca Levy, Urszula Eksmond, Julia Merkenschlager, George R Young, Juliette Roels, Jonathan P Stoye, Thomas Tüting, Dinis P Calado, George Kassiotis

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer immunology research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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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

10 authors at 2 institutions in 2 countries.

Eleonora OttinaRetroviral Immunology, The Francis Crick Institute, London, UK.ORCID 0000-0002-9630-496X
Prisca LevyRetroviral Immunology, The Francis Crick Institute, London, UK.
Urszula EksmondRetroviral Immunology, The Francis Crick Institute, London, UK.
Julia MerkenschlagerRetroviral Immunology, The Francis Crick Institute, London, UK.
George R YoungRetrovirus-Host Interactions, The Francis Crick Institute, London, UK.
Juliette RoelsRetroviral Immunology, The Francis Crick Institute, London, UK.
Jonathan P StoyeRetrovirus-Host Interactions, The Francis Crick Institute, London, UK.
Thomas TütingLaboratory of Experimental Dermatology, Department of Dermatology, University of Magdeburg, Magdeburg, Germany.
Dinis P CaladoImmunity and Cancer Laboratory, The Francis Crick Institute, London, UK.
George KassiotisRetroviral Immunology, The Francis Crick Institute, London, UK. george.kassiotis@crick.ac.uk.
The Francis Crick Institute · GBUniversity Hospital Magdeburg · DE

Funding

Cancer Research UK 22158Medical Research Council MC_U117512710Medical Research Council MR/J008060/1Wellcome Trust 102898/B/13/ZWellcome Trust FC001057Wellcome Trust FC001099Wellcome Trust FC001162
6 · The paper itself

Abstract

Mouse models have been instrumental in establishing fundamental principles of cancer initiation and progression and continue to be invaluable in the discovery and further development of cancer therapies. Nevertheless, important aspects of human disease are imperfectly approximated in mouse models, notably the involvement of endogenous retroviruses (ERVs). Replication-defective ERVs, present in both humans and mice, may affect tumor development and antitumor immunity through mechanisms not involving infection. Here, we revealed an adverse effect of murine ERVs with restored infectivity on the behavior of mouse cancer models. In contrast to human cancer, where infectious ERVs have never been detected, we found that ERV infectivity was frequently restored in transplantable, as well as genetic, mouse cancer models. Such replication-competent, ERV-derived retroviruses were responsible for unusually high expression of retroviral nucleic acids and proteins in mouse cancers. Infectious ERV-derived retroviruses produced by mouse cancer cells could directly infect tumor-infiltrating host immune cells and fundamentally modified the host's immune defenses to cancer, as well as the outcome of immunotherapy. Therefore, infectious retroviruses, variably arising in mouse cancer models, but not in human cancer, have the potential to confound many immunologic studies and should be considered as a variable, if not altogether avoided.

Indexed as

AnimalsCell Line, TumorEndogenous RetrovirusesFemaleLeukemia Virus, MurineLymphocytes, Tumor-InfiltratingMaleMice, Inbred C57BLMice, Inbred CBAMice, TransgenicNeoplasms, ExperimentalPositive Regulatory Domain I-Binding Factor 1Proto-Oncogene Proteins B-rafRetroviridae InfectionsViral TropismBraf protein, mousePositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseProto-Oncogene Proteins B-raf

Identifiers

PMID30143537
PMCPMC6485373
OpenAlexW2888615469

What OpenQuestion holds

Textmetadata
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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.