Evidence map›Paper›PMID 41564866›Full record

ArticleCell reports. Medicine2026

CRISPR screens in the context of immune selection identify CHD1 and MAP3K7 as mediators of cancer immunotherapy resistance.

Alex Watterson, Gabriele Picco, Vivien Veninga, Youhani Samarakoon, Chiara M Cattaneo, Sara F Vieira, Emre Karakoc, Shriram Bhosle, Thomas W Battaglia, Sarah Consonni and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

14 authors.

Alex WattersonCancer, Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, Cambridgeshire, UK; Open Targets, Cambridgeshire, UK.
Gabriele PiccoCancer, Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, Cambridgeshire, UK; Open Targets, Cambridgeshire, UK.
Vivien VeningaDepartment of Immunology and Molecular Oncology, Netherlands Cancer Institute, Amsterdam, the Netherlands; Oncode Institute, Utrecht, the Netherlands.
Youhani SamarakoonCancer Research UK, Cambridge Institute, University of Cambridge, Cambridge, UK.
Chiara M CattaneoDepartment of Immunology and Molecular Oncology, Netherlands Cancer Institute, Amsterdam, the Netherlands; Oncode Institute, Utrecht, the Netherlands.
Sara F VieiraCancer, Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, Cambridgeshire, UK; Open Targets, Cambridgeshire, UK.
Emre KarakocCancer, Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, Cambridgeshire, UK; Open Targets, Cambridgeshire, UK.
Shriram BhosleCancer, Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, Cambridgeshire, UK.
Thomas W BattagliaDepartment of Immunology and Molecular Oncology, Netherlands Cancer Institute, Amsterdam, the Netherlands.
Sarah ConsonniCancer, Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, Cambridgeshire, UK; Open Targets, Cambridgeshire, UK.
Timotheus Y F HalimCancer Research UK, Cambridge Institute, University of Cambridge, Cambridge, UK.
Emile E VoestDepartment of Immunology and Molecular Oncology, Netherlands Cancer Institute, Amsterdam, the Netherlands; Oncode Institute, Utrecht, the Netherlands.
Mathew J GarnettCancer, Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, Cambridgeshire, UK; Open Targets, Cambridgeshire, UK.
Matthew A CoelhoCancer, Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, Cambridgeshire, UK; Open Targets, Cambridgeshire, UK. Electronic address: matthew.coelho@sanger.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer immunotherapy is only effective in a subset of patients, highlighting the need for effective biomarkers and combination therapies. Here, we systematically identify genetic determinants of cancer cell sensitivity to anti-tumor immunity by performing whole-genome CRISPR-Cas9 knockout screens in autologous tumoroid-T cell co-cultures, isogenic cancer cell models deficient in interferon signaling, and in the context of four cytokines. We discover that loss of CHD1 and MAP3K7 (encoding TAK1) potentiates the transcriptional response to IFN-γ, thereby creating an acquired vulnerability by sensitizing cancer cells to tumor-reactive T cells. Immune checkpoint blockade is more effective in a syngeneic mouse model of melanoma deficient in Chd1 and Map3k7 and is associated with elevated intra-tumoral CD8

Indexed as

Clustered Regularly Interspaced Short Palindromic RepeatsDNA-Binding ProteinsDrug Resistance, NeoplasmImmunotherapyMAP Kinase Kinase KinasesAnimalsCD8-Positive T-LymphocytesCell Line, TumorCRISPR-Cas SystemsDNA HelicasesGene Expression Regulation, NeoplasticHumansImmune Checkpoint InhibitorsInterferon-gammaMAP Kinase Kinase Kinase 7MiceCHD1 protein, humanDNA-Binding ProteinsDNA HelicasesImmune Checkpoint InhibitorsInterferon-gammaMAP Kinase Kinase Kinase 7MAP Kinase Kinase Kinasescancer immunotherapyCHD1co-culture screenCRISPR-Cas9IFN-γimmmune checkpoint blockadeMAP3K7resistanceTAK1T cells

Identifiers

PMID41564866
PMCPMC12866162

What OpenQuestion holds

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LicenceCC BY
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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.