Evidence map›Paper›PMID 42521760›Full record

ArticleNature genetics2026

Paired mutation calling and spatial transcriptomics identify cellular neighborhoods associated with the neoplastic outcome of mouse colitis.

Elisa B Moutin, Linus L H Chang, Giada Giavara, Shenay Mehmed, Mathilde Colombé, Carla Boquetale, Kate Marks, Filipe C Lourenço, Nefeli Skoufou-Papoutsaki, Richard Kemp and 4 more

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Article in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Elisa B MoutinCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-9029-1520
Linus L H ChangSchool of Mathematics, University of Birmingham, Birmingham, UK.
Giada GiavaraCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Shenay MehmedCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0009-0006-2178-618X
Mathilde ColombéCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Carla BoquetaleCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Kate MarksLeeds Institute of Medical Research, University of Leeds, Leeds, UK.
Filipe C LourençoCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-9655-2488
Nefeli Skoufou-PapoutsakiCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Richard KempCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Philippe GascardDepartment of Pathology, University of California, San Francisco, San Francisco, CA, USA.ORCID http://orcid.org/0000-0001-5912-5228
Thea D TlstyDepartment of Pathology, University of California, San Francisco, San Francisco, CA, USA.
David S TourignySchool of Mathematics, University of Birmingham, Birmingham, UK. d.tourigny@bham.ac.uk.ORCID http://orcid.org/0000-0002-3987-8078
Douglas J WintonCRUK Cambridge Institute, University of Cambridge, Cambridge, UK. doug.Winton@cruk.cam.ac.uk.ORCID http://orcid.org/0000-0001-6067-7927

Funding

Plastic States Associated with Cellular Stress and Malignancy: Insights for Prevention and Treatment of Lethal Metaplastic CancersR35CA197694 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TLSTY, THEA D · 2016 to 2022
$6.1M
Defining a Stromal Signature that Facilitates Progression of Lethal CancersR50CA211543 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GASCARD, PHILIPPE · 2019 to 2023
$1.2M
Cancer Research UK (CRUK) A24456Cancer Research UK (CRUK) A27145Cancer Research UK (CRUK) A29074NCI NIH HHS R35 CA197694NCI NIH HHS R50 CA211543U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) 5R35CA197694U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) 5R50CA211543
6 · The paper itself

Abstract

In the progression from inflammatory bowel disease to associated cancer, the clonal mutational landscape shifts from selection of mutations in inflammatory genes to selection for cancer-driver mutations. How prevalence and expansion of either type of mutant clones could be impacted by the cellular environments in which they arise and how this affects the neoplastic outcome of colitis remains unknown. Here we combine in vivo lineage tracing, in silico modeling, mutational profiling and spatial transcriptomics in a mouse model of colitis-associated tumorigenesis to capture clone fates associated with chronic inflammation. We identify epithelial- and immune-enriched neighborhoods and propose a model in which establishment of a reparative tissue environment facilitates tumor initiation by promoting the selection and expansion of pro-oncogenic clones, reducing the span of inflammation-resistant neighborhoods containing nononcogenic clones.

Indexed as

ColitisMutationAnimalsDisease Models, AnimalGene Expression ProfilingMiceSpatial TranscriptomicsTranscriptome

Identifiers

PMID42521760
PMCPMC13447109

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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.