Evidence map›Paper›PMID 38405882›Full record

ArticlebioRxiv : the preprint server for biology2024

Epigenome and early selection determine the tumour-immune evolutionary trajectory of colorectal cancer.

Eszter Lakatos, Vinaya Gunasri, Luis Zapata, Jacob Househam, Timon Heide, Nicholas Trahearn, Ottilie Swinyard, Luis Cisneros, Claire Lynn, Maximilian Mossner and 12 more

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. 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, 5 citations in OpenAlex.

No citing paper in PubMed yet.

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

22 authors at 5 institutions in 4 countries.

Eszter LakatosDepartment of Mathematical Sciences, Chalmers University of Technology and University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0002-7221-6850
Vinaya GunasriUCL Cancer Institute, University College London, London, UK.ORCID 0000-0002-9292-6470
Luis ZapataCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0002-1386-2019
Jacob HousehamCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0003-3199-336X
Timon HeideCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0002-1386-7469
Nicholas TrahearnCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0002-8596-0996
Ottilie SwinyardCentre for Genomics and Computational Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0001-8474-8865
Luis CisnerosArizona Cancer Evolution Center, Biodesign Institute and School of Life Sciences Arizona State University, Tempe, USA.ORCID 0000-0002-7890-1269
Claire LynnCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0002-2630-4075
Maximilian MossnerCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0001-9751-3803
Chris KimberleyCentre for Genomics and Computational Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0002-9720-4434
Inmaculada SpiteriCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0002-1097-8972
George D CresswellCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0003-3303-068X
Gerard Llibre-PalomarCentre for Genomics and Computational Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0002-4741-3473
Miriam MitchisonHistopathology Department, University College London Hospitals NHS Foundation Trust, London, UK.ORCID 0000-0003-2520-2744
Carlo C MaleyArizona Cancer Evolution Center, Biodesign Institute and School of Life Sciences Arizona State University, Tempe, USA.ORCID 0000-0002-0745-7076
Marnix JansenUCL Cancer Institute, University College London, London, UK.ORCID 0000-0003-0645-564X
Manuel Rodriguez-JustoUCL Cancer Institute, University College London, London, UK.ORCID 0000-0001-5007-1761
John BridgewaterUCL Cancer Institute, University College London, London, UK.ORCID 0000-0001-9186-1604
Ann-Marie BakerCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0001-8905-9137
Andrea SottorivaCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0001-6709-9533
Trevor A GrahamCentre for Evolution and Cancer, The Institute of Cancer Research, London, UK.ORCID 0000-0001-9582-1597
Institute of Cancer Research · GBQueen Mary University of London · GBCRUK Lung Cancer Centre of Excellence · GBArizona State University · USUniversity College London Hospitals NHS Foundation Trust · GB

Funding

Molecular, Cellular and Tissue Characterization UnitU2CCA233254 · NCI · DUKE UNIVERSITY · PI HWANG, E.SHELLEY · 2018 to 2023
$11.4M
The Role of the Microbiome in Cancer Suppression and Susceptibility Across SpeciesU54CA217376 · NCI · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI MALEY, CARLO · 2018 to 2022
$8.6M
Modeling Neoplastic Progression in Barrett's Esophagus - Renewal -2R01CA140657 · NCI · WISTAR INSTITUTE · PI Carlo Maley · 2009 to 2026
$5.0M
NCI NIH HHS R01 CA140657NCI NIH HHS U2C CA233254NCI NIH HHS U54 CA217376Wellcome Trust
6 · The paper itself

Abstract

Immune system control is a major hurdle that cancer evolution must circumvent. The relative timing and evolutionary dynamics of subclones that have escaped immune control remain incompletely characterized, and how immune-mediated selection shapes the epigenome has received little attention. Here, we infer the genome- and epigenome-driven evolutionary dynamics of tumour-immune coevolution within primary colorectal cancers (CRCs). We utilise our existing CRC multi-region multi-omic dataset that we supplement with high-resolution spatially-resolved neoantigen sequencing data and highly multiplexed imaging of the tumour microenvironment (TME). Analysis of somatic chromatin accessibility alterations (SCAAs) reveals frequent somatic loss of accessibility at antigen presenting genes, and that SCAAs contribute to silencing of neoantigens. We observe that strong immune escape and exclusion occur at the outset of CRC formation, and that within tumours, including at the microscopic level of individual tumour glands, additional immune escape alterations have negligible consequences for the immunophenotype of cancer cells. Further minor immuno-editing occurs during local invasion and is associated with TME reorganisation, but that evolutionary bottleneck is relatively weak. Collectively, we show that immune evasion in CRC follows a "Big Bang" evolutionary pattern, whereby genetic, epigenetic and TME-driven immune evasion acquired by the time of transformation defines subsequent cancer-immune evolution.

Identifiers

PMID38405882
PMCPMC10888923
OpenAlexW4391920889

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.