ArticleBritish journal of cancer2023
Subclonal accumulation of immune escape mechanisms in microsatellite instability-high colorectal cancers.
Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Review
- Review
- Understanding the Promise and Challenges of Tumor-Agnostic Therapy: Could One Size Really Fit All?Cancers · 2026Review
- Of Context, Quality, and Complexity: Fine-Combing Tumor Mutational Burden in Immunotherapy-Treated Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- A bibliometric analysis of immune escape in colorectal cancer: research trends, key contributors, and future directions.Frontiers in immunology · 2025Review
- Precision prognosis of colorectal cancer: a multi-tiered model integrating microsatellite instability genes and clinical parameters.Frontiers in oncology · 2024Article
Corrections and comments
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Authors and funding
34 authors at 11 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntratumor heterogeneity (ITH) in microsatellite instability-high (MSI-H) colorectal cancer (CRC) has been poorly studied. We aimed to clarify how the ITH of MSI-H CRCs is generated in cancer evolution and how immune selective pressure affects ITH.
methodsWe reanalyzed public whole-exome sequencing data on 246 MSI-H CRCs. In addition, we performed a multi-region analysis from 6 MSI-H CRCs. To verify the process of subclonal immune escape accumulation, a novel computational model of cancer evolution under immune pressure was developed.
resultsOur analysis presented the enrichment of functional genomic alterations in antigen-presentation machinery (APM). Associative analysis of neoantigens indicated the generation of immune escape mechanisms via HLA alterations. Multiregion analysis revealed the clonal acquisition of driver mutations and subclonal accumulation of APM defects in MSI-H CRCs. Examination of variant allele frequencies demonstrated that subclonal mutations tend to be subjected to selective sweep. Computational simulations of tumour progression with the interaction of immune cells successfully verified the subclonal accumulation of immune escape mutations and suggested the efficacy of early initiation of an immune checkpoint inhibitor (ICI) -based treatment.
conclusionsOur results demonstrate the heterogeneous acquisition of immune escape mechanisms in MSI-H CRCs by Darwinian selection, providing novel insights into ICI-based treatment strategies.
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Registered trials
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 Socratic graph.