ArticleNature communications2026
Neoantigen evolution and response to checkpoint inhibitor immunotherapy in colorectal cancer.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Article
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Checkpoint-blockade immunotherapy enables the immune system to recognize tumor cells that were previously invisible due to immune escape, but these therapies lead to heterogeneous patient outcomes. Focusing on colorectal cancer, in which two subtypes have markedly different responses to immunotherapy, we query the relationship between a tumor's mutagenic landscape and therapeutic outcomes. First, we model neoantigen evolution in growing tumors using a stochastic branching-process model and label each neoantigen by its predicted immunogenicity, giving each in-silico tumor a unique pre-treatment mutational landscape. Next, we use a dynamical systems model of tumor-immune interactions under checkpoint-blockade therapy, parameterized using clinical trial data, to simulate immunotherapy. We relate therapeutic outcomes to the heterogeneity of tumor mutational landscape, finding that a strong clonal neoantigen appears crucial for a successful response. Additionally, the minimal neoantigen quality across all neoantigens contributing to response dynamics is one of the strongest predictors of durable response.
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Registered trials
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