ArticleBritish journal of cancer2023
Somatic mutations can induce a noninflamed tumour microenvironment via their original gene functions, despite deriving neoantigens.
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 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Clinicopathologic, genetic and immune cell infiltration analysis of colorectal signet ring cell carcinoma with comparison to conventional adenocarcinoma.Journal of the National Cancer Center · 2026Article
- Characterization of Tumor Antigens from Multi-omics Data: Computational Approaches and Resources.Genomics, proteomics & bioinformatics · 2025Review
- The genetic landscape of primary malignant melanoma of the cervix using integrated bioinformatics analysis and whole-exome sequencing.Frontiers in oncology · 2025Article
- Relevance of mutation-derived neoantigens and non-classical antigens for anticancer therapies.Human vaccines & immunotherapeutics · 2024Review
- Facts and Hopes in Immunotherapy Strategies Targeting Antigens Derived from KRAS Mutations.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Review
- Copy number loss of KDM5D may be a predictive biomarker for ATR inhibitor treatment in male patients with pulmonary squamous cell carcinoma.The journal of pathology. Clinical research · 2024Article
- "Paradoxical neoantigenic mutations": not simply a driver vs passenger dualism.British journal of cancer · 2023Article
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12 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundIdentifying biomarkers to predict immune checkpoint inhibitor (ICI) efficacy is warranted. Considering that somatic mutation-derived neoantigens induce strong immune responses, patients with a high tumour mutational burden reportedly tend to respond to ICIs. However, there are several conflicting data. Therefore, we focused on the original function of neoantigenic mutations and their impact on the tumour microenvironment (TME).
methodsWe evaluated 88 high-frequency microsatellite instability (MSI-H) colorectal cancers and analysed the function of the identified neoantigenic mutations and their influence on programmed cell death 1 (PD-1) blockade efficacy. The results were validated using The Cancer Genome Atlas (TCGA) datasets.
resultsWe identified frameshift mutations in RNF43 as a common neoantigenic gene mutation in MSI-H tumours. However, loss-of-function RNF43 mutations induced noninflamed TME by activating the WNT/β-catenin signalling pathway. In addition, loss of RNF43 function induced resistance to PD-1 blockade even in neoantigen-rich tumours. TCGA dataset analyses demonstrated that passenger rather than driver gene mutations were related to the inflamed TME in diverse cancer types.
conclusionsWe propose a novel concept of "paradoxical neoantigenic mutations" that can induce noninflamed TME through their original gene functions, despite deriving neoantigens, suggesting the significance of qualities as well as quantities in neoantigenic mutations.
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