ArticleGenome biology2024
Immune evasion impacts the landscape of driver genes during cancer evolution.
Article in Genome biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Cross-species insights from ART-D to uncover evolutionarily conserved oncogenic mechanisms.Molecular systems biology · 2026Article
- A Prognostic Risk Model Based on Immune Genes in Thyroid Cancer and Its Correlation With Tumor-Associated Immune Cell Infiltration Abundance.Cancer medicine · 2026Article
- A core driver gene set identified based on geMER reveals its potential driver mechanism in pan-cancer.NPJ precision oncology · 2025Article
- The role of Prolyl 3-Hydroxylase 1 (P3H1) in tumor development and prognosis: a pan-cancer analysis with validation in colonic adenocarcinoma.American journal of translational research · 2025Article
- Immune evasion impacts the landscape of driver genes during cancer evolution.Genome biology · 2024Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundCarcinogenesis is driven by interactions between genetic mutations and the local tumor microenvironment. Recent research has identified hundreds of cancer driver genes; however, these studies often include a mixture of different molecular subtypes and ecological niches and ignore the impact of the immune system.
resultsIn this study, we compare the landscape of driver genes in tumors that escaped the immune system (escape +) versus those that did not (escape -). We analyze 9896 primary tumors from The Cancer Genome Atlas using the ratio of non-synonymous to synonymous mutations (dN/dS) and find 85 driver genes, including 27 and 16 novel genes, in escape - and escape + tumors, respectively. The dN/dS of driver genes in immune escaped tumors is significantly lower and closer to neutrality than in non-escaped tumors, suggesting selection buffering in driver genes fueled by immune escape. Additionally, we find that immune evasion leads to more mutated sites, a diverse array of mutational signatures and is linked to tumor prognosis.
conclusionsOur findings highlight the need for improved patient stratification to identify new therapeutic targets for cancer treatment.
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