ArticleJournal of the Royal Society, Interface2018
Passenger mutations can accelerate tumour suppressor gene inactivation in cancer evolution.
Article in Journal of the Royal Society, Interface, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- The nuclease EXO1 promotes genomic instability by degrading nascent DNA in BRCA-proficient cells.Nature communications · 2026Article
- Identification of cancer mini-drivers by deciphering selective landscape in the cancer genome.Briefings in bioinformatics · 2026Article
- In Silico Characterization of PathogenicGenes · 2025Article
- Microenvironment and Tumor Heterogeneity as Pharmacological Targets in Precision Oncology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Podoplanin expression in various types of oral dysplasia and oral squamous cell carcinoma.Journal of Taibah University Medical Sciences · 2025Article
- Mechanism insights and therapeutic intervention of tumor metastasis: latest developments and perspectives.Signal transduction and targeted therapy · 2024Review
- Review
- CDMPred: a tool for predicting cancer driver missense mutations with high-quality passenger mutations.PeerJ · 2024Article
- Plasminogen missense variants and their involvement in cardiovascular and inflammatory disease.Frontiers in cardiovascular medicine · 2024Review
- BRCA-mutated gastric adenocarcinomas are associated with chromosomal instability and responsiveness to platinum-based chemotherapy.Journal of pathology and translational medicine · 2023Article
- Unraveling the Drivers of Tumorigenesis in the Context of Evolution: Theoretical Models and Bioinformatics Tools.Journal of molecular evolution · 2023Review
- Familial CCM Genes Might Not Be Main Drivers for Pathogenesis of Sporadic CCMs-Genetic Similarity between Cancers and Vascular Malformations.Journal of personalized medicine · 2023Review
- Variants Identified in theGenes · 2023Article
- Tumour Genetic Heterogeneity in Relation to Oral Squamous Cell Carcinoma and Anti-Cancer Treatment.International journal of environmental research and public health · 2023Review
- Non-Association of Driver Alterations in PTEN with Differential Gene Expression and Gene Methylation in IDH1 Wildtype Glioblastomas.Brain sciences · 2023Article
- Updated Views in Targeted Therapy in the Patient with Non-Small Cell Lung Cancer.Journal of personalized medicine · 2023Review
- Exploring histopathological and serum biomarkers in lung adenocarcinoma: Clinical applications and translational opportunities (Review).International journal of oncology · 2022Review
- Article
- Article
- Gene Therapy Targeting p53 and KRAS for Colorectal Cancer Treatment: A Myth or the Way Forward?International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Carcinogenesis is an evolutionary process whereby cells accumulate multiple mutations. Besides the 'driver mutations' that cause the disease, cells also accumulate a number of other mutations with seemingly no direct role in this evolutionary process. They are called passenger mutations. While it has been argued that passenger mutations render tumours more fragile due to reduced fitness, the role of passenger mutations remains understudied. Using evolutionary computational models, we demonstrate that in the context of tumour suppressor gene inactivation (and hence fitness valley crossing), the presence of passenger mutations can accelerate the rate of evolution by reducing overall population fitness and increasing the relative fitness of intermediate mutants in the fitness valley crossing pathway. Hence, the baseline rate of tumour suppressor gene inactivation might be faster than previously thought. Conceptually, parallels are found in the field of turbulence and pattern formation, where instabilities can be driven by perturbations that are damped (disadvantageous), but provide a richer set of pathways such that a system can achieve some desired goal more readily. This highlights, through a number of novel parallels, the relevance of physical sciences in oncology.
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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 OpenQuestion graph.