ReviewNature reviews. Cancer2015
The mini-driver model of polygenic cancer evolution.
Review in Nature reviews. Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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
74 citing papers in PubMed.
- Article
- The cumulative impact of passenger mutations on cancer development.Nature communications · 2026Article
- Mini-Galaxy: Rethinking Complex Human Diseases Through the Lens of Systems Biology and Multilayered AI Network Perspectives.International journal of molecular sciences · 2026Review
- Identification of cancer mini-drivers by deciphering selective landscape in the cancer genome.Briefings in bioinformatics · 2026Article
- Driver mutation impact in Chinese hepatocellular carcinoma.PloS one · 2026Article
- Mathematical Modeling Quantifies "Just-Right" APC Inactivation for Colorectal Cancer Initiation.Cancer research · 2025Article
- A set cover algorithm identifies minimal circulating tumour DNA sequencing targets for colorectal cancer detection.Scientific reports · 2025Article
- Encoding and decoding selectivity and promiscuity in the human chemokine-GPCR interaction network.Cell · 2025Article
- Biophysical Properties of Somatic Cancer Mutations in the S4 Transmembrane Segment of the Human Voltage-Gated Proton Channel hHBiomolecules · 2025Article
- Identifying functional roles and pathways of shared mutations in canine solid tumors by whole-genome sequencing.PloS one · 2025Article
- Rethinking cancer evolution: from genetic mutations to complex information systems in tumor reversion.Evolution, medicine, and public health · 2025Article
- Editorial: State-of-the-art hypothesis-driven systems pharmacology and artificial intelligence approaches to decipher disease complexity.Frontiers in pharmacology · 2025Article
- Language Modelling Techniques for Analysing the Impact of Human Genetic Variation.Bioinformatics and biology insights · 2025Review
- Oncometabolites at the crossroads of genetic, epigenetic and ecological alterations in cancer.Cell death and differentiation · 2024Review
- Hidden secrets of the cancer genome: unlocking the impact of non-coding mutations in gene regulatory elements.Cellular and molecular life sciences : CMLS · 2024Review
- In vivo CRISPR screens reveal SCAF1 and USP15 as drivers of pancreatic cancer.Nature communications · 2024Article
- Rare disease research workflow using multilayer networks elucidates the molecular determinants of severity in Congenital Myasthenic Syndromes.Nature communications · 2024Article
- Reuniting philosophy and science to advance cancer research.Biological reviews of the Cambridge Philosophical Society · 2023Article
- Unraveling the Drivers of Tumorigenesis in the Context of Evolution: Theoretical Models and Bioinformatics Tools.Journal of molecular evolution · 2023Review
- Sequential mutations in exponentially growing populations.PLoS computational biology · 2023Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Much of cancer genetics research has focused on the identification of the most-important somatic mutations ('major drivers') that cause tumour growth. However, many mutations found in cancer might not be major drivers or 'passenger' mutations, but instead might have relatively weak tumour-promoting effects. Our aim is to highlight the existence of these mutations (termed 'mini drivers' herein), as multiple mini-driver mutations might substitute for a major-driver change, especially in the presence of genomic instability or high mutagen exposure. The mini-driver model has clinical implications: for example, the effects of therapeutically targeting such genes may be limited. However, the main importance of the model lies in helping to provide a complete understanding of tumorigenesis, especially as we anticipate that an increasing number of mini-driver mutations will be found by cancer genome sequencing.
Indexed as
Identifiers
26456849What Socratic holds
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.