ReviewNature reviews. Genetics2021
Mutation-selection balance and compensatory mechanisms in tumour evolution.
Review in Nature reviews. Genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers, 1 of them a synthesis that pooled it.
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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Pooled it
- RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- [Prediction and verification of therapeutic drugs for triple-negative breast cancer using a knowledge graph-based drug repurposing model].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Fluctuating environment causes neoplastic transition and epithelial-mesenchymal plasticity in human cells.Research square · 2026Article
- Lineage plasticity: a new dilemma in lung cancer treatment.Molecular biology reports · 2026Review
- Low SVEP1 in intrahepatic cholangiocarcinoma mediates phenotype switching-driven metastasis by Jag2/Notch1/Hes5.Cell death & disease · 2025Article
- Compensatory evolution to DNA replication stress is robust to nutrient availability.Molecular systems biology · 2025Article
- Bistable Mutation-Selection Equilibria and Violations of Fisher's Theorem in Tetraploids: Insights from Nonlinear Dynamics.bioRxiv : the preprint server for biology · 2025Article
- Mitochondrial ROS inhibition prevents doxorubicin-induced breast cancer cell migration and invasion.iScience · 2025Article
- Genome-level selection in tumors as a universal marker of resistance to therapy.Nature communications · 2025Article
- Article
- Nutrient transporter-oriented nanoinhibitor counteracts intracellular metabolic reprogramming for RT-resistant HCC treatment.Materials today. Bio · 2025Article
- Gut Microbiota Secondary Metabolites: Key Roles in GI Tract Cancers and Infectious Diseases.Biomedicines · 2025Review
- Histological transformation in lung adenocarcinoma: Insights of mechanisms and therapeutic windows.Journal of translational internal medicine · 2024Article
- Cetuximab chemotherapy resistance: Insight into the homeostatic evolution of head and neck cancer (Review).Oncology reports · 2024Review
- Surviving the Storm: The Role of Poly- and Depolyploidization in Tissues and Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Synergistic epistasis among cancer drivers can rescue early tumors from the accumulation of deleterious passengers.PLoS computational biology · 2024Article
- Machine learning-based extrachromosomal DNA identification in large-scale cohorts reveals its clinical implications in cancer.Nature communications · 2024Article
- Molecular and immunohistochemical study ofHeliyon · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Intratumour heterogeneity and phenotypic plasticity, sustained by a range of somatic aberrations, as well as epigenetic and metabolic adaptations, are the principal mechanisms that enable cancers to resist treatment and survive under environmental stress. A comprehensive picture of the interplay between different somatic aberrations, from point mutations to whole-genome duplications, in tumour initiation and progression is lacking. We posit that different genomic aberrations generally exhibit a temporal order, shaped by a balance between the levels of mutations and selective pressures. Repeat instability emerges first, followed by larger aberrations, with compensatory effects leading to robust tumour fitness maintained throughout the tumour progression. A better understanding of the interplay between genetic aberrations, the microenvironment, and epigenetic and metabolic cellular states is essential for early detection and prevention of cancer as well as development of efficient therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.