ArticlePLoS computational biology2021
The role of memory in non-genetic inheritance and its impact on cancer treatment resistance.
Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Growth rate-driven modelling suggests that phenotypic adaptation drives drug resistance in BRAFV600E-mutant melanoma.Communications biology · 2026Article
- INHERITANCE OF INTRACELLULAR VIRAL RNA IN A MULTISCALE MODEL OF HEPATITIS C INFECTION.SIAM journal on applied mathematics · 2026Article
- Drug-tolerant persister cells in cancer: bridging the gaps between bench and bedside.Nature communications · 2025Review
- Inheritable cell-states shape drug-persister correlations and population dynamics in cancer cells.PLoS computational biology · 2025Article
- Reducing phenotype-structured partial differential equations models of cancer evolution to systems of ordinary differential equations: a generalised moment dynamics approach.Journal of mathematical biology · 2025Article
- Identifiability of phenotypic adaptation from low-cell-count experiments and a stochastic model.PLoS computational biology · 2025Article
- Systems Biology of the Cancer Cell.Annual review of biomedical engineering · 2025Review
- A multiscale model of the action of a capsid assembly modulator for the treatment of chronic hepatitis B.PLoS computational biology · 2025Article
- Spatially Resolved Tumor Ecosystems and Cell States in Gastric Adenocarcinoma Progression and Evolution.Cancer discovery · 2025Article
- A mathematical framework for comparison of intermittent versus continuous adaptive chemotherapy dosing in cancer.NPJ systems biology and applications · 2024Article
- Leveraging Cancer Phenotypic Plasticity for Novel Treatment Strategies.Journal of clinical medicine · 2024Article
- Modeling resistance to the broadly neutralizing antibody PGT121 in people living with HIV-1.PLoS computational biology · 2024Article
- A Nexus between Genetic and Non-Genetic Mechanisms Guides KRAS Inhibitor Resistance in Lung Cancer.Biomolecules · 2023Article
- Understanding and leveraging phenotypic plasticity during metastasis formation.NPJ systems biology and applications · 2023Article
- A Continuation Technique for Maximum Likelihood Estimators in Biological Models.Bulletin of mathematical biology · 2023Article
- Examining the efficacy of localised gemcitabine therapy for the treatment of pancreatic cancer using a hybrid agent-based model.PLoS computational biology · 2023Article
- Review
- Roadmap on plasticity and epigenetics in cancer.Physical biology · 2022Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
Intra-tumour heterogeneity is a leading cause of treatment failure and disease progression in cancer. While genetic mutations have long been accepted as a primary mechanism of generating this heterogeneity, the role of phenotypic plasticity is becoming increasingly apparent as a driver of intra-tumour heterogeneity. Consequently, understanding the role of this plasticity in treatment resistance and failure is a key component of improving cancer therapy. We develop a mathematical model of stochastic phenotype switching that tracks the evolution of drug-sensitive and drug-tolerant subpopulations to clarify the role of phenotype switching on population growth rates and tumour persistence. By including cytotoxic therapy in the model, we show that, depending on the strategy of the drug-tolerant subpopulation, stochastic phenotype switching can lead to either transient or permanent drug resistance. We study the role of phenotypic heterogeneity in a drug-resistant, genetically homogeneous population of non-small cell lung cancer cells to derive a rational treatment schedule that drives population extinction and avoids competitive release of the drug-tolerant sub-population. This model-informed therapeutic schedule results in increased treatment efficacy when compared against periodic therapy, and, most importantly, sustained tumour decay without the development of resistance.
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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.