ArticleJournal of theoretical biology2020
Understanding the role of phenotypic switching in cancer drug resistance.
Article in Journal of theoretical biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 79 citations in OpenAlex.
- Cell State Transitions Drive the Evolution of Disease Progression in B-Lymphoblastic Leukemia.Cancer research communications · 2026Article
- Targeting cancer stem cell plasticity and tumor microenvironment crosstalk: a comprehensive review.Discover oncology · 2025Review
- Transition between cell states of sensitivity reveals molecular vulnerability of drug-tolerant cells.Molecular systems biology · 2025Article
- Impacts of competition and phenotypic plasticity on the viability of adaptive therapy.Mathematical biosciences · 2025Article
- Inheritable cell-states shape drug-persister correlations and population dynamics in cancer cells.PLoS computational biology · 2025Article
- Chromosomal Instability as a Driver of Therapeutic Resistance and Phenotypic Plasticity in Non-Small Cell Lung Cancer.Journal of cellular and molecular medicine · 2025Article
- Optimal dosing of anti-cancer treatment under drug-induced plasticity.NPJ systems biology and applications · 2025Article
- A statistical framework for detecting therapy-induced resistance from drug screens.NPJ systems biology and applications · 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
- Article
- Quantitative measurement of phenotype dynamics during cancer drug resistance evolution using genetic barcoding.Nature communications · 2025Article
- Stochastic gene expression in proliferating cells: Differing noise intensity in single-cell and population perspectives.PLoS computational biology · 2025Article
- Identifiability of phenotypic adaptation from low-cell-count experiments and a stochastic model.PLoS computational biology · 2025Article
- Estimating treatment sensitivity in synthetic and in vitro tumors using a random differential equation model.NPJ systems biology and applications · 2025Article
- Optimisation of gene expression noise for cellular persistence against lethal events.Journal of theoretical biology · 2025Article
- Modeling critical dosing strategies for stromal-induced resistance to cancer therapy.NPJ systems biology and applications · 2025Article
- Modeling tumors as complex ecosystems.iScience · 2024Review
- Stochastic Gene Expression in Proliferating Cells: Differing Noise Intensity in Single-Cell and Population Perspectives.bioRxiv : the preprint server for biology · 2024Article
- Leveraging Cancer Phenotypic Plasticity for Novel Treatment Strategies.Journal of clinical medicine · 2024Article
- Modeling tumors as species-rich ecological communities.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The emergence of acquired drug resistance in cancer represents a major barrier to treatment success. While research has traditionally focused on genetic sources of resistance, recent findings suggest that cancer cells can acquire transient resistant phenotypes via epigenetic modifications and other non-genetic mechanisms. Although these resistant phenotypes are eventually relinquished by individual cells, they can temporarily 'save' the tumor from extinction and enable the emergence of more permanent resistance mechanisms. These observations have generated interest in the potential of epigenetic therapies for long-term tumor control or eradication. In this work, we develop a mathematical model to study how phenotypic switching at the single-cell level affects resistance evolution in cancer. We highlight unique features of non-genetic resistance, probe the evolutionary consequences of epigenetic drugs and explore potential therapeutic strategies. We find that even short-term epigenetic modifications and stochastic fluctuations in gene expression can drive long-term drug resistance in the absence of any bona fide resistance mechanisms. We also find that an epigenetic drug that slightly perturbs the average retention of the resistant phenotype can turn guaranteed treatment failure into guaranteed success. Lastly, we find that combining an epigenetic drug with an anti-cancer agent can significantly outperform monotherapy, and that treatment outcome is heavily affected by drug sequencing.
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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.