ArticlePLoS computational biology2021
Drug-induced resistance evolution necessitates less aggressive treatment.
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 24 papers.
What it found
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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
24 citing papers in PubMed.
- The shared evolutionary capacities of plasmids and extrachromosomal DNA.Nature reviews. Genetics · 2026Review
- Mapping the landscape of mathematical models for antimicrobial resistance: a scoping review.BMC public health · 2026Article
- Differential association of fluticasone furoate and budesonide with clinically detected COVID-19: a retrospective cohort study.BMJ open respiratory research · 2026Article
- Stochastic Evolutionary Control in Heterogeneous Populations.bioRxiv : the preprint server for biology · 2026Article
- Stress-driven emergence of heritable non-genetic drug resistance.Research square · 2025Article
- The role of environmental stress in promoting mutators through evolutionary rescue: quantitative predictions.Genetics · 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
- Personalized cancer treatment strategies incorporating irreversible and reversible drug resistance mechanisms.NPJ systems biology and applications · 2025Article
- Quantitative measurement of phenotype dynamics during cancer drug resistance evolution using genetic barcoding.Nature communications · 2025Article
- Bringing evolutionary cancer therapy to the clinic: a systems approach.NPJ systems biology and applications · 2025Review
- Modeling critical dosing strategies for stromal-induced resistance to cancer therapy.NPJ systems biology and applications · 2025Article
- Circulating tumor cell markers for early detection and drug resistance assessment through liquid biopsy.Frontiers in oncology · 2025Review
- A mathematical framework for comparison of intermittent versus continuous adaptive chemotherapy dosing in cancer.NPJ systems biology and applications · 2024Article
- Resistance Management for Cancer: Lessons from Farmers.Cancer research · 2024Review
- Threshold-awareness in adaptive cancer therapy.PLoS computational biology · 2024Article
- The first-in-class pro-apoptotic peptide PEP-010 is effective in monotherapy and in combination with paclitaxel on resistant ovarian adenocarcinoma cell models.Frontiers in pharmacology · 2024Article
- Steering and controlling evolution - from bioengineering to fighting pathogens.Nature reviews. Genetics · 2023Review
- Statistical inference of the rates of cell proliferation and phenotypic switching in cancer.Journal of theoretical biology · 2023Article
- A survey of open questions in adaptive therapy: Bridging mathematics and clinical translation.eLife · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Increasing body of experimental evidence suggests that anticancer and antimicrobial therapies may themselves promote the acquisition of drug resistance by increasing mutability. The successful control of evolving populations requires that such biological costs of control are identified, quantified and included to the evolutionarily informed treatment protocol. Here we identify, characterise and exploit a trade-off between decreasing the target population size and generating a surplus of treatment-induced rescue mutations. We show that the probability of cure is maximized at an intermediate dosage, below the drug concentration yielding maximal population decay, suggesting that treatment outcomes may in some cases be substantially improved by less aggressive treatment strategies. We also provide a general analytical relationship that implicitly links growth rate, pharmacodynamics and dose-dependent mutation rate to an optimal control law. Our results highlight the important, but often neglected, role of fundamental eco-evolutionary costs of control. These costs can often lead to situations, where decreasing the cumulative drug dosage may be preferable even when the objective of the treatment is elimination, and not containment. Taken together, our results thus add to the ongoing criticism of the standard practice of administering aggressive, high-dose therapies and motivate further experimental and clinical investigation of the mutagenicity and other hidden collateral costs of therapies.
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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.