ArticleNPJ systems biology and applications2025
Understanding therapeutic tolerance through a mathematical model of drug-induced resistance.
Article in NPJ systems biology and applications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- A three-gene signature correlated with MAPK/ERK activation characterizes acquired resistance to EGFR-tyrosine kinase inhibitors in non-small cell lung cancer.Oncology letters · 2026Article
- Cancer drug response and resistance: molecular mechanisms and combating strategies.Signal transduction and targeted therapy · 2026Review
- Growth rate-driven modelling suggests that phenotypic adaptation drives drug resistance in BRAFV600E-mutant melanoma.Communications biology · 2026Article
- 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
- A statistical framework for detecting therapy-induced resistance from drug screens.NPJ systems biology and applications · 2025Article
- Modeling critical dosing strategies for stromal-induced resistance to cancer therapy.NPJ systems biology and applications · 2025Article
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.
Funding
Abstract
There is growing recognition that phenotypic plasticity enables cancer cells to adapt to various environmental conditions. An example of this adaptability is the ability of an initially sensitive population of cancer cells to acquire resistance and persist in the presence of therapeutic agents. Understanding the implications of this drug-induced resistance is essential for predicting transient and long-term tumor dynamics subject to treatment. This paper introduces a mathematical model of drug-induced resistance which provides excellent fits to time-resolved in vitro experimental data. From observational data of total numbers of cells, the model unravels the relative proportions of sensitive and resistance subpopulations and quantifies their dynamics as a function of drug dose. The predictions are then validated using data on drug doses that were not used when fitting parameters. Optimal control techniques are then utilized to discover dosing strategies that could lead to better outcomes as quantified by lower total cell volume.
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.