ArticleScience translational medicine2011
Optimization of dosing for EGFR-mutant non-small cell lung cancer with evolutionary cancer modeling.
Article in Science translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 307 papers, 2 of them syntheses that pooled it.
What it found
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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
307 citing papers in PubMed, 2 syntheses or guidelines pooled it, 527 citations in OpenAlex.
- Comparison of T790M Acquisition After Treatment With First- and Second-Generation Tyrosine-Kinase Inhibitors: A Systematic Review and Network Meta-Analysis.Frontiers in oncology · 2022Pooled it
- Pooled it
- Identification of optimal dosing schedules of dacomitinib and osimertinib for a phase I/II trial in advanced EGFR-mutant non-small cell lung cancer.Nature communications · 2021Trial
- Efficacy and Safety of First-Generation EGFR-TKIs Combined with Chemotherapy for Treatment-Naïve Advanced Non-Small-Cell Lung Cancer Patients Harboring SensitiveJournal of inflammation research · 2021Trial
- Urinary circulating DNA detection for dynamic tracking of EGFR mutations for NSCLC patients treated with EGFR-TKIs.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017Trial
- Trial
- Afatinib beyond progression in patients with non-small-cell lung cancer following chemotherapy, erlotinib/gefitinib and afatinib: phase III randomized LUX-Lung 5 trial.Annals of oncology : official journal of the European Society for Medical Oncology · 2016Trial
- Trial
- Evolutionary Antifragile Therapy Is a Treatment Strategy to Suppress Drug Resistance by Exploiting Dose-Response Convexity.Cancer research · 2026Article
- Quantum-Augmented Federated AI for Adaptive Pharmacogenomic Precision Oncology: A Perspective.ACS pharmacology & translational science · 2026Review
- Mutation-Specific Response to Ramucirumab inJTO clinical and research reports · 2026Article
- Towards evolutionary guided precision medicine of acute myeloid leukemia and Fanconi anemia associated bone marrow failure.Stem cells translational medicine · 2026Article
- Can evolutionary therapy be applied in non-small cell lung cancer?Scientific reports · 2026Article
- Mathematical Oncology: How Modeling Is Transforming Clinical Decision-Making.Cancer research · 2025Review
- Prevalence and therapeutic response of EGFR T790I mutation in NSCLC patients with acquired resistance to EGFR-TKIs: a retrospective cohort study.BMC cancer · 2025Article
- Probability Distribution for Rare Neutral Mutations in Cancers and Application to Dynamic Precision Medicine of Cancer.bioRxiv : the preprint server for biology · 2025Article
- Evolutionary antifragile therapy.bioRxiv : the preprint server for biology · 2025Article
- Inheritable cell-states shape drug-persister correlations and population dynamics in cancer cells.PLoS computational biology · 2025Article
- Dauricine Overcomes Osimertinib Resistance in Lung Cancer by Inducing Ferroptosis via Stabilizing SAT1.Cancer science · 2025Article
- Personalized cancer treatment strategies incorporating irreversible and reversible drug resistance mechanisms.NPJ systems biology and applications · 2025Article
247 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 1 country.
Funding
Abstract
Non-small cell lung cancers (NSCLCs) that harbor mutations within the epidermal growth factor receptor (EGFR) gene are sensitive to the tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib. Unfortunately, all patients treated with these drugs will acquire resistance, most commonly as a result of a secondary mutation within EGFR (T790M). Because both drugs were developed to target wild-type EGFR, we hypothesized that current dosing schedules were not optimized for mutant EGFR or to prevent resistance. To investigate this further, we developed isogenic TKI-sensitive and TKI-resistant pairs of cell lines that mimic the behavior of human tumors. We determined that the drug-sensitive and drug-resistant EGFR-mutant cells exhibited differential growth kinetics, with the drug-resistant cells showing slower growth. We incorporated these data into evolutionary mathematical cancer models with constraints derived from clinical data sets. This modeling predicted alternative therapeutic strategies that could prolong the clinical benefit of TKIs against EGFR-mutant NSCLCs by delaying the development of resistance.
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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.