ArticleNature communications2013
Non-Darwinian dynamics in therapy-induced cancer drug resistance.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 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
164 citing papers in PubMed.
- Time-Resolved Network Entropy Analysis Identifies a CTNND1-VAV3 Subnetwork in Gefitinib-Resistant NSCLC.International journal of molecular sciences · 2026Article
- Molecular Characterization of PARP Inhibitor Response Reveals Co-Targeting Strategies in Advanced Prostate Cancer.Cancers · 2026Article
- Pre-existing cell states predict resistance to multiple treatments.Cell genomics · 2026Article
- Two Worlds, One Battle: How Bacteria and Malignancies Converge on Drug Resistance.International journal of molecular sciences · 2026Review
- Review
- Review
- Dying cells as architects of the stem cell niche: a conserved mechanism driving tissue regeneration and tumor therapy resistance.Cell communication and signaling : CCS · 2026Review
- First Line and Treatment Sequencing in EGFR-Mutated Metastatic NSCLC: What is Right for Which Patient?Drugs · 2026Review
- Review
- The Divide-Survive Matrix: decoupling proliferative drive from intrinsic survival architecture in oncology.Frontiers in oncology · 2026Article
- Cellular memory after cancer therapy: persistence after drug withdrawal, maintenance across cell divisions, and responses to rechallenge.Frontiers in pharmacology · 2026Review
- A Systematic Review of Evidence for the Cost of Therapeutic Resistance in Cancer.bioRxiv : the preprint server for biology · 2025Article
- Transition between cell states of sensitivity reveals molecular vulnerability of drug-tolerant cells.Molecular systems biology · 2025Article
- Reinforcement learning for adaptive control of phenotypically heterogeneous bacterial populations.bioRxiv : the preprint server for biology · 2025Article
- Review
- SOX9 drives a stem-like transcriptional state and platinum resistance in high-grade serous ovarian cancer.The Journal of clinical investigation · 2025Article
- H3K27me3 chromatin heterogeneity reveals variable cell responses to estrogen and endocrine treatment.bioRxiv : the preprint server for biology · 2025Article
- Inheritable cell-states shape drug-persister correlations and population dynamics in cancer cells.PLoS computational biology · 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
104 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
The development of drug resistance, the prime cause of failure in cancer therapy, is commonly explained by the selection of resistant mutant cancer cells. However, dynamic non-genetic heterogeneity of clonal cell populations continuously produces metastable phenotypic variants (persisters), some of which represent stem-like states that confer resistance. Even without genetic mutations, Darwinian selection can expand these resistant variants, which would explain the invariably rapid emergence of stem-like resistant cells. Here, by using quantitative measurements and modelling, we show that appearance of multidrug resistance in HL60 leukemic cells following treatment with vincristine is not explained by Darwinian selection but by Lamarckian induction. Single-cell longitudinal monitoring confirms the induction of multidrug resistance in individual cells. Associated transcriptome changes indicate a lasting stress response consistent with a drug-induced switch between high-dimensional cancer attractors. Resistance induction correlates with Wnt pathway upregulation and is suppressed by β-catenin knockdown, revealing a new opportunity for early therapeutic intervention against the development of drug 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.