ArticleNature communications2015
Temporally sequenced anticancer drugs overcome adaptive resistance by targeting a vulnerable chemotherapy-induced phenotypic transition.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.
What it found
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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.
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Who cites it
159 citing papers in PubMed, 286 citations in OpenAlex.
- NRF2 activation is required for chemotherapy resistance acquisition in medulloblastoma via metabolic and redox adaptation.Redox biology · 2026Article
- Growth rate-driven modelling suggests that phenotypic adaptation drives drug resistance in BRAFV600E-mutant melanoma.Communications biology · 2026Article
- Identification, functional insights and therapeutic targeting of EMT tumour states.Nature reviews. Cancer · 2026Review
- A Systematic Review of Evidence for the Cost of Therapeutic Resistance in Cancer.bioRxiv : the preprint server for biology · 2025Article
- Ultrasound-responsive hydrogels for bone and cartilage tissue engineering.Materials today. Bio · 2025Review
- 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
- A CD24BMC biology · 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
- Stochastic variation in the FOXM1 transcription program mediates replication stress tolerance.Molecular oncology · 2025Article
- Low-cost robotic manipulation of live microtissues for cancer drug testing.Science advances · 2025Article
- Phenotypic plasticity and secretory heterogeneity in subpopulations derived from single cancer cell.Acta pharmaceutica Sinica. B · 2025Article
- Towards understanding cancer dormancy over strategic hitching up mechanisms to technologies.Molecular cancer · 2025Review
- Modeling critical dosing strategies for stromal-induced resistance to cancer therapy.NPJ systems biology and applications · 2025Article
- Modeling Drug Responses and Evolutionary Dynamics Using Patient-Derived Xenografts Reveals Precision Medicine Strategies for Triple-Negative Breast Cancer.Cancer research · 2025Article
- Crosstalk between lipid metabolism and EMT: emerging mechanisms and cancer therapy.Molecular and cellular biochemistry · 2025Article
- The LRP4/YAP axis drives the radiation-tolerant persister (RTP) cell state in breast cancer.Theranostics · 2025Article
- Modeling tumors as complex ecosystems.iScience · 2024Review
- Chemoresistance to additive PARP/PI3K dual inhibition in triple-negative breast cancer cell lines is associated with adaptive stem cell-like prevalence.bioRxiv : the preprint server for biology · 2024Article
- Modeling tumors as species-rich ecological communities.bioRxiv : the preprint server for biology · 2024Article
99 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
8 authors at 5 institutions in 3 countries.
Funding
Abstract
Understanding the emerging models of adaptive resistance is key to overcoming cancer chemotherapy failure. Using human breast cancer explants, in vitro cell lines, mouse in vivo studies and mathematical modelling, here we show that exposure to a taxane induces phenotypic cell state transition towards a favoured transient CD44(Hi)CD24(Hi) chemotherapy-tolerant state. This state is associated with a clustering of CD44 and CD24 in membrane lipid rafts, leading to the activation of Src Family Kinase (SFK)/hemopoietic cell kinase (Hck) and suppression of apoptosis. The use of pharmacological inhibitors of SFK/Hck in combination with taxanes in a temporally constrained manner, where the kinase inhibitor is administered post taxane treatment, but not when co-administered, markedly sensitizes the chemotolerant cells to the chemotherapy. This approach of harnessing chemotherapy-induced phenotypic cell state transition for improving antitumour outcome could emerge as a translational strategy for the management of cancer.
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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.