ArticleScience advances2020
Prior acquired resistance to paclitaxel relays diverse EGFR-targeted therapy persistence mechanisms.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Prognostic value of receptor tyrosine kinases in malignant melanoma patients: A systematic review and meta-analysis of immunohistochemistry.Frontiers in oncology · 2022Pooled it
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Osimertinib activates a TGF-β2-dependent secretory program that drives lung adenocarcinoma progression.The Journal of clinical investigation · 2026Article
- Chemotherapy-Treated Breast Cancer Cells Activate the WNT Signaling Pathway to Enter a Diapause-Like Early Persister State.Cancer research · 2026Article
- Mitochondrial fatty acid oxidation as the target for blocking therapy-resistance and inhibiting tumor recurrence: The proof-of-principle model demonstrated for ovarian cancer cells.Journal of advanced research · 2026Article
- Targeting Drug-Tolerant Persister Cancer Cells: Can Nanomaterial-Based Strategies Be Helpful for Anti-DTP Therapies?Pharmaceutics · 2025Review
- Enhanced bioluminescence imaging of tumor cells surviving chemotherapy in a murine model of triple-negative breast cancer.NPJ breast cancer · 2025Article
- Matrix-bound EGF promotes malignant phenotypes of breast cancer organoids in the biomimetic ECM of alginate.Materials today. Bio · 2025Article
- Single-organoid analysis reveals clinically relevant treatment-resistant and invasive subclones in pancreatic cancer.NPJ precision oncology · 2023Article
- Article
- Targeting drug-tolerant cells: A promising strategy for overcoming acquired drug resistance in cancer cells.MedComm · 2023Review
- Article
- Targeting epidermal growth factor receptor in paclitaxel-resistant human breast and lung cancer cells with upregulated glucose-6-phosphate dehydrogenase.British journal of cancer · 2022Article
- Review
- Modulating environmental signals to reveal mechanisms and vulnerabilities of cancer persisters.Science advances · 2022Article
- Engaging plasticity: Differentiation therapy in solid tumors.Frontiers in pharmacology · 2022Review
- Overcoming therapeutic resistance to platinum-based drugs by targeting Epithelial-Mesenchymal transition.Frontiers in oncology · 2022Review
- Perspectives of metal-organic framework nanosystem to overcome tumor drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Modeling adaptive drug resistance of colorectal cancer and therapeutic interventions with tumor spheroids.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Chemotherapy confers a conserved secondary tolerance to EGFR inhibition via AXL-mediated signaling bypass.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary drug resistance stems from dynamic clonal evolution during the development of a prior primary resistance. This collateral type of resistance is often a characteristic of cancer recurrence. Yet, mechanisms that drive this collateral resistance and their drug-specific trajectories are still poorly understood. Using resistance selection and small-scale pharmacological screens, we find that cancer cells with primary acquired resistance to the microtubule-stabilizing drug paclitaxel often develop tolerance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), leading to formation of more stable resistant cell populations. We show that paclitaxel-resistant cancer cells follow distinct selection paths under EGFR-TKIs by enriching the stemness program, developing a highly glycolytic adaptive stress response, and rewiring an apoptosis control pathway. Collectively, our work demonstrates the alterations in cellular state stemming from paclitaxel failure that result in collateral resistance to EGFR-TKIs and points to new exploitable vulnerabilities during resistance evolution in the second-line treatment setting.
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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.