ArticleNature communications2018
Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
What it found
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Who cites it
111 citing papers in PubMed, 179 citations in OpenAlex.
- An Annotated Biobank of Triple-Negative Breast Cancer Patient-Derived Xenografts Features Treatment-Naïve and Longitudinal Samples during Neoadjuvant Chemotherapy.Cancer research · 2025Trial
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- Reframing cancer therapy through tumor plasticity.Nature cancer · 2026Review
- Varying susceptibility of subpopulations along the epithelial-mesenchymal spectrum to undergo EMT.The FEBS journal · 2026Article
- Regulated cell death plasticity in cancer: thresholds, reversibility, and therapeutic failure.Journal of translational medicine · 2026Review
- 3D EM uncovers mitochondrial network remodeling in residual triple negative breast cancer after conventional chemotherapy treatments.iScience · 2026Article
- Single-cell morphodynamical trajectories enable prediction of gene expression accompanying cell state change.Cell systems · 2026Article
- Cell-intrinsic and tumor microenvironmental determinants of platinum resistance in epithelial ovarian cancer.Discover oncology · 2026Review
- Growth factors maintain intratumoral heterogeneity and drive therapeutic resistance in triple-negative breast cancer.Cell reports · 2026Article
- Drug-tolerant persister cells: the deadly survivors in hematological malignancies.Frontiers in pharmacology · 2026Review
- KLF5 enables dichotomous lineage programs in pancreatic cancer via the AAA+ ATPase coactivators RUVBL1 and RUVBL2.Nature communications · 2025Article
- Targeting Drug-Tolerant Persister Cancer Cells: Can Nanomaterial-Based Strategies Be Helpful for Anti-DTP Therapies?Pharmaceutics · 2025Review
- The interplay of DNA damage, epigenetics and tumour heterogeneity in driving cancer cell fitness.Nature communications · 2025Review
- Enhanced bioluminescence imaging of tumor cells surviving chemotherapy in a murine model of triple-negative breast cancer.NPJ breast cancer · 2025Article
- Diagnosis and therapeutic targeting of quiescent cancer cells: road to conquer cancer recurrence.BMB reports · 2025Review
- Chromatin-focused genetic and chemical screens identify BRPF1 as a targetable vulnerability in Taxol-resistant triple-negative breast cancer.Experimental & molecular medicine · 2025Article
- How memory and adaptation cost shape cell phenotypic dynamics in response to fluctuating environments.bioRxiv : the preprint server for biology · 2025Article
- Drug-induced tolerant persisters in tumor: mechanism, vulnerability and perspective implication for clinical treatment.Molecular cancer · 2025Review
- Phenotypic plasticity and secretory heterogeneity in subpopulations derived from single cancer cell.Acta pharmaceutica Sinica. B · 2025Article
- An integrative phenotype-structured partial differential equation model for the population dynamics of epithelial-mesenchymal transition.NPJ systems biology and applications · 2025Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 4 institutions in 1 country.
Funding
Abstract
Intratumoral heterogeneity in cancers arises from genomic instability and epigenomic plasticity and is associated with resistance to cytotoxic and targeted therapies. We show here that cell-state heterogeneity, defined by differentiation-state marker expression, is high in triple-negative and basal-like breast cancer subtypes, and that drug tolerant persister (DTP) cell populations with altered marker expression emerge during treatment with a wide range of pathway-targeted therapeutic compounds. We show that MEK and PI3K/mTOR inhibitor-driven DTP states arise through distinct cell-state transitions rather than by Darwinian selection of preexisting subpopulations, and that these transitions involve dynamic remodeling of open chromatin architecture. Increased activity of many chromatin modifier enzymes, including BRD4, is observed in DTP cells. Co-treatment with the PI3K/mTOR inhibitor BEZ235 and the BET inhibitor JQ1 prevents changes to the open chromatin architecture, inhibits the acquisition of a DTP state, and results in robust cell death in vitro and xenograft regression in vivo.
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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.