ArticleScience translational medicine2019
Resistance to neoadjuvant chemotherapy in triple-negative breast cancer mediated by a reversible drug-tolerant state.
Article in Science translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 3 of them syntheses that pooled it.
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
200 citing papers in PubMed, 3 syntheses or guidelines pooled it, 300 citations in OpenAlex.
- Efficacy, safety, and PD-L1-defined outcomes of neoadjuvant immune checkpoint inhibitors in early-stage triple-negative breast cancer: a systematic review and meta-analysis.Frontiers in immunology · 2026Pooled it
- A systematic review of progress toward unlocking the power of epigenetics in breast cancer: latest updates and perspectives.Frontiers in pharmacology · 2025Pooled it
- Recurrence-free survival dynamics following adjuvant chemotherapy for resected colorectal cancer: A systematic review of randomized controlled trials.Cancer medicine · 2024Pooled it
- An Annotated Biobank of Triple-Negative Breast Cancer Patient-Derived Xenografts Features Treatment-Naïve and Longitudinal Samples during Neoadjuvant Chemotherapy.Cancer research · 2025Trial
- Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy-Tolerant Persister Cells in ER+ Breast Cancer.Cancer research · 2025Trial
- Targeting fibroblast activation suppresses chemotherapy-induced pro-invasive remodeling of the extracellular matrix.bioRxiv : the preprint server for biology · 2026Article
- Epithelial-mesenchymal transition in carcinoma: navigating phenotypic states to target resistance and metastasis.Cancer metastasis reviews · 2026Review
- Multiple distinct metastatic cell states are induced by epithelial-mesenchymal plasticity.bioRxiv : the preprint server for biology · 2026Article
- Integrative Single-Cell and Bulk Transcriptomic Analyses with Spatial Validation Identify a Residual Fatty Acid-EMT Subset Driving Chemotherapy Resistance in Triple-Negative Breast Cancer via MIF- and MK-Mediated Ligand-Receptor Signaling.International journal of molecular sciences · 2026Article
- Chronotherapeutic administration of neoadjuvant chemotherapy reduces cancer-related fatigue-like behavior.Brain, behavior, & immunity - health · 2026Article
- 3D EM uncovers mitochondrial network remodeling in residual triple negative breast cancer after conventional chemotherapy treatments.iScience · 2026Article
- Spatiotemporal organisation of residual disease in mouse and human BRCA1-deficient mammary tumours and breast cancer.Nature communications · 2026Article
- Geospatial genetic evolution and phenotypic plasticity in triple-negative breast cancer.Genome medicine · 2026Article
- Ferrous Iron Accumulation Is a Hallmark and Therapeutic Vulnerability of Therapy-Induced Senescence.bioRxiv : the preprint server for biology · 2026Article
- Inhibitory Effect of Melatonin on the Proliferation of Breast Cancer Cells MDA-MB-468 by Antioxidants Superoxide Dismutase and Glutathione Peroxidase.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Review
- Game of clones: decipher lineage plasticity in hormone-driven cancers.Cellular and molecular life sciences : CMLS · 2026Review
- Profile of Helen M. Piwnica-Worms.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Metabolic Response to CDK4/6 Inhibition in ER+ Breast Cancer Creates a Therapeutic Vulnerability in Drug-Tolerant Persister Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Co-occurrence of transcriptionally distinct persister cell states underpins neoadjuvant therapy resistance in triple‑negative breast cancer.Genome medicine · 2026Article
140 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
30 authors at 3 institutions in 1 country.
Funding
Abstract
Eradicating triple-negative breast cancer (TNBC) resistant to neoadjuvant chemotherapy (NACT) is a critical unmet clinical need. In this study, patient-derived xenograft (PDX) models of treatment-naïve TNBC and serial biopsies from TNBC patients undergoing NACT were used to elucidate mechanisms of chemoresistance in the neoadjuvant setting. Barcode-mediated clonal tracking and genomic sequencing of PDX tumors revealed that residual tumors remaining after treatment with standard frontline chemotherapies, doxorubicin (Adriamycin) combined with cyclophosphamide (AC), maintained the subclonal architecture of untreated tumors, yet their transcriptomes, proteomes, and histologic features were distinct from those of untreated tumors. Once treatment was halted, residual tumors gave rise to AC-sensitive tumors with similar transcriptomes, proteomes, and histological features to those of untreated tumors. Together, these results demonstrated that tumors can adopt a reversible drug-tolerant state that does not involve clonal selection as an AC resistance mechanism. Serial biopsies obtained from patients with TNBC undergoing NACT revealed similar histologic changes and maintenance of stable subclonal architecture, demonstrating that AC-treated PDXs capture molecular features characteristic of human TNBC chemoresistance. Last, pharmacologic inhibition of oxidative phosphorylation using an inhibitor currently in phase 1 clinical development delayed residual tumor regrowth. Thus, AC resistance in treatment-naïve TNBC can be mediated by nonselective mechanisms that confer a reversible chemotherapy-tolerant state with targetable vulnerabilities.
Indexed as
Identifiers
What OpenQuestion holds
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.