ArticleBreast cancer research : BCR2024
Metabolic adaptation towards glycolysis supports resistance to neoadjuvant chemotherapy in early triple negative breast cancers.
Article in Breast cancer research : BCR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
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The trial behind it
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.
- Pooled it
- Neoadjuvant chemotherapy with angiogenesis inhibitor in early-stage breast cancer: a systematic review and meta-analysis.Frontiers in oncology · 2026Pooled it
- Response to neoadjuvant chemotherapy in early breast cancers is associated with epithelial-mesenchymal transition and tumor-infiltrating lymphocytes.Molecular oncology · 2025Trial
- Surgery-first versus neoadjuvant chemotherapy in stage I (cT1c) triple-negative breast cancer: A critical reappraisal.Breast (Edinburgh, Scotland) · 2026Review
- A CXCR4/PD-L1 Bispecific Nanobody Engineered for Tumor Microenvironment Retention Mediates Sustained Synergy with Chemotherapy via Remodeling Immunity in TNBC.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Distinct metabolic dependency on BCAA defines cancer stemness and malignancy in human triple-negative breast cancer.Cell reports · 2026Article
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- Machine Learning-Based Analysis of Large-Scale Transcriptomic Data Identifies Core Genes Associated with Multi-Drug Resistance.International journal of molecular sciences · 2026Article
- Ensemble Machine Learning on Bulk RNA-Seq Identifies 17-Gene Signature Predicting Neoadjuvant Chemotherapy Response in Breast Cancer.Current issues in molecular biology · 2026Article
- Divergent transcriptional programs and constrained metabolic states reveal selective metabolic dependencies in chemoresistant luminal breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2026Article
- Breast Cancer Progression by the FGF/FGFR Axis: A Metabolic Perspective.Journal of mammary gland biology and neoplasia · 2025Review
- Future perspective of clinical usefulness of metabolic and mitochondrial heterogeneity in triple-negative breast cancers.International journal of clinical oncology · 2025Review
- Alternative Promoters Drive Transcriptomic Reprogramming and Prognostic Stratification in TNBC.NPJ systems biology and applications · 2025Article
- Metabolomics as a tool for understanding and treating triple-negative breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Role of intratumoral heterogeneity in metastatic progression and drug resistance.Discover oncology · 2025Review
- RnaXtract, a tool for extracting gene expression, variants, and cell-type composition from bulk RNA sequencing.Scientific reports · 2025Article
- Resistance to neoadjuvant chemotherapy in breast cancers: a metabolic perspective.Journal of experimental & clinical cancer research : CR · 2025Review
- ALKBH3-regulated mActa pharmaceutica Sinica. B · 2025Article
- Jacaric Acid Empowers RSL3-Induced Ferroptotic Cell Death in Two- and Three-Dimensional Breast Cancer Cell Models.International journal of molecular sciences · 2025Article
- Predictive Value ofPharmaceuticals (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeoadjuvant chemotherapy (NAC) is the standard of care for patients with early-stage triple negative breast cancers (TNBC). However, more than half of TNBC patients do not achieve a pathological complete response (pCR) after NAC, and residual cancer burden (RCB) is associated with dismal long-term prognosis. Understanding the mechanisms underlying differential treatment outcomes is therefore critical to limit RCB and improve NAC efficiency.
methodsHuman TNBC cell lines and patient-derived organoids were used in combination with real-time metabolic assays to evaluate the effect of NAC (paclitaxel and epirubicin) on tumor cell metabolism, in particular glycolysis. Diagnostic biopsies (pre-NAC) from patients with early TNBC were analyzed by bulk RNA-sequencing to evaluate the predictive value of a glycolysis-related gene signature.
resultsPaclitaxel induced a consistent metabolic switch to glycolysis, correlated with a reduced mitochondrial oxidative metabolism, in TNBC cells. In pre-NAC diagnostic biopsies from TNBC patients, glycolysis was found to be upregulated in non-responders. Furthermore, glycolysis inhibition greatly improved response to NAC in TNBC organoid models.
conclusionsOur study pinpoints a metabolic adaptation to glycolysis as a mechanism driving resistance to NAC in TNBC. Our data pave the way for the use of glycolysis-related genes as predictive biomarkers for NAC response, as well as the development of inhibitors to overcome this glycolysis-driven resistance to NAC in human TNBC patients.
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