ReviewCells2019
Metabolic Reprogramming in Breast Cancer and Its Therapeutic Implications.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 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.
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
147 citing papers in PubMed, 225 citations in OpenAlex.
- Pathological response and metabolites' prognostic role in HER2-positive breast cancer treated with neoadjuvant pyrotinib, trastuzumab, nab-paclitaxel, and carboplatin: a single-arm phase II trial.Breast cancer research : BCR · 2025Trial
- A Phase II Clinical Study on Apatinib Plus Vinorelbine in Refractory HER2-Negative Breast Cancer and its Metabolic Implications of Drug Resistance.Current cancer drug targets · 2025Trial
- Trial
- Article
- Incremental Value of Synthetic MRI Radiomics in Predicting Neoadjuvant Response in Human Epidermal Growth Factor Receptor 2-Positive Breast Cancer.Radiology. Imaging cancer · 2026Article
- LncRNA PCAT7 drives tumorigenesis and glycolytic reprogramming in breast cancer via the ceRNA-mediated miR-204-5p/RUNX2 axis.Cancer gene therapy · 2026Article
- Integrated data-independent acquisition and thermal proteome profiling for proteomic characterization of lamotrigine-treated MCF-7 cells.Analytical and bioanalytical chemistry · 2026Article
- A novel combination for in vivo breast cancer treatment: TAK1 inhibition combined with metformin and Lentinula edodes compounds synergistically reinvigorates CD8Journal of translational medicine · 2026Article
- Therapy as a State-Generator: Dynamic Phenotypic Landscapes and Adaptive Stress Circuits in Chemotherapy Resistance of Breast Cancer.Antioxidants (Basel, Switzerland) · 2026Review
- Unraveling the αVβ5-GLUT5 axis in breast cancer: linking extracellular matrix signaling to fructose metabolism: a scoping review.Molecular biology reports · 2026Article
- Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer.Current oncology (Toronto, Ont.) · 2026Review
- Ophiobolin A impacts mitochondrial redox biology in an epithelial-mesenchymal transition (EMT)-specific manner.Cancer cell international · 2026Article
- UNC93B1 drives IL-6/STAT3-dependent tumor-macrophage crosstalk and epithelial-mesenchymal transition in breast cancer.Frontiers in pharmacology · 2026Article
- Article
- Mortality differences in coronary patients with breast cancer treated with trimetazidine dihydrochloride: potential therapeutic implications.Cardio-oncology (London, England) · 2025Article
- Decoding breast cancer: insights into molecular pathways & therapeutic approaches.Discover oncology · 2025Review
- Adaptability of lung and liver metastatic breast cancer cells to glucose.Cancer cell international · 2025Article
- Prediction of Lung Cancer Metastasis Risk Based on Single-Cell Metabolic Profiling of Circulating Tumor Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mammary adipose dysfunction in the dual epidemic of obesity and breast cancer.Carcinogenesis · 2025Review
- Landscape of metabolic alterations and treatment strategies in breast cancer.Genes & diseases · 2025Review
87 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Current standard-of-care (SOC) therapy for breast cancer includes targeted therapies such as endocrine therapy for estrogen receptor-alpha (ERα) positive; anti-HER2 monoclonal antibodies for human epidermal growth factor receptor-2 (HER2)-enriched; and general chemotherapy for triple negative breast cancer (TNBC) subtypes. These therapies frequently fail due to acquired or inherent resistance. Altered metabolism has been recognized as one of the major mechanisms underlying therapeutic resistance. There are several cues that dictate metabolic reprogramming that also account for the tumors' metabolic plasticity. For metabolic therapy to be efficacious there is a need to understand the metabolic underpinnings of the different subtypes of breast cancer as well as the role the SOC treatments play in targeting the metabolic phenotype. Understanding the mechanism will allow us to identify potential therapeutic vulnerabilities. There are some very interesting questions being tackled by researchers today as they pertain to altered metabolism in breast cancer. What are the metabolic differences between the different subtypes of breast cancer? Do cancer cells have a metabolic pathway preference based on the site and stage of metastasis? How do the cell-intrinsic and -extrinsic cues dictate the metabolic phenotype? How do the nucleus and mitochondria coordinately regulate metabolism? How does sensitivity or resistance to SOC affect metabolic reprogramming and vice-versa? This review addresses these issues along with the latest updates in the field of breast cancer metabolism.
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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.