ReviewSeminars in radiation oncology2019
Targeting Cancer Stem Cell Redox Metabolism to Enhance Therapy Responses.
Review in Seminars in radiation oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis 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
54 citing papers in PubMed, 1 synthesis or guideline pooled it.
- PGC1α-Mediated Metabolic Reprogramming Drives the Stemness of Pancreatic Precursor Lesions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Pooled it
- Cancer stem cells and drug resistance in cancer: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Clinical significance and expression of ALDH1 in triple-negative breast cancer.Diagnostic pathology · 2025Article
- Bibliometric-driven research on chemoresistance in breast cancer: knowledge mapping, hotspot evolution, and emerging insights (1994-2024).Discover oncology · 2025Article
- Decoding the NRF2-NOTCH Crosstalk in Lung Cancer-An Update.Antioxidants (Basel, Switzerland) · 2025Review
- Oxidative Stress and Redox Imbalance: Common Mechanisms in Cancer Stem Cells and Neurodegenerative Diseases.Cells · 2025Review
- Autophagy as a Therapeutic Target in Breast Tumors: The Cancer stem cell perspective.Autophagy reports · 2024Article
- Simultaneous Targeting of NQO1 and SOD1 Eradicates Breast Cancer Stem Cells via Mitochondrial Futile Redox Cycling.Cancer research · 2024Article
- Medicinal plants as a potential resource for the discovery of novel structures towards cancer drug resistance treatment.Heliyon · 2024Review
- mTORC2-driven chromatin cGAS mediates chemoresistance through epigenetic reprogramming in colorectal cancer.Nature cell biology · 2024Article
- A Novel Signature Based on Angiogenesis-Related Genes Predicts the Prognosis and Immunotherapy Response in HER2-Positive Breast Cancer.Journal of Cancer · 2024Article
- A Green Synthesis of Au-Ag Alloy Nanoparticles using Polydopamine Chemistry: Evaluation of their Anticancer Potency Towards Both MCF-7 Cells and their Cancer Stem Cells Subgroup.Anti-cancer agents in medicinal chemistry · 2024Article
- Review
- Cancer stem cells: an insight into the development of metastatic tumors and therapy resistance.Stem cell reviews and reports · 2023Review
- Review
- Cancer Metabolism: The Role of ROS in DNA Damage and Induction of Apoptosis in Cancer Cells.Metabolites · 2023Review
- Cancer stem cell fate determination: mito-nuclear communication.Cell communication and signaling : CCS · 2023Review
- A comparative study of smart nanoformulations of diethyldithiocarbamate with CuScientific reports · 2023Article
- Anticancer Analysis of CD44 Targeted Cyclosporine Loaded Thiolated Chitosan Nanoformulations for Sustained Release in Triple-Negative Breast Cancer.International journal of nanomedicine · 2023Article
- Targeting cancer stem cell plasticity in triple-negative breast cancer.Exploration of targeted anti-tumor therapy · 2023Review
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.
Funding
Abstract
Cancer has long been viewed as a disease of altered metabolism. Although it has long been recognized that the majority of cancer cells display increased dependence on glycolysis, the metabolism of "cancer stem-like cells" (CSCs) that drive tumor growth and metastasis is less well characterized. In this chapter, we review the current state of knowledge of CSC metabolism with an emphasis on the development of therapeutic strategies to exploit the metabolic vulnerabilities of these cells. We outline emerging evidence indicating distinct metabolic pathways active in the proliferative, epithelial- (E) and quiescent, mesenchymal-like (M) CSC states in triple negative breast cancer. These CSC states are characterized by their different redox potentials and divergent sensitivities to inhibitors of glycolysis and redox metabolism. We highlight the roles of two redox-regulated signaling pathways, hypoxia-inducible factor 1α and nuclear factor erythroid 2-related factor 2, in regulating CSC epithelial-mesenchymal plasticity during metabolic and/or oxidative stress, and discuss clinical strategies using combinations of pro-oxidant-based therapeutics simultaneously targeting E- and M-like CSCs. By specifically targeting CSCs of both states, these strategies have the potential to increase the therapeutic efficacy of traditional chemotherapy and radiation therapy.
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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.