ReviewCancers2020
Insights into the New Cancer Therapy through Redox Homeostasis and Metabolic Shifts.
Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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
27 citing papers in PubMed, 49 citations in OpenAlex.
- Deciphering autophagy-metabolism interactions in cancer drug resistance: a comprehensive review.Cancer chemotherapy and pharmacology · 2026Review
- Redox processes in the treatment of advanced skin cancers.Clinical & experimental metastasis · 2026Review
- Redox Homeostasis as a Therapeutic Target in Chronic Oxidative Diseases: Implications for Cancer Treatment.Antioxidants (Basel, Switzerland) · 2026Review
- Whey Protein Mitigates Oxidative Stress Injury and Improves Protein Synthesis in Mouse Skeletal Muscle by Regulating the SIRT1/Nrf2/HO-1 Axis and AMPK/TSC2/mTOR/4EBP1 Pathway.Journal of food science · 2025Article
- Chronic Psychological Stress Activates TRP/TAM/CXCL1 Signaling to Promote Breast Cancer Adipocyte Lipolysis via KEAP1 mResearch (Washington, D.C.) · 2025Article
- Harnessing the interaction between redox signaling and senescence to restrain tumor drug resistance.Frontiers in cell and developmental biology · 2025Review
- P53 Regulation upon Lipid Peroxidation and Ferroptosis for Intervention against Atherogenesis.Current medicinal chemistry · 2025Review
- ACSL3 regulates breast cancer progressionCancer biology & medicine · 2024Article
- The regulatory roles and clinical significance of glycolysis in tumor.Cancer communications (London, England) · 2024Review
- The role and mechanism of cinnamaldehyde in cancer.Journal of food and drug analysis · 2024Review
- Transcriptomic analysis reveals the crosstalk between type 2 diabetes and chronic pancreatitis.Health science reports · 2024Article
- Research Progress of Disulfide Bond Based Tumor Microenvironment Targeted Drug Delivery System.International journal of nanomedicine · 2024Review
- Review
- PTMA binds to HMGB1 to regulate mitochondrial oxidative phosphorylation and thus affect the malignant progression of esophageal squamous cell carcinoma.Journal of thoracic disease · 2023Article
- Pan-cancer and single-cell analysis reveal the prognostic value and immune response of NQO1.Frontiers in cell and developmental biology · 2023Article
- ROS regulation in gliomas: implications for treatment strategies.Frontiers in immunology · 2023Review
- Targeting Glucose Metabolism Enzymes in Cancer Treatment: Current and Emerging Strategies.Cancers · 2022Review
- Metabolic Reprogramming in Hematologic Malignancies: Advances and Clinical Perspectives.Cancer research · 2022Review
- Article
- Synergic effect of anticancer peptide CIGB-552 and Cisplatin in lung cancer models.Molecular biology reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Modest levels of reactive oxygen species (ROS) are necessary for intracellular signaling, cell division, and enzyme activation. These ROS are later eliminated by the body's antioxidant defense system. High amounts of ROS cause carcinogenesis by altering the signaling pathways associated with metabolism, proliferation, metastasis, and cell survival. Cancer cells exhibit enhanced ATP production and high ROS levels, which allow them to maintain elevated proliferation through metabolic reprograming. In order to prevent further ROS generation, cancer cells rely on more glycolysis to produce ATP and on the pentose phosphate pathway to provide NADPH. Pro-oxidant therapy can induce more ROS generation beyond the physiologic thresholds in cancer cells. Alternatively, antioxidant therapy can protect normal cells by activating cell survival signaling cascades, such as the nuclear factor erythroid 2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) pathway, in response to radio- and chemotherapeutic drugs. Nrf2 is a key regulator that protects cells from oxidative stress. Under normal conditions, Nrf2 is tightly bound to Keap1 and is ubiquitinated and degraded by the proteasome. However, under oxidative stress, or when treated with Nrf2 activators, Nrf2 is liberated from the Nrf2-Keap1 complex, translocated into the nucleus, and bound to the antioxidant response element in association with other factors. This cascade results in the expression of detoxifying enzymes, including NADH-quinone oxidoreductase 1 (NQO1) and heme oxygenase 1. NQO1 and cytochrome b5 reductase can neutralize ROS in the plasma membrane and induce a high NAD
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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.