The DOI matches its Crossref record; 406 of the 406 references it cites were found in a registry or an index.
Redox-Directed Cancer Therapeutics: Molecular Mechanisms and Opportunities
Open accessAbstract
Redox dysregulation originating from metabolic alterations and dependence on mitogenic and survival signaling through reactive oxygen species represents a specific vulnerability of malignant cells that can be selectively targeted by redox chemotherapeutics. This review will present an update on drug discovery, target identification, and mechanisms of action of experimental redox chemotherapeutics with a focus on pro- and antioxidant redox modulators now in advanced phases of preclinal and clinical development. Recent research indicates that numerous oncogenes and tumor suppressor genes exert their functions in part through redox mechanisms amenable to pharmacological intervention by redox chemotherapeutics. The pleiotropic action of many redox chemotherapeutics that involves simultaneous modulation of multiple redox sensitive targets can overcome cancer cell drug resistance originating from redundancy of oncogenic signaling and rapid mutation.Moreover, some redox chemotherapeutics may function according to the concept of synthetic lethality (i.e., drug cytotoxicity is confined to cancer cells that display loss of function mutations in tumor suppressor genes or upregulation of oncogene expression). The impressive number of ongoing clinical trials that examine therapeutic performance of novel redox drugs in cancer patients demonstrates that redox chemotherapy has made the crucial transition from bench to bedside.
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“current pro-oxidant strategies often cause serious collateral damage, resulting in a narrow therapeutic window20”
From Targeting cancer vulnerabilities with high-dose vitamin C (2019) · cites this paper as [20]
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Sorted by citations
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Targeting cancer vulnerabilities with high-dose vitamin C
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Metadata
- Authors
- Wondrak, G. T.
- Affiliations
- University of Arizona (US)
- Corresponding author
- Wondrak, Georg T.
- ORCID
- Wondrak, Georg T.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2009-12
- Volume
- 11
- Issue
- 12
- Pages
- 3013-3069
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- PMC
- PMC2824519
- OpenAlex
- W2000718634
- Cited by
- 462
- References
- 406
- Citations by year
- 2026: 7 · 2025: 24 · 2024: 16 · 2023: 18 · 2022: 18 · 2021: 23 · 2020: 25 · 2019: 29 · 2018: 26 · 2017: 35 · 2016: 44 · 2015: 42 · 2014: 40 · 2013: 33 · 2012: 34
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antioxidants and Redox Signaling (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Arizona Cancer Center (CA023074)
- Servier
- National Institutes of Health (CA023074, ES 06694)
- National Cancer Institute (R01CA122484, CA-023074, P30CA023074)
- National Institute of Environmental Health Sciences (ES 06694, P30ES006694)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Keywords
- reactive oxygen species, redox dysregulation, cancer cell vulnerability, oncogene function, tumor suppressor, chemoresistance, synthetic lethality, redox signaling, drug discovery, clinical trials
- MeSH terms
- Antineoplastic Agents, Humans, Neoplasms, Oxidation-Reduction
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