Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?

By D. Trachootham, J. Alexandre, Peng Huang. Nature reviews. Drug discovery, 2009

5,133 citations recorded by the source corpus.

Subfields: Molecular Biology, Organic Chemistry

View Paper: https://www.semanticscholar.org/paper/2141fcfe719cd89baf34f8881fa06656db8dfa0e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Hayes
2. K. Jomová
3. Geou-Yarh Liou
4. M. Valko
5. Ming Tan
6. I. Harris
7. Michael T. McMahon
8. A. Cuadrado

In Organic Chemistry

1. K. Jomová
2. Geou-Yarh Liou
3. M. Valko
4. David B. Graves

Citations in the corpus

• An Integrated Metabolic Atlas of Clear Cell Renal Cell Carcinoma (2016, neutral): “…was not only associated with poor clinical outcome but also enriched in somatic alterations of central redox regulators KEAP1 and NRF2 (Jaramillo and Zhang, 2013), supporting the proposed roles of reactive oxygen species (ROS) and altered redox state in certain cancers (Trachootham et al., 2009).”
• PGC1α Expression Defines a Subset of Human Melanoma Tumors with Increased Mitochondrial Capacity and Resistance to Oxidative Stress (2013, neutral): “On the other hand, above a certain threshold, ROS can be toxic and induce cellular damage, leading to cell death (Trachootham et al., 2009; Diehn et al., 2009).”
• CD44 variant regulates redox status in cancer cells by stabilizing the xCT subunit of system xc(-) and thereby promotes tumor growth. (2011, background): “High levels of GSH as well as increased expression of antioxidant enzymes promote cancer cell survival and resistance to anticancer agents (Trachootham et al., 2009).”
• Reactive oxygen species in cancer (2010, background): “However, it is possible that a threshold of toxicity in these cancer cells is not reached and that the additional increase in ROS further causes more mutations or drives cell migration and invasion [221, 273].”
• Regulation of cancer cell metabolism (2011, background): “In the absence of the redox maintenance pathway that is supported by these tumour suppressors, malignant cells might be selectively kille”
• Antimicrobial strategies centered around reactive oxygen species--bactericidal antibiotics, photodynamic therapy, and beyond. (2013, background): “…limited to atherosclerosis (Paravicini & Touyz, 2006), diabetes (Paravicini & Touyz, 2006), carcinogenesis, and tumor metastasis through gene activation (Ishikawa et al., 2008; Trachootham et al., 2009), neurodegeneration (Andersen, 2004; Shukla et al., 2011), and aging (Haigis & Yankner, 2010).”
• The Oxygen Rich Postnatal Environment Induces Cardiomyocyte Cell Cycle Arrest Through DNA Damage Response (2014, neutral): “In contrast, ROS-mediated senescence and cell-cycle exit is a well-recognized characteristic of stem cells (Takahashi et al., 2006; Trachootham et al., 2009).”
• The emerging role of reactive oxygen and nitrogen species in redox biology and some implications for plasma applications to medicine and biology (2012, background): “Figure 27 (following Trachootham et al [139]), illustrates the basic idea.”
• BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells (2013, background): “This notion has provided the impetus to explore redox modulation as a therapeutic target in cancer, with the rationale that pro-oxidants may eradicate tumor cells by pushing them beyond the limits of viability (Trachootham et al., 2009).”