ROS stress in cancer cells and therapeutic implications.

By H. Pelicano, D. Carney, Peng Huang. Drug resistance updates, 2004

1,967 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/b72b5db2350bba90d43ef1f15f3920be99113f96

How researchers see this paper

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

In Cancer Research

1. Yongqiang Chen
2. S. Gibson
3. M. Azad
4. H. Pelicano
5. Peng Huang
6. G. Barrera
7. D. Trachootham

In Molecular Biology

1. Yongqiang Chen
2. S. Gibson
3. M. Azad
4. H. Pelicano
5. D. Trachootham
6. Peng Huang
7. J. Alexandre
8. G. Barrera

In Nutrition and Dietetics

1. Yongqiang Chen
2. S. Gibson
3. M. Azad
4. J. Kong

Citations in the corpus

• Regulation of reactive oxygen species generation in cell signaling (2011, neutral): “1989; Miyajima et al., 1997; Pelicano et al., 2003; 2004; Tan et al., 1998).”
• Redox Regulation of Cell Survival (2008, neutral): “89 and 239).”
• Oxidative stress is inherent in prostate cancer cells and is required for aggressive phenotype. (2008, background): “Inherent oxidative stress may affect several functions in cancer cells or tumor tissue, such as cell proliferation, promotion of mutations and genetic instability, alterations in cellular sensitivity to anticancer agents, invasion, and metastasis (7, 9).”
• Oxidative stress induces autophagic cell death independent of apoptosis in transformed and cancer cells (2008, background): “Cancer cells produce higher levels of ROS than normal cells, and this contributes to cancer progression.(14,17,18) Trachootham et al.”
• Inhibition of glycolysis in cancer cells: a novel strategy to overcome drug resistance associated with mitochondrial respiratory defect and hypoxia. (2005, background): “The constant generation of reactive oxygen species within the mitochondria and the increased free radical stress in cancer cells may cause further damage to both mtDNA and the electron transport chain, thus amplifying respiratory malfunctions and dependency on glycolysis (7).”
• Oxidative Stress and Lipid Peroxidation Products in Cancer Progression and Therapy (2012, background): “However, excessive levels of ROS stress can also be toxic to the cells: cancer cells with increased oxidative stress are likely to be more vulnerable to damage by further ROS insults induced by exogenous agents [109].”
• Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach? (2009, background): “However, as excessive levels of ROS stress can also be toxic to the cells, cancer cells with increased oxidative stress are likely to be more vulnerable to damage by further ROS insults induced by exogenous agent”
• Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for Cancer Progression and Treatment (2009, positive): “Cancer cells, both in vivo and in vitro , characteristically have higher ROS levels compared with normal cells (87) (Fig.”