Reactive oxygen species in cancer cells: live by the sword, die by the sword.

By P. Schumacker. Cancer Cell, 2006

1,245 citations recorded by the source corpus.

Reactive oxygen species and tumor biology are intertwined in a complex web, making it difficult to understand which came first, whether oxidants are required for tumor cell growth, and whether oxidant stress can be exploited therapeutically. Evidence suggests that transformed cells use ROS signals to drive proliferation and other events required for tumor progression. This confers a state of increased basal oxidative stress, making them vulnerable to chemotherapeutic agents that further augment ROS generation or that weaken antioxidant defenses of the cell. In this respect, it appears that tumor cells may die by the same systems they require.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e7c0887be1bb35dcd01433c02a6469a39f5cde74

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. Peng Huang
4. M. Sporn
5. G. Barrera
6. D. Trachootham

In Molecular Biology

1. Yongqiang Chen
2. S. Gibson
3. D. Trachootham
4. Peng Huang
5. J. Alexandre
6. M. Sporn
7. K. Liby
8. G. Barrera

Citations in the corpus

• Oxidative stress induces autophagic cell death independent of apoptosis in transformed and cancer cells (2008, background): “Indeed, ROS have many effects on cells including DNA damage, mitochondrial dysfunction, activation of signaling pathways and activation of transcription factors leading to upregulation of genes.(17) We have demonstrated that ROS induced beclin-1 expression and beclin-1 is required for ROSinduced aut”
• Upsides and Downsides of Reactive Oxygen Species for Cancer: The Roles of Reactive Oxygen Species in Tumorigenesis, Prevention, and Therapy (2012, neutral): “On the other hand, normal cells appear to have, under lower basal stress and reserve, a higher capacity to cope with additional ROS-generating insults than cancer cells do (271, 300).”
• Triterpenoids and rexinoids as multifunctional agents for the prevention and treatment of cancer (2007, background): “In malignant cells that are already oxidatively stressed, the addition of a drug that further increases the production of ROS can kill the malignant cel”
• Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling (2018, neutral): “Tumor cells often display enhanced intracellular ROS levels (Schumacker, 2006; Sabharwal and Schumacker, 2014).”
• Oxidative Stress and Lipid Peroxidation Products in Cancer Progression and Therapy (2012, background): “Therefore, manipulating ROS levels by redox modulation is a way to selectively kill cancer cells without causing significant toxicity to normal cells [110].”
• Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach? (2009, background): “Therefore, manipulating ROS levels by redox modulation is a way to selectively kill cancer cells without causing significant toxicity to normal cell”