The contribution of endogenous sources of DNA damage to the multiple mutations in cancer.

By A. Jackson, Lawrence Loeb. Mutation research, 2001

642 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/d127f252d9149fae2260bfc24e1479e65e991c2a

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. Subash C. Gupta
2. P. Storz
3. Lawrence Loeb
4. Morgane Macheret
5. Bharat B. Aggarwal
6. Carol Prives
7. S. Hecht
8. T. Halazonetis

In Molecular Biology

1. Subash C. Gupta
2. A. Budanov
3. P. Storz
4. Bharat B. Aggarwal
5. Morgane Macheret
6. Constantinos Fiotakis
7. Lawrence Loeb
8. Carol Prives

In Pathology and Forensic Medicine

1. P. Storz
2. Lawrence Loeb

Citations in the corpus

• A mutator phenotype in cancer. (2001, background): “In vitro (42) and inEscherichia coli(43), damage to DNA containing repetitive sequences by oxygen-reactive species results in mutations within repeats.”
• DNA replication stress as a hallmark of cancer. (2015, background): “Reactive oxygen species (ROS)–induced genetic and epigenetic alterations in human carcinogenesis.”
• ROS, stress‐activated kinases and stress signaling in cancer (2002, background): “Oxidative stress can also induce DNA damage that leads to genomic instability, which may contribute to cancer progression (Jackson and Loeb, 2001).”
• Environmental and chemical carcinogenesis. (2004, background): “Similar changes, but at lower frequencies, have been reported in a variety of tumors that are not known to be associated with mutations or silencing in mismatch repair genes [56].”
• Reactive oxygen species in tumor progression. (2005, background): “Initial experiments on the role of ROS in tumor initiation revealed that ROS act as DNA-damaging agents, effectively increasing the mutation rate within cells and thus promoting oncogenic transformation (6).”
• Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species (2010, background): “High levels of ROS lead to formation of 8-hydroxy-2′-deoxyguanosine (8-OH-dG), the main source of oxidation-associated mutagenesis (25).”
• Upsides and Downsides of Reactive Oxygen Species for Cancer: The Roles of Reactive Oxygen Species in Tumorigenesis, Prevention, and Therapy (2012, neutral): “Evidence accumulated over the past several years has indicated an association between ROS and malignant transformation (141, 311, 318).”
• Oxidative stress, inflammation, and cancer: how are they linked? (2010, background): “effectively increasing the mutation rate within cells and thus promoting oncogenic transformation [159].”
• Role of oxidative stress and DNA damage in human carcinogenesis. (2011, background): “3Gy) contributing significantly in the accumulationof mutations in cells and tissues [5–7].”
• 8-hydroxy-2′ -deoxyguanosine (8-OHdG): A Critical Biomarker of Oxidative Stress and Carcinogenesis (2009, background): “The in vivo studies have to overcome the additional influence of inflammation, which increases the level of oxidative damage and contributes to the increase of progression to cancer (64, 70).”
• The antioxidant function of the p53 tumor suppressor (2005, background): “Indeed, endogenous ROS are the major source of DNA damag”
• Molecular biomarkers of oxidative stress in aquatic organisms in relation to toxic environmental pollutants. (2006, background): “…free radical of biological and toxicological importance, because of its potent oxidative potential and indiscriminate reactivity with cellular components, such as lipids of biological membranes, proteins of enzymes, and DNA (Stadtman and Levine, 2000; Richter, 1987; Jackson and Loeb, 2001).”