Radical causes of cancer

By S. Hussain, L. Hofseth, C. Harris. Nature Reviews. Cancer, 2003

1,717 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/204e70ad6e7a5c0376290ae5b500babd382105a4

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Citations in the corpus

Oxidative Stress, Mitochondrial Dysfunction, and Aging (2011, neutral): “hyperoxia, toxins, and transition metals [16–26].”
TP53 mutations and hepatocellular carcinoma: insights into the etiology and pathogenesis of liver cancer (2007, background): “Chronic inflammation and infection is frequently associated with increased cancer risk, although exceptions can be cited, including rheumatoid arthritis and human papillomavirus infection (Table 3; Hussain et al., 2003).”
Immunity, Inflammation, and Cancer (2010, neutral): “It has therefore been debated whether immune-mediated mechanisms as opposed to dietary and environmental mutagens are the critical driving forces behind tumor initiation (Hussain et al., 2003).”
Inflammation and cancer IV. Colorectal cancer in inflammatory bowel disease: the role of inflammation. (2004, background): “Indeed, IBD is considered one of the main “oxyradical overload” diseases whereby chronic inflammation, be it inherited or acquired, results in a cancer-prone phenotype (44).”
Inflammation and Cancer: Triggers, Mechanisms and Consequences (2019, background): “Indeed, chronic intestinal inflammation leads to accumulation of mutations in Tp53 and other cancer related genes in intestinal epithelial cells (Canli et al., 2017; Chang et al., 2007; Hussain et al., 2003; Robles et al., 2016) and can trigger tumor formation even without additional extrinsic mutag”
On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death (2017, neutral): “5,6 However, only recently has the accumulation of LOOH been directly related to a speci ﬁ c cell death pathway, coined ferroptosis.”
The potential effects of chlorogenic acid, the main phenolic components in coffee, on health: a comprehensive review of the literature (2017, background): “Cancers and CGA Early in-vitro observations suggest that cellular damage caused by reactive oxygen species (ROS) is related to the incidence of a number of diseases, including coronary heart disease, diabetes and cancers [102, 103].”
Therapeutic targeting of the tumor microenvironment. (2005, neutral): “This class of inflammatory cells can also enhance the genomic instability of the tumor through the production of reactive oxygen and nitrogen species, which can form peroxynitrate, a DNA-damaging agent (Maeda and Akaike, 1998; reviewed in Hussain et al., 2003).”
Inflammation and cancer: An ancient link with novel potentials (2007, background): “the field of cancer biology because of its proneoplastic and antineoplastic functions.(3,21) These antagonistic functions of NO are primarily governed by the quantity of NO , cell type, redox status and the inflammatory microenvironment.”
Regulation of Ferroptotic Cancer Cell Death by GPX4 (2014, background): “, 1997), are under high levels of oxidative stress (Szatrowski and Nathan, 1991), which therefore needs to be counteracted by increasing the ROS-scavenging capacity, to prevent oxidative damage (Hussain et al., 2003).”