Chemical Carcinogenesis: From Animal Models To Molecular Models In One Decade
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2018, Studies in Natural Products ChemistryCitation Excerpt :Next, in vivo assays imply the use of animal models, usually rodents, to monitor carcinogenesis inhibition. In contrast to chemical carcinogen-induced models used in the last decades [112], transgenic rodent models are used nowadays, since they were found more relevant to the better understanding of human carcinogenesis complexity [113]. One of the best examples is Apcmin mice, a mutant model affecting APC gene functionality, which induces intestinal adenomas and simulates, with high fidelity, physiopathological conditions associated with human colon carcinogenesis [114].
Bulky DNA Adducts, Tobacco Smoking, Genetic Susceptibility, and Lung Cancer Risk
2017, Advances in Clinical ChemistryCitation Excerpt :These are well-known carcinogens present in cigarette smoke and motor vehicle exhaust and fumes from industrial processes and residential heating [7–9]. Interest in the analysis of the bulky DNA adducts is derived from early experimental animal models that demonstrated that DNA damage is necessary but insufficient for cancer development [2,10,11]. At the beginning of the 21st century, most evidence supported the notion that exposure to environmental carcinogens [3,5,12–28], including cigarette smoke [1,3,5,29–35], resulted in alterations to the structural integrity of DNA, i.e., bulky DNA adducts and oxidative DNA damage [1,12,19,36–46].
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2014, Infection, Genetics and EvolutionCitation Excerpt :Neoplastic cells show impaired defence systems, as well as a lack of adhesion, spreading and phagocyte behaviour (Beckmann et al., 1992; Diaz et al., 2011). Basic underlying mechanisms of carcinogenesis are evolutionary conserved (Yuspa and Poirier, 1988) and highly conserved domains of neoplasia-related genes suggest that their functional roles may also be conserved (Ciocan and Rotchell, 2005). The molecular mechanisms of cancer are based on an uncontrolled cell growth and loss of cell’s ability to undergo apoptosis (Hanahan and Weinberg, 2000).
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2013, Journal of Experimental and Clinical Medicine(Taiwan)Citation Excerpt :When the tumor promoter disappears, regression of the tumor occurs, possibly through apoptosis mechanisms. Some tumor promoters are tissue-specific, but others act simultaneously on several different tissues.34 A long-term and/or high-dose exposure, a tumor promoter can sometimes induce preneoplasms and neoplasms even without initiation stimuli.11