Epigenetic carcinogens: Evaluation and risk assessment
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Global and region-specific post-transcriptional and post-translational modifications of bisphenol A in human prostate cancer cells
2019, Environmental PollutionCitation Excerpt :BPA exposure and action mechanisms associated with chronic diseases could be related to oxidative stress, mitochondrial dysfunctions, genotoxic effects, epigenetic modifications including alterations of cell signaling pathways (Kundakovic and Champagne, 2011; Rezg et al., 2014). Environmental chemicals have been linked to aberrant changes in epigenetic regulation in tumor have been gained considerable attention (Williams and Whysner, 1996; Klaunig et al., 2000; Esteller and Herman, 2002; Bombail et al., 2004; Fleisch et al., 2012; Pogribny and Beland, 2013; Greally ve Jacobs, 2013). BPA exposure could change cellular pathways through epigenetic mechanisms including global and gene-specific DNA methylation, histone modifications, miRNA regulations and also alterations on gene expression levels of chromatin modifying enzymes through in vitro and in vivo studies (Collett et al., 2006; Dolinoy et al., 2007; Avissar-Whiting et al., 2010; Doherty et al., 2010; Chao et al., 2012; Zhou et al., 2013; Singh and Li, 2012; Bhan et al., 2014; Faulk et al., 2015; Ho et al., 2015; Cheong et al., 2016; Hayes et al., 2016; Laing et al., 2016; Anderson et al., 2017; Chen et al., 2017; Kumar and Thakur, 2017; Prins et al., 2017; Desai et al., 2018; Gao et al., 2018; Neff et al., 2019).
An integrated approach for prospectively investigating a mode-of-action for rodent liver effects
2013, Toxicology and Applied PharmacologyCitation Excerpt :The induction of cytochrome P450 (Cyp) enzyme activity has long been associated with chemically-induced rodent hepatocarcinogenesis (Guengerich, 1988). An example of one such compound that induces tumors through a non-DNA-reactive mechanism involving liver hyperplasia is phenobarbital (PB) (Williams and Whysner, 1996). Rodents chronically treated with PB show activation of CAR as evidenced by elevation of associated gene transcripts (mainly Cyp2b), enzyme activity, hepatocellular proliferation, and eventually proliferative liver lesions (Wei et al., 2000; Yamamoto et al., 2004).
Guidelines and pharmacopoeial standards for pharmaceutical impurities: Overview and critical assessment
2012, Regulatory Toxicology and PharmacologyCitation Excerpt :TD50 of 2.65 mg/kg/day (an identical value being cited by Cheeseman et al.) shows that the compound has been treated as a strong carcinogen, more potent than many N-nitrosamines, in relation to the determination of the TTC. Simple linear extrapolation is inappropriate for the risk assessment of non-genotoxic compounds (which comprise the majority of the drug substances shown in Table 3, and there are many more in the Bassan et al. dataset) since such compounds are normally considered to be thresholded in relation to dose–response relationships (Williams and Whysner, 1996; EU Scientific Committees, 2009). A further consideration is that numerous structurally alerting compounds in the current CPDB reported as yielding “no positive test” are excluded from the TTC datasets; examples of these compounds, along with their Ames-test status, are shown in Table 4. (
Diagnostic Challenge
2012, Journal of Exotic Pet MedicineApplication of the DNA adductome approach to assess the DNA-damaging capability of in vitro micronucleus test-positive compounds
2011, Mutation Research - Genetic Toxicology and Environmental MutagenesisCitation Excerpt :Kirkland et al. demonstrated recently that the results from in vitro genotoxicity tests, especially the chromosome aberration assay and the micronucleus test in Chinese hamster cells and the mouse lymphoma tk locus assay, are highly discrepant from the results from rodent in vivo carcinogenicity tests [1]. Direct or indirect DNA reaction with a compound is an example of MOA, and should be first considered after a positive result is obtained in in vitro genotoxicity tests [2]. Direct DNA-reactive compounds are considered to have a non-effective threshold in the dose–response relationship in carcinogenesis; however, non-DNA-reactive (indirect) compounds have a threshold.
Chemicals with Carcinogenic Activity in Rodent Liver
2010, Comprehensive Toxicology, Second Edition