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Disruptive chemicals, senescence and immortality Public Deposited

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  • Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of prosurvival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of proapoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.
  • The publisher and the author(s) have made this article open access. This is the publisher’s final pdf. The published article is copyrighted by the author(s) and published by Oxford University Press. The published article can be found at: http://carcin.oxfordjournals.org/
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  • Carnero, A., Blanco-Aparicio, C., Kondoh, H., Lleonart, M. E., Martinez-Leal, J. F., Mondello, C., ... & Yasaei, H. (2015). Disruptive chemicals, senescence and immortality. Carcinogenesis, 36(Suppl 1), S19-S37. doi:10.1093/carcin/bgv029
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  • 36
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  • Supp. 1
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  • This research was supported by Yeungnam University research grants in 2014 to Hyun Ho Park. Po Sing Leung was supported by the Health and Medical Research Fund of Food and Health Bureau, Hong Kong Special Administrative Region, Ref. No: 10110021. Yon Rojanasakul was supported by NIH (R01-ES022968) and NSF (CBET-1434503). Rita Dornetshuber-Fleiss was supported by the Austrian Science Fund (FWF, project number T 451-B18) and the Johanna Mahlke, geb.-Obermann-Stiftung. Clement Yedjou was supported by National Institutes of Health (Grant No. NIMHDG12MD007581, Grant No. NIGMS- P20GM103476).
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