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The effect of environmental chemicals on the tumor microenvironment Público Deposited

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https://ir.library.oregonstate.edu/concern/articles/xs55md79g

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  • Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex interaction among blood vessels that feed the tumor, the extracellular matrix that provides structural and biochemical support, signaling molecules that send messages and soluble factors such as cytokines. The tumor microenvironment also consists of many host cellular effectors including multipotent stromal cells/mesenchymal stem cells, fibroblasts, endothelial cell precursors, antigen-presenting cells, lymphocytes and innate immune cells. Carcinogens can influence the tumor microenvironment through effects on epithelial cells, the most common origin of cancer, as well as on stromal cells, extracellular matrix components and immune cells. Here, we review how environmental exposures can perturb the tumor microenvironment. We suggest a role for disrupting chemicals such as nickel chloride, Bisphenol A, butyltins, methylmercury and paraquat as well as more traditional carcinogens, such as radiation, and pharmaceuticals, such as diabetes medications, in the disruption of the tumor microenvironment. Further studies interrogating the role of chemicals and their mixtures in dose-dependent effects on the tumor microenvironment could have important general mechanistic implications for the etiology and prevention of tumorigenesis.
  • 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/. The publisher and the author(s) have made this article open access.
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  • Casey, S. C., Vaccari, M., Al-Mulla, F., Al-Temaimi, R., Amedei, A., Barcellos-Hoff, M. H., ... & Felsher, D. W. (2015). The effect of environmental chemicals on the tumor microenvironment. Carcinogenesis, 36(Suppl 1), S160-S183. doi:10.1093/carcin/bgv035
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  • 36
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  • Supp. 1
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  • The authors would like to acknowledge the NIH National Institute of Environmental Health Sciences (R01ES017452) and travel grant support. The authors also acknowledge Fondazione Cariplo (2011-0370 to C.M.), Kuwait Institute for the Advancement of Sciences (2011-1302-06 to F.Al-M.), Grant University Scheme (RUGs) Ministry of Education Malaysia (04-02-12-2099RU to R.A.H.), Italian Ministry of University and Research (2009FZZ4XM_002 to A.A.), the University of Florence (ex60%2012 to A.A.), US Public Health Service Grants (RO1 CA92306, RO1 CA92306-S1, RO1 CA113447 to R.R.), Department of Science and Technology, Government of India (SR/FT/LS-063/2008 to N.S.), a grant from the National Cancer Institute (R01CA552679 to S.R.), the Miguel Servet Program (CP10/00656 to L.S.), the Italian Association for Cancer Research (IG 14640 to E.L.), the RAS (Sardinian Regional Government to E.L.) and grants from the National Institute of Environmental Health Sciences (T32ES007015 to C.C. and P30 ES000210 to W.H.B.). P.H. acknowledges the Charles University in Prague projects (UNCE 204015 and PRVOUK P31/2012), by the Czech Science Foundation project (P301/12/1686) and by the Internal Grant Agency of the Ministry of Health of the Czech Republic project (NT13663-3/2012). P.K.K. thanks the Center for Environment and Water, Research Institute, KFUPM for research facilities and King Abdulaziz City for Science and Technology for funding no. T.K. 11-0629. V.M.-S. and M.C. thank Canceropôle Rhone-Auvergne (CLARA), La Ligue Nationale Contre le Cancer (Ain, Rhône) and INCA, ANR (ANR-10-LABX-0061 and 2011 ANR-CESA-018-04) and Region Rhône-Alpes (CMIRA-COOPERA-12-004945-01) grants. D.W.F. acknowledges support from the National Cancer Institute (R01CA17037801, R01CA89305, R01CA105102, P50CA114747, P01CA034233, U56CA112973) and the Leukemia and Lymphoma Society (R6223-07). S.C.C. is currently supported by National Cancer Institute (F32CA177139), and D.C.K. is supported by National Cancer Institute (T32CA09151) and a Postdoctoral Enrichment Award from the Burroughs Wellcome fund.
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