p-Benzoquinone initiates non-invasive urothelial cancer through aberrant tyrosine phosphorylation of EGFR, MAP kinase activation and cell cycle deregulation: Prevention by vitamin C

DOI: 10.1016/j.toxrep.2017.06.005

Keywords: Bax, BCL2-associated X protein, Bcl-2, B-cell lymphoma 2, CS, cigarette smoke, DNPH, 2 4-dinitrophenylhydrazine, GAPDH, glyceraldehyde 3-phosphate dehydrogenase, IARC, International Agency for Research on Cancer, p-BQ, p-benzoquinone, p-BSQ, p-benzosemiquinone, PAHs, polycyclic aromatic hydrocarbons, PBS, phosphate buffered saline, ROS, reactive oxygen species, SDS PAGE, sodium dodecyl sulfate polyacrylamide gel electrophoresis, TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labelling, WHO, World Health Organization, UC, urothelial carcinoma, CIS, carcinoma in situ, EGFR, epidermal growth factor receptor, MAPK, mitogen activated protein kinase p-Benzoquinone, Carcinoma in situ, Dysplasia, Aberrant EGFR activation, Cell cycle deregulation, Vitamin C

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