Chemically-Induced DNA Damage, Mutagenesis, and Cancer

© 2019 by the authors; CC BY license

supercritical-carbon dioxide fluid of C. indicum (CI_SCFE); BLM; anti-tumor effect; pulmonary fibrosis; synergism effect; hexavalent chromium Cr(VI); coenzyme Q10; reactive oxygen species (ROS); mitochondrial membrane potential (MMP); L-02 hepatocytes; apoptosis; chemical genotoxic agents; p53 signaling; p21^WAF1 (CDKN1A); DNAJB9; multinucleated giant cells; premature senescence; apoptosis; mutational processes; magnetic therapy; nanotoxicity; M1dG; 8-oxodG; human hepatocarcinoma cells; VPA; DNA double-strand breaks; radiosensitivity; DNA repair; U2OS; chemical carcinogen (DMBA)-induced tumor; engineered nanomaterials; DNA damage; nanotoxicity; DNA repair proteins/genes; DNA repair pathways; PrimPol; replication; DNA damage; mitochondria; oxoguanine glycosylase 1 (Ogg1); 8-hydroxy-2′-deoxyguanosine; DNA repair; multiorgan carcinogenesis bioassay; DNA adducts; DNA adductomics; DNA damage; genotoxicity; chemical carcinogenesis; high resolution accurate mass (HRAM) mass spectrometry; constant neutral loss; apoptosis; apoptotic microtubule network; microtubules; actin filaments; genotoxic drugs; Resveratrol; cancer; molecular targets; apoptosis; chemoprevention; therapy; DNA repair; alkylation damage; conformational changes; protein structure; protein stability; protein-tag; melanoma; reactive oxygen species; ROS; NADPH oxidase; single nucleotide polymorphisms; SNP; superoxide dismutase; SOD2; SOD3; RAC1; NOTCH signaling; HNSCC; overall survival; carcinogenesis; carcinogen; mutagen; metabolism; DNA adduct; tumor; chronic exposure; somatic mutation; n/a