Mutagenesis, apoptosis, basic relation to carcinogenic models.
Cancer arises from an accumulation of mutations as well as changes in the expression pattern of genes mainly involved in cell cycle regulation, DNA repair and apoptosis, which promote clonal selection of cells with an increasingly malignant phenotype. Although a single mutant gene may not be able to redirect the growth program of a normal cell, the multiplicity of downstream targets of a deregulated molecule and the extensive cross-talk between biochemical pathways suggest that cellular context and genotype are of great importance in cancer initiation, while gene activation and inactivation events may not be independent. Complex exposure patterns affecting molecular targets exhibiting multiple intracellular interactions add a significant percentage of uncertainty when assessing cancer risk.
Voutsinas
G
G
Institute of Biology, NCSR, Demokritos, Athens, Greece. mvoutsin@mail.demokritos.gr
D017209:Apoptosis / Q000187:drug effects*; D004249:DNA Damage; D006801:Humans; D009153:Mutagens / Q000009:adverse effects*; D009369:Neoplasms / Q000453:epidemiology* / Q000235:genetics / Q000473:pathology; D011336:Probability; D018570:Risk Assessment
D009153:Mutagens