Molecular epidemiology of human cancer risk. Gene-environment interactions and p53 mutation spectrum in human lung cancer.
Molecular epidemiology of cancer risk utilizes knowledge of both the genetic changes in cancer and the current hypothesis of chemical carcinogenesis when selecting possible markers for individual susceptibility, early disease, and biologically significant exposure. Polymorphisms of drug-metabolizing enzymes, especially CYP enzymes, and mutations in the p53 tumor-suppressor gene have been in the center of interest for the past decade. Both have shown promise, CYP polymorphisms as markers for individual susceptibility and p53 mutation spectrum at population level for specific exposure. However, it is probable that very few markers, if any, are sufficient alone. Future challenges for molecular epidemiology in the lung cancer field include pursuing ethically the best performance in applying that knowledge, in addition to the development of reliable and well-validated markers.
Vähäkangas
Kirsi
K
Department of Pharmacology and Toxicology, University of Kuopio, Finland.
D014408:Biomarkers, Tumor / Q000235:genetics*; D004777:Environment; D052138:Genes, Neoplasm / Q000235:genetics*; D006801:Humans; D008175:Lung Neoplasms / Q000453:epidemiology* / Q000235:genetics; D017720:Molecular Epidemiology; D009154:Mutation; D012307:Risk Factors; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
D014408:Biomarkers, Tumor; D016159:Tumor Suppressor Protein p53