Chemical Carcinogenesis

Abstract

Overview Human exposure to chemical carcinogens can result in cancer. What dictates this outcome is relatively predictable but highly variable. Factors governing the outcome include type of exposure, amount of exposure, time of exposure, and genetic makeup of the host (i.e., humans). The latter is comprised of variations in single nucleotides within genes (e.g., single nucleotide polymorphisms in deoxyribonucleic acid–repair genes), as well as the metabolomic, proteomic, microbiomic, transcriptomic, and epigenomic background of the individual. It is becoming increasingly clear that these endpoints can be modified by chemical carcinogens and that inflammatory load influences outcome. To this end, the past decade has seen an explosion of extremely sensitive and highly accurate technology. Linking this technology to the rapid development of bioinformatics has enabled us to begin merging the totality of lifetime exposure (exposome) with the totality of metabolomic, proteomic, microbiomic, transcriptomic, epigenomic, and other “omic” profiles. We feel optimistic that the next decade will bring the development of tools to identify an individual's weighted risk signature as a biomarker for cancer risk and develop a personalized and precise approach to cancer chemoprevention and treatment.