Chemical-induced Carcinogenesis

Historically, evidence of chemical carcinogenesis has played a significant role in verifying conclusions draw from epidemiological studies. Chemical agents that were suspected to have a certain role in human chronic diseases, such as cancers, have been tested in animals to establish firmly a causative risk or link to risk. The three best examples are: (1) tobacco smoke and lung cancer; (2) asbestos and mesothelioma; and (3) aflatoxin and hepatic cancer. New chemical compounds are synthesized every day, and a number of natural or synthetic compounds are incorporated in foods either as a result of their processing or to preserve or enhance them. Chemical carcinogenesis studies using model animals have greatly contributed to understanding the mechanisms underlying the development and prevention of carcinogenesis. The carcinogenesis process is generally considered to include three steps: initiation, promotion, and progression. Each step is characterized by morphological and biochemical alterations resulting from genetic and epigenetic changes, including mutations in proto-oncogenes and tumor suppressor genes that control proliferation, cell death, and cellular repair. Long-term in vivo assays using laboratory animals enable the identification of carcinogenic compounds and their modes of action. Based on these findings, we should be able to establish effective strategies to treat and prevent malignancies resulting from exposure to potentially carcinogenic chemicals.