2.4 Chemically induced tumors
The chemical carcinogen-induced tumours originate from the host’s own cells, therefore closer than other transplantable neoplasms, closer to the human clinical tumours. The potential effects of the carcinogen on tumour physiology, as well as the risks to other animals and persons posed by the carcinogen and its metabolites released in the chemically induced animal’s faeces and urine, are all the boundaries of chemically produced tumours. There are two types of chemical carcinogens:(Homburger et al., 1962)
i. Direct acting agents—carcinogenicity is induced without the need for a chemical transition.
ii. Indirect acting agents—agents that only become active after undergoing metabolic conversion. Procarcinogens are another name for them, and ultimate carcinogens are the active end products.
When electron-rich atoms in RNA, DNA, and cellular proteins interact with electrophiles (atoms lacking an electron), both ultimate and direct carcinogens are created. Although TP53 and RAS gene mutations have traditionally been the main targets, chemical carcinogens can affect any gene. For instance, DMBA and DMAB both caused colon and breast cancer in rats. Mice developed fibrosarcomas after exposure to 3,4,9,10 dibenzopyrene, spindle cell sarcomas after exposure to 3,4 benzopyrene, and leukaemia and sarcomas after exposure to 20-methylcholanthrene.