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.