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Mechanisms of human carcinogens
1Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.
Progress in Clinical and Biological Research
|January 1, 1992
Summary
Human carcinogens cause cancer through genetic mutations and epigenetic changes. Both DNA-damaging and non-DNA-damaging agents alter gene expression and cell proliferation, contributing to multistep carcinogenesis.
Area of Science:
- Toxicology
- Molecular Biology
- Cancer Research
Background:
- Carcinogens induce genetic mutations by altering DNA.
- Some carcinogens, like hormones and asbestos, lack direct DNA interaction but cause genetic effects.
- Non-genotoxic carcinogens often operate through epigenetic mechanisms.
Purpose of the Study:
- To explore the diverse mechanisms of human carcinogen activity.
- To investigate the roles of both genetic and epigenetic processes in carcinogenesis.
- To understand how carcinogens influence gene expression and cell proliferation.
Main Methods:
- Review of existing literature on carcinogen mechanisms.
- Analysis of in vitro assays for chromosomal mutations.
- Examination of evidence for epigenetic effects of carcinogens.
Main Results:
- Many carcinogens are electrophilic or metabolically activated to DNA-reactive molecules.
- Non-DNA-reactive carcinogens can induce genetic effects via epigenetic pathways.
- Both genotoxic and non-genotoxic carcinogens modulate gene expression and cell proliferation.
Conclusions:
- Carcinogen mechanisms involve both genetic mutations and epigenetic alterations.
- Epigenetic effects, including altered gene expression and cell proliferation, are crucial in multistep carcinogenesis.
- Understanding these dual mechanisms is key to comprehending human cancer development.