Journal Article

Environmental factors as regulators and effectors of multistep carcinogenesis

Toshinari Minamoto, Masayoshi Mai and Ze'ev Ronai

in Carcinogenesis

Volume 20, issue 4, pages 519-527
Published in print April 1999 | ISSN: 0143-3334
Published online April 1999 | e-ISSN: 1460-2180 | DOI: https://dx.doi.org/10.1093/carcin/20.4.519
Environmental factors as regulators and effectors of multistep carcinogenesis

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This review highlights current knowledge of environmental factors in carcinogenesis and their cellular targets. The hypothesis that environmental factors influence carcinogenesis is widely supported by both epidemiological and experimental studies. The fact that only a small fraction of cancers can be attributed to germline mutations in cancer-related genes further buttresses the importance of environmental factors in carcinogenesis. Furthermore, penetrance of germline mutations may be modified by either environmental or other genetic factors. Examples of environmental factors that have been associated with increased cancer risk in the human population include chemical and physical mutagens (e.g. cigarette smoke, heterocyclic amines, asbestos and UV irradiation), infection by certain viral or bacterial pathogens, and dietary non-genotoxic constituents (e.g. macro- and micronutrients). Among molecular targets of environmental influences on carcinogenesis are somatic mutation (genetic change) and aberrant DNA methylation (epigenetic change) at the genomic level and post-translational modifications at the protein level. At both levels, changes elicited affect either the stability or the activity of key regulatory proteins, including oncoproteins and tumor suppressor proteins. Together, via multiple genetic and epigenetic lesions, environmental factors modulate important changes in the pathway of cellular carcinogenesis.

Keywords: CREB, cyclic AMP response element binding protein; EGFR, epidermal growth factor receptor; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HPV, human papilloma virus; IGFR, insulin-like growth factor receptor; MAPK, mitogen activated protein kinase; NO, nitric oxide; PKA, protein kinase A; PKC, protein kinase C; ROS, reactive oxygen species; TFIIH, transcription factor IIH; TPA, 12-O-tetradecanoylphorbol-13-acetate.

Journal Article.  7832 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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