chemical carcinogenesis

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chemical carcinogenesis

The induction of malignancy by a known or putative chemical carcinogen, which can be occupational (e.g., aromatic amines, arsenic, benzene, cadmium, chromium ores, soots, tars, vinyl chloride), environmental (e.g., aflatoxin, asbestos, tobacco) or iatrogenic (e.g., alkylating agents, anabolic steroids, phenacetin).
Initiation of the carcinogenic cascade occurs when an electrophilically reactive chemical (initiator) or, more often, one or more of its metabolites interacts with DNA, and repair of the damaged DNA is unsuccessful; this is followed by a sequence of events known as tumour promotion.


production of cancer.

biological carcinogenesis
viruses and some parasites are capable of initiating neoplasia. See viral oncogenesis, Spirocercalupi.
chemical carcinogenesis
numerous chemicals have been identified as carcinogenic.
physical carcinogenesis
includes ultraviolet radiation, ionizing radiation and asbestos.
References in periodicals archive ?
Conflicting views on chemical carcinogenesis arising from the design and evaluation of rodent carcinogenicity studies.
They present the core concepts, skills, and methods to perform risk assessments, including the fundamentals of cancer biology, chemical carcinogenesis, hormesis, and experimental evidence of thresholds for genotoxic carcinogens; guidelines and regulations for in vitro and in vivo testing; and evaluation of toxicological data and its relevance to hazard evaluation and cancer risk estimation.
Topics include the comparative pathology of mammary gland cancers in domestic and wild animals, neoplasia in nonhuman primates, mouse models of breast cancer, comparison of genetically engineered mouse mammary cancer models and human breast cancer by expression profiling, genetically engineered rat models, chemical carcinogenesis of rat and mouse mammary glands, comparative genetics and genomes of rat models, toxicogenomic analyses of genetic susceptibility to mammary gland carcinogenesis in rodents and the applications for breast cancer, and the relationship between comparative medicine, "one medicine," and genomic pathology.
In various models of chemical carcinogenesis, carcinogen induces ODC activity and inhibitors of ODC suppress cancer development.
Next come chapters on tissue context as a determinant of the tumor-suppressive or oncogenic function of certain genes, cancer stem cells, pharmacogenomics and determination of therapeutic efficacy, chemical carcinogenesis, hormones and cancer, and viral oncogenesis.
In Chapter six the author missed a good opportunity to discuss biochemical principles in more detail such processes like mutagenesis, chemical carcinogenesis, teratogenesis and immunotoxicity, which are fundamental in toxicology.
Although assumed, proof of the direct emergence of epithelial CSCs from an NSC population is not available, and the identity of the cells that acquire the molecular lesions initiating chemical carcinogenesis remains undefined (Perez-Losada and Balmain 2003).
They were instead designed to assist epidemiologists in making inductive inferences about the causal relationship of observed associations or, in the language of chemical carcinogenesis, as an aid in addressing the question, "Does a chemical exposure cause cancer?