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.
Inhibitory effects of Nigella sativa and saffron (Crocus sativus) on chemical carcinogenesis
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.
The role of glutathione and glutathione S-transferase in chemical carcinogenesis
A multihit, multistage model of chemical carcinogenesis
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?