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Summary Oncology first year researchmaster medical biology Radboud university
Chemical carcinogenesis The Hallmarks of Cancer + therapeutic targeting
Sustaining proliferative signaling EGFR inhibitors evading growth suppressors cyclin-dependent kinase inhibitors avoiding immune destruction immune activating anti-CTLA4 mAb enabling replicative immortality telomerase inhibitors tumor promoting inflammations selective anti inflammatory drugs activating invasion & metastasis inhibitors of HGF-c-Met inducing angiogenesis inhibitors of VEGF signaling genome instability & mutation PARP inhibitors resisting cell death proapatotoic BH3 mimetics deregulating cellular energetics aerobic glycolysis inhibitors
Mutagen is always toxic or growth inhibitory at high concentrations Exposure to chemical carcinogens Xenobiotic metabolizing enzymes DNA reactive metabolites mutations in cancer susceptibility genes Age-adjusted death rate per 100,000 stomach cancer in Japan high colon and rectum in USA higher than Japan. Mortality rates for gastrointestinal cancer (0-74 jr) for Japanese in Japan, and Japanese en Caucasians in California Japan stomach high, colon/rectum low. Foreign but born in Japan stomach lower then Japan and slightly higher colon/ rectum, in USA born Japan stomach lower and colon/ rectum, higher. Caucasians low stomach higher rectum/colon. There is a proportion of cancer deaths attributed to non-genetic factors that could have been avoided by changes in each category of non-genetic cancer causes History of chemical carcinogenesis Scrotumcancer in chimney sweepers PAHs high in chimney sweepers Nicotine is the addictive alkaloid constituent of tobacco. Nicotine stimulates tobacco use (does not cause cancer directly but indirectly). Orally ingested tobacco is very rapidly metabolized by hepatic cytochrome P450 (“first pass” effect). Only active when it is absorbed into the bloodstream via lungs, nasal epithelium, oral epithelium, or skin. PAHs induce cancer. nicotine (most likely) not! Smokers are addicted to nicotine and adjust their smoking habits as to maintain their blood nicotine levels above a threshold level to avoid the unpleasant effects of nicotine withdrawal. Cytochrome P450 2A6, which is highly variable in the population is a major determinant of smoking behavior. Individuals with high activity metabolize nicotine quickly, and smoke frequently – in some cases, waking with nicotine cravings and smoking at night. The metabolic activity level does not affect the likelihood of addiction or the ability to quit; these factors are probably influenced more by the physiology and genetics of the receptors for nicotine.
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