By Ronald G. Harvey (auth.), Trevor M. Penning (eds.)
This monograph offers a latest account of advances in chemical carcinogenesis. It promotes the view that it truly is alteration of the DNA by way of endogenous and exogenous cancer agents that finally results in sporadic mutations that are a root explanation for many human cancers. It offers with the metabolic activation of universal sessions of chemical cancer causing agents (tobacco cancer agents, heterocyclic amines, polycyclic fragrant hydrocarbons) and their detoxication. It describes the DNA-adducts that take place and their fix mechanisms. It covers advances in structural-biology that supply a glimpse of either the DNA-repair strategy and the by-pass of DNA-lesions and the way this informs the mutational code. It additionally bargains with the recommendations of chemoprevention and biomarkers for biomonitoring human publicity. Many modern texts at the biology of melanoma now concentration nearly completely at the molecular and mobilephone biology of the ailment and don't hide the beginning (DNA harmful occasions) of chemical carcinogenesis intensive. it's with this perceived gap-in wisdom that global specialists of their specific fields have contributed to this monograph. This monograph should be a big reference re-source for college students in education, postdoctoral scientists, and senior scientists a professional within the field.
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Additional info for Chemical Carcinogenesis
Comfrey, a popular herbal tea, frequently contains PAs that can cause moderate to severe liver damage. Although the FDA took official action in 2001 to ban comfrey as a dietary supplement, comfrey in various forms is still readily available, and its supposed health benefits are widely touted on the Internet. Human exposure to PAs may also result from food contamination. Several examples of large-scale poisoning associated with consumption of bread made from wheat flour contaminated with PAs have been reported (Fu et al.
Kinosita R (1936) Gann 30:423–426. Kmet J (1970) J. Chronic Dis. 23:305–315. Kolonel LN, Altshuler D, Henderson BE (2004) Nat. Rev. Cancer 4:519–527. Lai C-C, Miller JA, Miller EC, Liem A (1985) Carcinogenesis 6:1037–1045. 1 Historical Overview of Chemical Carcinogenesis 25 Lawley PD (1990) In Handbook of Experimental Pharmacology, Cooper CS, Grover PI (eds), Vol. 94/1, Springer-Verlag, Berlin, pp. 409–469. Lehr R, Kumar S, Levin W, Wood AW, Chang RL, Conney A, Yagi H, Sayer JM, Jerina DM (1985) In Polycyclic Hydrocarbons and Carcinogenesis, Harvey RG (ed), American Chemical Society, Washington, DC, pp.
1992; Rehman et al. 2000). Confirmation that mutations in Hras1 represent an initiating event in mouse skin carcinogenesis comes from several lines of evidence including (1) different mutation spectra depending on the initiating carcinogen and the types of DNA adducts they produce (reviewed in DiGiovanni 1992); (2) transgenic mice expressing a mutant Ha-ras gene develop skin tumors at sites of skin irritation (Bailleul et al. 1990); (3) knockout of Hras1 significantly reduced susceptibility to skin tumor development in mice exposed to a two-stage carcinogenesis protocol (Ise et al.