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Carcinogenesis Drugs

Monoclonal antibodies that are specific for sites of base modificadon in DNA have a number of applications in, for example, studies of carcinogenesis, drug action, or DNA repair (1). The production of antibodies of the appropriate specificity entails practical considerations that are specific to this type of antigen. [Pg.321]

Drug allergies, idiosynchratic, mutagenesis, carcinogenesis, drug dependency... [Pg.171]

Turesky, R.J. (2002) Heterocyclic aromatic amine metabolism, DNA adduct formation, mutagenesis, and carcinogenesis. Drug Metab. Rev., 34, 625-650. [Pg.180]

Ruch RJ, Trosko JE (2001) Gap-junction communication in chemical carcinogenesis. Drug Metab Rev 33 117-124... [Pg.114]

Since their discovery, P450s have been studied in enormous detail because of their involvement in a plethora of crucial cellular roles - from carbon source assimilation, through biosynthesis ofhormones, to carcinogenesis, drug activation, and degradation of xenobiotics. [Pg.429]

E (1997) Mechanism of action of dietary chemoprotective agents in rat liver induction of phase I and II drug metabolizing enzymes and aflatoxin B1 metabolism . Carcinogenesis, 18 1729-38. [Pg.61]

KALL M A, VANG o and CLAUSEN J (1996) Effects of dietary broccoli on human in vivo drug metabolising enzymes Evaluation of caffeine, oestrone and chloroxazone metabolism. Carcinogenesis 17 793-9. [Pg.237]

The N-nitroso compounds are a potential source of carcinogenesis in humans. N-nltroso compounds appear to be ubiquitous in our environment, being present in low levels in foods, cosmetics, drugs, atmosphere, etc., and also appear to be formed endogenously in vivo. [Pg.201]

Damage to connective caused by leakage of elastases leads to damage associated with inflammatory diseases, such as pulmonary emphysema, adult respiratory distress syndrome, septic shock, cystic fibrosis, carcinogenesis, chronic bronchitis, and rheumatoid arthritis. Compounds that directly inhibit elastase or its release from human neutrophils are of enormous pharmaceutical and cosmetological interest in the development of new anti-inflammatory drugs. A possible source for elastase inhibitors are the medicinal Asteraceae and Droseraceae, particularly those used as traditional medicine in Asia. [Pg.46]

Rydstrom, J. Montelius, J. Bengtsson, M. "Extrahepatic Drug Metabolism and Chemical Carcinogenesis" Elsevier New York, 1983. [Pg.327]

Baskin, L.S., and Yang, C.S. (1980b) Microsomes, Drug Oxidations, and Chemical Carcinogenesis. pp. 103-106. Academic Press, New York. [Pg.1045]

Pohl, L.R., Martin, J.L., Taburet, A.M. and George, J.W. 1980b. Oxidative bioactivation of haloforms into hepatotoxins. In Microsomes, Drug Oxidations, and Chemical Carcinogenesis, Vol. II. Coon, M.J., et al., Eds. Academic Press, New York. Pp. 881—884. [Pg.79]

Walle T, Walle UK, Sedmera D, and Klausner, M (2006) Benzo[A]pyrene-induced oral carcinogenesis and chemoprevention Studies in bioengineered human tissue. Drug Metab. Dispos. 34 346-350. [Pg.179]

Carcinogenesis involves a complex series of genetic and biochemical events that enable transformed cells to proliferate, metastasize, migrate to secondary sites, and, sometimes, acquire resistance to chemotherapy. In Sect. 25.4.1, we will discuss how caveolin-1 expression correlates with cancerous growth, a potential mechanism of chemotherapy drug resistance, and how caveolae may be particularly exploited for cancer therapeutic strategies. [Pg.604]

Lee YJ, Park SJ, Ciccone SL, Kim CR, Lee SH (2006) An in vivo analysis of MMC-induced DNA damage and its repair. Carcinogenesis 27(3) 446-453 Loehrer PJ, Einhom LH (1984) Drugs five years later. Cisplatin. Ann Intern Med 100(5) 704-713 Li G, Widom J (2004) Nucleosomes facilitate their own invasion. Nat Struct Mol Biol 11 763-769 Liu W, Sun D, Hurley LH (2005) Binding of G-quadruplex interactive agents to distinct G-quadruplexes induces different biological effects in MiaPaca cells. Nucleosides Nucleotides Nucleic Acids 24(10-12) 1801-1815... [Pg.185]

Anti-neoplastic activity of UDCA was demonstrated first in the context of ulcerative colitis-associated colorectal carcinogenesis. Subsequently, encouraging (but not definitive) results have been obtained in clinical trials of UDCA for prevention of sporadic colorectal adenoma recurrence, which should prompt further evaluation of UDCA for polyp prevention, particularly given its excellent safety profile compared with other candidate chemoprevention agents such as the nonsteroidal anti-inflammatory drugs. [Pg.93]

These above-mentioned studies quantifying bile acid reflux have been fundamental to allowing in vitro analysis of bile acid effects at physiological doses (Table 6.2). These in vitro studies have crucially, identified molecular mechanisms important in bile-driven carcinogenesis. These molecular events will undoubtedly be important in future years as drug-able targets and as biomarkers of cancer risk. Prior to bile acid quantification in the refluxate, there... [Pg.109]

Druckrey H Quantitative aspects in chemical carcinogenesis. In Trichaut R (ed) Potential Carcinogenic Hazards from Drugs. UICC Monograph Series 7 60-78, 1967... [Pg.263]


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Carcinogenesis

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