Chemistry meets biology in colitis-associated carcinogenesis

Autor:	Gerald N. Wogan, James G. Fox, Aswin Mangerich, Peter C. Dedon, Steven R. Tannenbaum
Přispěvatelé:	Massachusetts Institute of Technology. Center for Environmental Health Sciences, Massachusetts Institute of Technology. Department of Biological Engineering, Massachusetts Institute of Technology. Department of Chemistry, Massachusetts Institute of Technology. Division of Comparative Medicine, Dedon, Peter C., Mangerich, Aswin, Fox, James G., Tannenbaum, Steven Robert, Wogan, Gerald N.
Rok vydání:	2013
Předmět:	Innate immune system Carcinogenesis Inflammation General Medicine Disease Biology Gut flora medicine.disease_cause medicine.disease biology.organism_classification Colitis Inflammatory Bowel Diseases Biochemistry Inflammatory bowel disease Article Mice Immunology Colonic Neoplasms medicine Animals Humans medicine.symptom Genetic Toxicology
Zdroj:	Prof. Dedon via Howard Sliver
ISSN:	1029-2470
Popis:	The intestine comprises an exceptional venue for a dynamic and complex interplay of numerous chemical and biological processes. Here, multiple chemical and biological systems, including the intestinal tissue itself, its associated immune system, the gut microbiota, xenobiotics, and metabolites meet and interact to form a sophisticated and tightly regulated state of tissue homoeostasis. Disturbance of this homeostasis can cause inflammatory bowel disease (IBD)—a chronic disease of multifactorial etiology that is strongly associated with increased risk for cancer development. This review addresses recent developments in research into chemical and biological mechanisms underlying the etiology of inflammation-induced colon cancer. Beginning with a general overview of reactive chemical species generated during colonic inflammation, the mechanistic interplay between chemical and biological mediators of inflammation, the role of genetic toxicology, and microbial pathogenesis in disease development are discussed. When possible, we systematically compare evidence from studies utilizing human IBD patients with experimental investigations in mice. The comparison reveals that many strong pathological and mechanistic correlates exist between mouse models of colitis-associated cancer, and the clinically relevant situation in humans. We also summarize several emerging issues in the field, such as the carcinogenic potential of novel inflammation-related DNA adducts and genotoxic microbial factors, the systemic dimension of inflammation-induced genotoxicity, and the complex role of genome maintenance mechanisms during these processes. Taken together, current evidence points to the induction of genetic and epigenetic alterations by chemical and biological inflammatory stimuli ultimately leading to cancer formation. Massachusetts Institute of Technology. Center for Environmental Health Sciences (ES002109) National Institutes of Health (U.S.) (NIH (CA26731))
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9cd1edfaaf988a2eed8a955ae092ec53 https://pubmed.ncbi.nlm.nih.gov/23926919 Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
Nepřihlášeným uživatelům se plný text nezobrazuje	K zobrazení výsledku je třeba se přihlásit.