Differential response of flat and polypoid colitis-associated colorectal neoplasias to chemopreventive agents and heterocyclic amines

Individuals with ulcerative colitis face an increased risk of developing colorectal cancer and would benefit from early chemopreventive intervention. Results from preclinical studies in the mouse model of dextran sulfate sodium-induced colitis demonstrate that flat and polypoid colitis-associated dy...

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Bibliographic Details
Published in:Cancer letters 2013-06, Vol.334 (1), p.62-68
Main Authors: Chang, Wen-Chi L, Zenser, Terry V, Cooper, Harry S, Clapper, Margie L
Format: Article
Language:English
Subjects:
5-Aminosalicylic acid
Amines - toxicity
animal models
Animals
Anti-Inflammatory Agents, Non-Steroidal - pharmacology
Apoptosis - drug effects
Carcinogens - toxicity
Cell Proliferation - drug effects
Chemoprevention
colitis
Colitis - chemically induced
Colitis, Ulcerative - complications
Colitis, Ulcerative - drug therapy
Colitis, Ulcerative - pathology
Colorectal cancer
colorectal neoplasms
Colorectal Neoplasms - drug therapy
Colorectal Neoplasms - etiology
dextran
Dextran Sulfate - toxicity
Disease Models, Animal
Hematology, Oncology and Palliative Medicine
Heterocyclic amines
Humans
Inflammatory bowel disease
Meat Products
Mesalamine - pharmacology
Mice
Mouse
Mutation
Nitric Oxide Synthase Type II - antagonists & inhibitors
patients
quinoline
Quinolines - toxicity
risk
Rodents
therapeutics
Ulcerative colitis
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Summary:Individuals with ulcerative colitis face an increased risk of developing colorectal cancer and would benefit from early chemopreventive intervention. Results from preclinical studies in the mouse model of dextran sulfate sodium-induced colitis demonstrate that flat and polypoid colitis-associated dysplasias arise via distinct genetic pathways, impacted by the allelic status of p53. Furthermore, flat and polypoid dysplasias vary in their response to induction by the heterocyclic amine 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and inhibition by 5-aminosalicylic acid, a common therapy for the maintenance of colitis patients. These data suggest that use of combination therapy is essential for the optimal inhibition of colitis-associated colorectal cancer.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2013.02.013