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

Wen Chi L. Chang; Terry V. Zenser; Harry S. Cooper; Margie L. Clapper

doi:10.1016/j.canlet.2013.02.013

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

Wen Chi L. Chang, Terry V. Zenser, Harry S. Cooper, Margie L. Clapper

Research output: Contribution to journal › Review article › peer-review

4 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	62-68
Number of pages	7
Journal	Cancer Letters
Volume	334
Issue number	1
DOIs	https://doi.org/10.1016/j.canlet.2013.02.013
State	Published - Jun 28 2013

Keywords

Amines/toxicity
Animals
Anti-Inflammatory Agents, Non-Steroidal/pharmacology
Apoptosis/drug effects
Carcinogens/toxicity
Cell Proliferation/drug effects
Colitis, Ulcerative/complications
Colitis/chemically induced
Colorectal Neoplasms/drug therapy
Dextran Sulfate/toxicity
Disease Models, Animal
Humans
Meat Products
Mesalamine/pharmacology
Mice
Nitric Oxide Synthase Type II/antagonists & inhibitors
Quinolines/toxicity

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.canlet.2013.02.013

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

abstract = "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.",

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T1 - Differential response of flat and polypoid colitis-associated colorectal neoplasias to chemopreventive agents and heterocyclic amines

AU - Chang, Wen Chi L.

AU - Zenser, Terry V.

AU - Cooper, Harry S.

AU - Clapper, Margie L.

PY - 2013/6/28

Y1 - 2013/6/28

N2 - 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.

AB - 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.

KW - Amines/toxicity

KW - Animals

KW - Anti-Inflammatory Agents, Non-Steroidal/pharmacology

KW - Apoptosis/drug effects

KW - Carcinogens/toxicity

KW - Cell Proliferation/drug effects

KW - Colitis, Ulcerative/complications

KW - Colitis/chemically induced

KW - Colorectal Neoplasms/drug therapy

KW - Dextran Sulfate/toxicity

KW - Disease Models, Animal

KW - Humans

KW - Meat Products

KW - Mesalamine/pharmacology

KW - Mice

KW - Nitric Oxide Synthase Type II/antagonists & inhibitors

KW - Quinolines/toxicity

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DO - 10.1016/j.canlet.2013.02.013

M3 - Review article

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SN - 0304-3835

VL - 334

SP - 62

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JO - Cancer Letters

JF - Cancer Letters

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ER -

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

Abstract

Keywords

UN SDGs

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