Mouse models for the study of colon carcinogenesis

被引：286

作者：

Rosenberg, Daniel W. ^{[1
,2
]}

Giardina, Charles ^{[3
]}

Tanaka, Takuji ^{[4
]}

机构：

[1] Univ Connecticut, Ctr Hlth, Neag Canc Ctr, Ctr Mol Med, Farmington, CT USA

[2] Univ Connecticut, Ctr Hlth, Neag Canc Ctr, Colon Canc Prevent Program, Farmington, CT USA

[3] Univ Connecticut, Dept Mol & Cell Biol, Storrs, CT 06113 USA

[4] Kanazawa Med Univ, Dept Oncol Pathol, Uchinada, Ishikawa 9200293, Japan

来源：

CARCINOGENESIS | 2009年 / 30卷 / 02期

基金：

美国国家卫生研究院;

关键词：

ABERRANT CRYPT FOCI; DEXTRAN SODIUM-SULFATE; BETA-CATENIN GENE; PUTATIVE PRENEOPLASTIC LESIONS; MUCIN-DEPLETED FOCI; GROWTH-FACTOR-BETA; NONSTEROIDAL ANTIINFLAMMATORY DRUG; ORNITHINE-DECARBOXYLASE ACTIVITY; CYTOSOLIC PHOSPHOLIPASE A(2); AZOXYMETHANE-INDUCED TUMORS;

D O I：

10.1093/carcin/bgn267

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The study of experimental colon carcinogenesis in rodents has a long history, dating back almost 80 years. There are many advantages to studying the pathogenesis of carcinogen-induced colon cancer in mouse models, including rapid and reproducible tumor induction and the recapitulation of the adenoma-carcinoma sequence that occurs in humans. The availability of recombinant inbred mouse panels and the existence of transgenic, knock-out and knock-in genetic models further increase the value of these studies. In this review, we discuss the general mechanisms of tumor initiation elicited by commonly used chemical carcinogens and how genetic background influences the extent of disease. We will also describe the general features of lesions formed in response to carcinogen treatment, including the underlying molecular aberrations and how these changes may relate to the pathogenesis of human colorectal cancer.

引用

页码：183 / 196

页数：14

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