Mouse models of colorectal cancer: Past, present and future perspectives

被引:110
作者
Buertin, Florian [1 ]
Mullins, Christina S. [2 ]
Linnebacher, Michael [3 ]
机构
[1] Univ Rostock, Univ Med Ctr Rostock, Dept Gen Visceral Vasc & Transplantat Surg, D-18057 Rostock, Germany
[2] Univ Rostock, Dept Thorac Surg, Univ Med Ctr Rostock, D-18057 Rostock, Germany
[3] Univ Med Ctr Rostock, Dept Gen Visceral Vasc & Transplantat Surg, Mol Oncol & Immunotherapy, Schillingallee 69, D-18057 Rostock, Germany
关键词
Colorectal cancer; Mouse models; Patient-derived xenografts; Carcinogen-induced models; Genetically engineered mouse models; Preclinical drug development; DEXTRAN SODIUM-SULFATE; PATIENT-DERIVED XENOGRAFTS; FAMILIAL ADENOMATOUS POLYPOSIS; MULTIPLE INTESTINAL NEOPLASIA; INDUCED COLON CARCINOGENESIS; DNA MISMATCH REPAIR; K-RAS ONCOGENE; CRE-MEDIATED INACTIVATION; COMPOUND MUTANT MICE; BETA-CATENIN GENE;
D O I
10.3748/wjg.v26.i13.1394
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Colorectal cancer (CRC) is the third most common diagnosed malignancy among both sexes in the United States as well as in the European Union. While the incidence and mortality rates in western, high developed countries are declining, reflecting the success of screening programs and improved treatment regimen, a rise of the overall global CRC burden can be observed due to lifestyle changes paralleling an increasing human development index. Despite a growing insight into the biology of CRC and many therapeutic improvements in the recent decades, preclinical in vivo models are still indispensable for the development of new treatment approaches. Since the development of carcinogen-induced rodent models for CRC more than 80 years ago, a plethora of animal models has been established to study colon cancer biology. Despite tenuous invasiveness and metastatic behavior, these models are useful for chemoprevention studies and to evaluate colitis-related carcinogenesis. Genetically engineered mouse models (GEMM) mirror the pathogenesis of sporadic as well as inherited CRC depending on the specific molecular pathways activated or inhibited. Although the vast majority of CRC GEMM lack invasiveness, metastasis and tumor heterogeneity, they still have proven useful for examination of the tumor microenvironment as well as systemic immune responses; thus, supporting development of new therapeutic avenues. Induction of metastatic disease by orthotopic injection of CRC cell lines is possible, but the so generated models lack genetic diversity and the number of suited cell lines is very limited. Patient-derived xenografts, in contrast, maintain the pathological and molecular characteristics of the individual patient's CRC after subcutaneous implantation into immunodeficient mice and are therefore most reliable for preclinical drug development - even in comparison to GEMM or cell line-based analyses. However, subcutaneous patient-derived xenograft models are less suitable for studying most aspects of the tumor microenvironment and anti-tumoral immune responses. The authors review the distinct mouse models of CRC with an emphasis on their clinical relevance and shed light on the latest developments in the field of preclinical CRC models.
引用
收藏
页码:1394 / 1426
页数:33
相关论文
共 393 条
[1]   CLUES TO THE PATHOGENESIS OF FAMILIAL COLORECTAL-CANCER [J].
AALTONEN, LA ;
PELTOMAKI, P ;
LEACH, FS ;
SISTONEN, P ;
PYLKKANEN, L ;
MECKLIN, JP ;
JARVINEN, H ;
POWELL, SM ;
JEN, J ;
HAMILTON, SR ;
PETERSEN, GM ;
KINZLER, KW ;
VOGELSTEIN, B ;
DELACHAPELLE, A .
SCIENCE, 1993, 260 (5109) :812-816
[2]   Expression and Mutation Pattern of β-Catenin and Adenomatous Polyposis Coli in Colorectal Cancer Patients [J].
Abdelmaksoud-Damak, Rania ;
Miladi-Abdennadher, Imen ;
Triki, Mouna ;
Khabir, Abdelmajid ;
Charfi, Slim ;
Ayadi, Lobna ;
Frikha, Mounir ;
Sellami-Boudawara, Tahia ;
Mokdad-Gargouri, Raja .
ARCHIVES OF MEDICAL RESEARCH, 2015, 46 (01) :54-62
[3]   Regorafenib Inhibits Growth, Angiogenesis, and Metastasis in a Highly Aggressive, Orthotopic Colon Cancer Model [J].
Abou-Elkacem, Lotfi ;
Arns, Susanne ;
Brix, Gunnar ;
Gremse, Felix ;
Zopf, Dieter ;
Kiessling, Fabian ;
Lederle, Wiltrud .
MOLECULAR CANCER THERAPEUTICS, 2013, 12 (07) :1322-1331
[4]   THE C-MYC ONCOGENE DRIVEN BY IMMUNOGLOBULIN ENHANCERS INDUCES LYMPHOID MALIGNANCY IN TRANSGENIC MICE [J].
ADAMS, JM ;
HARRIS, AW ;
PINKERT, CA ;
CORCORAN, LM ;
ALEXANDER, WS ;
CORY, S ;
PALMITER, RD ;
BRINSTER, RL .
NATURE, 1985, 318 (6046) :533-538
[5]   Tumor macrophages are pivotal constructors of tumor collagenous matrix [J].
Afik, Ran ;
Zigmond, Ehud ;
Vugman, Milena ;
Klepfish, Mordehay ;
Shimshoni, Elee ;
Pasmanik-Chor, Metsada ;
Shenoy, Anjana ;
Bassat, Elad ;
Halpern, Zamir ;
Geiger, Tamar ;
Sagi, Irit ;
Varol, Chen .
JOURNAL OF EXPERIMENTAL MEDICINE, 2016, 213 (11) :2315-2331
[6]   Heterogeneity in Circulating Tumor Cells: The Relevance of the Stem-Cell Subset [J].
Agnoletto, Chiara ;
Corra, Fabio ;
Minotti, Linda ;
Baldassari, Federica ;
Crudele, Francesca ;
Cook, William Joseph James ;
Di Leva, Gianpiero ;
D'Adamo, Adamo Pio ;
Gasparini, Paolo ;
Volinia, Stefano .
CANCERS, 2019, 11 (04)
[7]  
Akyol A, 2008, NAT METHODS, V5, P231, DOI [10.1038/nmeth.1182, 10.1038/NMETH.1182]
[8]   Higher metastatic efficiency of KRas G12V than KRas G13D in a colorectal cancer model [J].
Alamo, Patricia ;
Gallardo, Alberto ;
Di Nicolantonio, Federica ;
Pavon, Miguel Angel ;
Casanova, Isolda ;
Trias, Manuel ;
Mangues, Maria Antonia ;
Lopez-Pousa, Antonio ;
Villaverde, Antonio ;
Vazquez, Esther ;
Bardelli, Alberto ;
Cespedes, Maria Virtudes ;
Mangues, Ramon .
FASEB JOURNAL, 2015, 29 (02) :464-476
[9]   Subcutaneous preconditioning increases invasion and metastatic dissemination in mouse colorectal cancer models [J].
Alamo, Patricia ;
Gallardo, Alberto ;
Pavon, Miguel A. ;
Casanova, Isolda ;
Trias, Manuel ;
Mangues, Maria A. ;
Vazquez, Esther ;
Villaverde, Antonio ;
Mangues, Ramon ;
Cespedes, Maria V. .
DISEASE MODELS & MECHANISMS, 2014, 7 (03) :387-396
[10]   Smad4 haploinsufficiency in mouse models for intestinal cancer [J].
Alberici, P ;
Jagmohan-Changur, S ;
De Pater, E ;
Van Der Valk, M ;
Smits, R ;
Hohenstein, P ;
Fodde, R .
ONCOGENE, 2006, 25 (13) :1841-1851