Experimental Liver Metastasis

Ravikumar, Thanjavur S.; D'Emilia, J; Cocchiaro, Celia; Wolf, Barbara C.; King, Vincent; Steele, Glenn

doi:10.1001/archsurg.1989.01410010059013

Cited by 22 publications

(2 citation statements)

References 22 publications

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“…WB-2054 is a poorly differentiated mucin-producing colon adenocarcinoma which is induced by administration of 1,2-dimethylhydrazine to WF×BN F 1 rats (16). WB-2054-M 5 is a fifth generation metastatic variant derived through serial applications of the Fidler hypothesis in our laboratory (17, 18).…”

Section: Methodsmentioning

confidence: 99%

In vivo Recombinant Adenovirus-mediated p53 Gene Therapy in a Syngeneic Rat Model for Colorectal Cancer

et al. 2004

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The p53 gene has a significant role in controlling genomic stability of cancer. The purpose of this study was to evaluate the tumor response of allograft colorectal tumor treated with Ad5CMV-p53 in a syngeneic rat model. Two weeks after the inoculation of WB-2054-M5 tumor cells in the flank of rats, rats were randomly assigned by tumor size to one of three groups (n=18 in each): phosphate buffered saline (PBS), Ad5CMV, and Ad5CMV-p53. Recombinant adenovirus or PBS was administered through intratumoral injection at three divided doses every other day for 4 weeks. Apoptosis of the tumors was evaluated using TUNEL assay. After 2 and 4 weeks of treatment, the volume (cm3) of tumors in PBS, Ad5CMV, and Ad5CMV-p53 was as follows: 2 week: 1.66±0.43, 1.40±0.47, 0.75±0.26 (p<0.001), 4 week: 4.41±0.88, 3.93±1.86, 2.33±0.51 (p<0.001). Tumor growth showed no statistically significant difference between the PBS and Ad5CMV groups (6-week vol. p=0.32). The TUNEL assay results revealed more apparent apoptotic cells in Ad5CMV-p53-treated tumors than in other groups. Growth of allograft colorectal cancer in the syngeneic rat model was significantly suppressed by intratumoral Ad5CMV-p53 gene therapy. These results demonstrate that gene replacement therapy with p53 may provide a novel modality of treatment in conjunction with other present treatments for metastatic colorectal cancer.

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Section: Methodsmentioning

confidence: 99%

In vivo Recombinant Adenovirus-mediated p53 Gene Therapy in a Syngeneic Rat Model for Colorectal Cancer

et al. 2004

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“…Partial hepatic ischemia before injection of tumor cells further increases the number of hepatic metastases, likely due to up-regulation of expression of adhesion molecules induced during hepatic ischemia[163],[164]. WB-2054-M cells, originally from a lung metastasis, yielded liver metastases in 50% of Wistar/Furth x Brown-Norwegian hybrid rats [165]. Colon cancer CC531, LDLX40, DHDK12/TR, and LMCR cells developed liver metastasis in all Wistar, WAG/Rij, and BDIX rats when injected into the portal vein[166]–[172].…”

Section: Metastatic Colorectal Cancer Modelsmentioning

confidence: 99%

Mouse models of colorectal cancer

Tong¹,

Yang²,

Koeffler³

2011

Chin J Cancer

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Colorectal cancer is one of the most common malignancies in the world. Many mouse models have been developed to evaluate features of colorectal cancer in humans. These can be grouped into genetically-engineered, chemically-induced, and inoculated models. However, none recapitulates all of the characteristics of human colorectal cancer. It is critical to use a specific mouse model to address a particular research question. Here, we review commonly used mouse models for human colorectal cancer.

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