Spontaneous Tumor Mice & Rat Models Overview
Spontaneous tumor models can be challenging to work with, as tumor development is often inconsistent from animal to animal and may only take place in aged animals. The advantage of cancer genetically engineered models (GEMs) is that the tumors develop de novo in the appropriate tissue, with the appropriate microenvironment. One way to more easily develop a simultaneous study cohort is to collect tumors from the cancer GEM (with or without further in vitro expansion) and implant into wild type mice of the same background strain in a syngeneic tumor experiment.
|Accelerated and amplified development of chemically-induced and spontaneous tumors.
|Knockout of the Trp53 tumor suppressor gene predisposes homozygous mice to development of various tumors, primarily lymphomas and sarcomas.
|Excellent model for study of human familial colon cancer. Contains a truncating mutation in the Apc gene at a site corresponding to the human mutation hotspot region of the gene. Heterozygotes develop multiple tumors in the small intestine and colon by 2-4 months of age.
|Invasive Lobular Breast Cancer Model*
|Tissue-specific conditional knockout of Cdh1 (E-cadherin) and Trp53 in mice induces metastatic mammary carcinomas that resemble human invasive lobular carcinoma (ILC), the second most common type of primary breast cancer. Females develop multiple skin and mammary tumors with a median latency of 214 days according to published reports. Note: that 20-30% of mice will develop non-mammary epithelial tumors.
|Brca1-Associated Breast Cancer Model*
|Conditional mouse mutant with somatic deletion of Brca1 and Trp53 in several epithelial tissues including mammary epithelium. Female mice of this strain show a high incidence of mammary tumors that mimic many aspects of human BRCA1-mutated basal-like breast cancer. ~80% of females develop multiple mammary and skin epithelial tumors with onset between 140 and 280 days according to published reports. Note: that 20-30% of mice will develop non-mammary epithelial tumors.
|Floxed Ink4a/Arf Mouse*
|Contains a targeted mutation of Cdkn2a (Ink4a/Arf) which introduced LoxP sites upstream of exon 2 and downstream of exon 3. Cross with the tissue-specific cre of your choice to develop a tumor model, including ones which development sarcomas, carcinomas, lymphomas, and metastatic melanoma.
|Floxed p53 Mouse*
|Contains a targeted mutation of Trp53 which introduced LoxP sites flanking exons 2 through 10. Cross with the tissue-specific cre of your choice to generate a conditional disruption of the Trp53 tumor suppressor gene, the most commonly mutated gene in human cancers. Conditional deletion avoids the predominance of non-epithelial tumors observed in constitutive Trp53 knockouts.
*Available from Taconic's cryopreserved repository.