Discussion

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Molecular lesions causing breast cancer in human have proven to cause breast cancer in Genetically Engineered Mice.	Some molecular lesions causing breast cancer in mice have not been found in human breast cancer

A number of molecular lesions have been associated with human breast cancer. HER2/neu (c-erbB2) was the one of the first to be associated with human breast cancer. It is now the basis for novel immunotherapy for breast cancer. Other lesions in genes such as BrCa1, p53, Cyclin D1, ras, myc, neu and many others have been identified in association with human breast cancer. Genetic engineering of mice to overexpress putative oncogenes or underexpress putative tumor suppressor genes is one of the most important techniques for the verification of biological activity. The panel of experimental models included in this collection illustrate some of the genes that can cause mouse mammary malignancy.

Unfortunately, the genes that have been identified in the mouse have not proven to be mutated or activated in many human breast cancers. However, they are activated in other cancers or the pathways that they activate are associated with other cancers. For example, chemical carcinogenesis is generally associated with ras mutations in the mammary gland (e.g. NMU and DMBA). The genes activated by the insertion of the mouse mammary tumor virus are occasionally found in human breast cancers (e.g. wnt 1, int2, notch 4, and wnt10b). These genes generally produce mammary tumors that closely resemble those produced by MMRV insertion -activation of the same genes. Although they do not particularly resemble the human tumor phenotype, the members of the FGF family are activated in a number of human cancers and the wnt pathway interacts with a number of proteins that are thought to be important in human breast cancer such as beta-catenin and E-cadherin.