Abstract
A series of allelic mutations in the tumor suppressor Brca1 have been created to study mechanisms underlying BRCA1-associated tumorigenesis. Brca1 is essential in maintaining genome integrity through its involvement in DNA damage repair, G 2–M cell-cycle checkpoint and centrosome duplication. The loss of Brca1 is not sufficient for malignant transformation, rather, it triggers multiple genetic alterations, including the inactivation of p53 and activation of a number of oncogenes, that ultimately result in mammary tumorigenesis.
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