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Women with mutations in hereditary cancer genes, BRCA1 and BRCA2, are highly predisposed to breast cancer (lifetime risk 50-80%) and ovarian cancer (lifetime risk 15-40%). Men with mutations in BRCA2 are predisposed to pancreatic and prostate cancer. How a normal, presumably healthy cell in these mutation carriers transform into a tumor cell is largely unknown.
Primary Research Interests:
1. How and when normal, presumably healthy cells become tumor cells?
2. How can we leverage these mechanistic insights to design better preventive and therapeutic treatment strategies?
We are addressing these questions in the setting of hereditary breast and ovarian cancer by studying genes like BRCA 1, BRCA2, PALB2, Rad51C and many others.
Our ongoing projects aim to give us a better understanding of the different functions of these cancer predisposing genes, with special focus on DNA damage repair function, given that it is the most commonly disrupted function in the tumor cells of the mutation carriers. We are addressing these questions in primary cells derived from patient tissues, as well as in transgenic murine models.