|Dr. Eva Lee, PhD
Assistant Professor of Radiological Sciences and Physics in Residence (Medical Physics)
Department of Developmental & Cell Biology / Department of Biological Chemistry
122 Sprague Hall -- 140 Sprague Hall
Dr. Eva Lee, PhD studies how alterations in various genes impact the development of breast cancer using sophisticated genetic models. Dr. Lee's work is providing tools to understand why each individual's tumor is different and ultimately how this might impact their treatment. Dr. Eva Lee works with with Drs Wen-Hwa Lee and Rainer Brachmann on breast cancer projects.
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The research objective in the Lee laboratory is the understanding of molecular events underlying tumorigenesis and the identification of drug targets for cancer therapy. Many genes critical for cancer prevention such as tumor suppressor genes have been shown to be required for proper cellular response to DNA damage and replication blocks. We have investigated the function of several of these genes including gene mutated in ataxia telangiectasia (ATM) and its related kinase, ATR; genes mutated in Nijmegen breakage syndrome, NBS1 and A-T like syndrome, Mre11; and Li-Fraumeni syndrome (p53). The organization of these tumor suppressors in DNA damage response and the roles of phosphorylation in the regulation of checkpoint activities and cell survival upon DNA damage are being investigated.
Mutations of the breast cancer susceptibility genes, BRCA1 and BRCA2, account for a significant percentage of familial breast cancer. The p53 gene is frequently mutated in breast cancer in patients without family history of breast cancer. The p53 gene is also mutated at very high frequencies in breast cancers developed in BRCA1 carriers. BRCA1 protein is involved in DNA repair, cell cycle checkpoint, growth regulation, and steroid hormone actions. We have developed model systems of human breast cancer using the Cre/loxP system for tissue-specific inactivation of p53, breast cancer susceptibility genes (BRCA1 & 2), and PTEN.
These models are used to study processes regulating cancer development and molecular basis of differential responses to steroid hormones and chemotherapy in vivo. Our studies indicate that mutations of Brca1 modify regulation of cell proliferation by steroid hormones and responses of tumor cells to chemotherapy. Comparisons of molecular profiles among human breast cancer and tumors in our model systems identify specific markers that are likely to be useful for cancer detection, prognosis, and tailored treatment.
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