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Our research focuses on elucidating the molecular mechanism of gene transcriptional regulation and its desregulation in breast cancer, with an ultimate goal to provide novel insights and potential therapeutic targets for better diagnosis, prognosis and individualized treatment of the disease.
Breast cancer is the most common type of cancer and one of the leading causes of death among western women. A vast majority (75%) of breast cancer was found to express estrogen receptor (ER)a, which is the key mediator of estrogen functions and plays prominent roles in breast tumorigenesis and drug resistance.
Anti-estrogens such as tamoxifen have been widely used in their treatment but acquired resistance greatly limited their usages. Hence, further development of novel strategies to selectively block estrogen signaling pathways is urgently needed.
Our previous work has established MED1 as a key transcription coregulator that plays important roles in ERa-mediated transcription and estrogen-dependent breast cancer cell growth. Significantly, MED1 has been reported to be over-expressed or amplified in a high percentage (40 to 50%) of primary breast cancer and breast cancer cell lines.
Building upon these promising results, we have centered our studies on the role and underlying molecular mechanism of MED1 in regulating estrogen receptor functions in breast cancer, and to devise innovative therapeutic approaches to target MED1 for their treatments.
Vontz Center for Molecular Studies 3125 Eden AvenuePO Box 670521Cincinnati, OH 45267-0521
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