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Research | Core Facilities | Patient Studies | Tech Transfer | Seminars | Intranet | Careers | Search | Contact Us | Ways To Give HOME |
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More about Arthritis and Immunology Research Program
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Research Interests From over a decade of work on the genetics of SLE, it is now clear that the risk of developing SLE is strongly influenced by genetic polymorphisms inherited within families. We use rapid high-capacity genotyping technology to systematically evaluate genetic polymorphisms associated with human SLE. With the completion of our genome-wide association study many new genetic targets will be identified and will require further replication. We are engaged in all phases of genetic evaluation from discovery to validation to functional characterization in model systems. The overall objective of these studies is to develop a comprehensive view of the genetic landscape of SLE and then use that information to develop new and improved treatments, predictive tools and monitoring programs for patients with SLE. Molecular mechanisms that influence aggressiveness of squamous cell carcinoma (SCCA) represent another major research emphasis. Recent work is focused on the role of Snail Homolog 2 (SNAI2) or Slug in modulating the malignant phenotype in SCCA. SCCA is the most common form of cancer originating from the upper aerodigestive tract and is diagnosed in over 45,000 patients annually in the United States. Previous studies from our lab demonstrated that Slug is over-expressed in tumor tissues from a subset of patients experiencing tumor relapse following treatment. In other model systems Slug promotes epithelial to mesenchymal transition (EMT) through repression of epithelial cadherins and modulates apoptosis responses through the p53/PUMA pathway. Preliminary studies using SCCA cell lines concur with these observations and show that forced expression of Slug results in molecular and morphologic evidence of EMT and repression of E-cadherin. Slug also confers resistance to common therapeutic treatments including taxanes and ionizing radiation in our SCCA cell line models. Future work will focus on defining the precise molecular mechanisms for these effects in Slug expressing cell lines and xenograft mouse models. Joined OMRF Scientific Staff in 2007. Mailing Address
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