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        Cancer development is a multi-step process. Although a large number of genes have been suggested to regulate cancer progression, only a limited number of those have proven to be critical for the initiation of cancer and are altered at early stages. Much evidence about these early genes came from gene aberrations including gene amplifications and chromosome translocations and rearrangements. Some of these genes are frequently linked to transcriptional regulation including coactivator functions.

        Our research focus is transcriptional coactivators in human cancer development. We are studying a number of coactivators that we have previously cloned, including TRBP, CoAA and GT198. These genes are located in the cancer susceptibility locus, and their alterations have been detected in human primary cancers at multiple levels, including gene aberration and protein overexpression. Some coactivators are developmentally expressed, and they participate in stem cell differentiation. Coactivator proteins are key regulators in gene expression cascades, and thus they are prone to be targeted as oncoproteins.

        We are focusing on the role of coactivators in the aspects of gene aberration, stem cell differentiation, apoptosis, protein interactions.  Research approaches include transgenic mouse models fluorescent in situ hybridization (FISH) analysis, yeast two-hybrid screens, cloning, immunohistochemistry, kinase phosphorylation, DNA methylation, RNA splicing, and protein structure analysis and transgenic mice.

         Our goal is to understand how coactivators are regulated cell-specifically to control cancer and embryonic development and to identify tumor-related genes that involve coactivators in human cancers.