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Edmond J. Feris

Ed is a doctoral student in the Program in Experimental & Molecular Medicine in the department of Pharmacology and Toxicology at the Geisel School of Medicine at Dartmouth College. Born and raised in Barranquilla, Colombia, he completed his BS at Boston College with double Majors in Economics and Biochemistry. In the Cole lab, he studies the mechanisms of oncogenic transformation, focusing on the functional interaction between the Myc transcription factor family and the TRRAP-containing histone acetyltransferase complexes, with the goal of targeting this protein-protein interaction therapeutically in cancer. Prior to joining the Cole Lab, Ed began his scientific career studying the molecular inhibition of the aggregation structure of amyloid beta proteins; major components of the neurotoxic plaques found in Alzheimer's patients. Later moved on to studying population genetics of HLA haplotypes, comparing octogenarian populations with systemic lupus populations stratified by socioeconomic class and ethnicity. Previously he has also consulted for construction companies in his native Colombia, developing budget and procurement planning strategies to maximize efficient allocation of funds. Upon completion of his Ph.D Ed would like to combine his professional and academic experiences to overcome the difficulties of bringing new therapies to patient care.

Research Interests
molecular therapeutics; drug screening/discovery/development; cancer genetics; gene regulation; pharmacogenomics

Research Summary
MYC is a potent oncogene that drives unrestrained cell growth and proliferation. Approximately 70% of human tumors have elevated MYC expression, and suppression of MYC expression can lead to the regression of tumors. The prevailing model of MYC-mediated transcription postulates that MYC increases local histone acetylation at promoters. MYC binds to histone acetyltransferase complexes through TRRAP (transformation/transcription-domain-associated protein). In the Cole lab, we have shown that MYC transactivation is dependent on a highly conserved region of the gene product known as MYC Box 2 (MB2) and that this region is also essential for MYC:TRRAP interaction. Therefore, we hypothesize that inhibition of the MYC:TRRAP interaction, more specifically MB2 can be exploited therapeutically in cancer treatment. For this purpose, we have determined the minimal interacting domains of both proteins and are developing a molecular screening assay to determine potential lead compounds.