Post-baccalaureate

Duke University (Durham, NC)

Investigated truncated CYLD genes and then synthesized plasmids with these deletions for future application in later stages of a multi-year clinical study.

The cylindromatosis gene (CYLD) has been recognized as a tumor suppressor because of its genetic association with neoplasms occurring in skin appendages. The mechanism of CYLD's action is indicated in a highly orchestrated regulation of cell signaling pathways. Previous studies to determine such roles were performed in specialized cell lines and not in actual tissue. The cellular processes of major import are cell growth and apoptosis (pre-programmed cell death), and abnormalities in these are associated with cancers such as cylindromatosis. Thus, the research focused, as an independent part of a larger collaborative study, the effects of altered CYLD function on the cell cycle of human epidermal cells, with the ultimate goal of determining the role of the CYLD gene in epidermal homeostasis and the correlation to its downstream signaling pathways.

2005-2006 Undergraduate Prep Room Assistant - Duke University Chemistry

2003-2004 Duke University Peer Tutoring Program - Physics, Biology, Spanish

2002 Duke University FOCUS Program - Healthcare and Society