Notch is a powerful regulator for the development and homeostasis of various tissues. Dysregulation of Notch signaling has been implicated in a number of pathological conditions including cancer. The Fringe glycosyltransferases modify Notch receptor and modulate Notch activation. Fine-tuning of Notch signaling by Fringe is critical in the regulation of stem cell function. We are interested in understanding roles of Fringe-modulated Notch signaling in tissue development and tumorigenesis in the following areas:
Notch controls pancreatic differentiation during development and is reactivated in pancreatic cancer. We recently discovered that Lfng is uniquely expressed in a subset of acinar cells in pancreas. Deletion of Lfng in the mouse pancreas caused increased Notch activation associated with accumulation of stem-like cells, and dramatically accelerated Kras-induced PDAC development. We hypothesize that Lfng-expressing acinar cells represent a cellular origin of Kras-induced PDAC, and Lfng-positive PDAC cells may be enriched for cancer stem cells. We are currently testing this hypothesis and identifying genes that are critical for PDAC initiation and progression.
*In last four years. A complete publication list can be accessed through MyBibliography at NCBI.
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