Prostaglandins
We are interested in the role of prostaglandins in pancreatic tumorigenesis. We want to understand how prostaglandin-mediated communication within the tumor microenvironment contributes to disease progression and how these pathways can be targeted therapeutically. By utilizing immortalized human fibroblast lines, we aim to better understand prostacyclin signaling through a variety of molecular biology techniques. Additionally, using clinically relevant inhibitors, we examine the ability to affect tumor development and progression in mouse models of pancreatic cancer.
Epithelial Plasticity
The lab investigates the fundamental mechanisms that regulate epithelial plasticity, cell fate, and differentiation during tissue injury, regeneration, development, and disease. By integrating single-cell genomics, genetically engineered mouse models, and organoid systems, we examine how epithelial cells transition through distinct cell states across different tissues.
In the pancreas, we focus on understanding how these dynamic states influence key processes in pancreatic regeneration and neoplasia, including cellular differentiation, proliferation, and the formation and progression of pancreatic intraepithelial neoplasia (PanIN). Additionally, in the intestinal epithelium, we study how transcriptional regulators such as ZFP800 (ZNF800 in humans) regulate cell lineage allocation, secretory differentiation, and barrier integrity.
Neuron Remodeling
The lab investigates how extracellular vesicles released by intraductal papillary mucinous neoplasms (IPMNs)—precursor lesions of pancreatic ductal adenocarcinoma—promote neural infiltration and tumor progression. Using extracellular vesicle isolation, murine dorsal root ganglion models, immunofluorescence imaging, and quantitative image analysis, we are uncovering how tumor-derived signaling drives neural remodeling within the pancreatic tumor microenvironment. Additionally, we actively integrate human subjects research by managing longitudinal biospecimen collection and processing, collaborating with multidisciplinary clinical teams to advance patient-centered translational research.
Incretins
We are interested in the role of incretin receptor signaling in pancreatitis and pancreatic tumorigenesis, with the goal of uncovering novel biological consequences of incretin signaling within the pancreatic epithelium during disease. By utilizing genetically engineered mouse models, histological analyses, and organoid models of pancreatic metaplasia and dysplasia, we examine how endogenous and exogenous incretin signaling influence key oncogenic processes, including cellular survival, proliferation, inflammation, and remodeling of the tumor microenvironment.
Glycans
The DelGiorno lab investigates the critical role glycans play in the development and stratification of intraductal papillary mucinous neoplasms (IPMNs), a common precancerous lesion of the pancreas. As a complex post-translational modification, glycans act as promising diagnostic and functional drivers of disease. We are interested in understanding how specific glycan structures can reliably distinguish benign from malignant IPMNs, providing clinicians with biomarkers to guide surgical intervention. By integrating cell culture, computational, and biochemical approaches, we are uncovering how these dynamic structures not only aid in stratification but also actively promote or inhibit pancreatic cancer development.
Tuft Cells
Pancreatitis is a major risk factor for pancreatic cancer. We have identified formation of these rare cell populations in the injured pancreas and are currently investigating their role in injury, healing, and pancreatic regeneration (Red, Actin; Green, YFP).
Combining 3View serial block face scanning electron microscopy and imaging software, we generate 3D images of secretory cell types, like tuft cells, to understand their subcellular structures and their interactions with stromal cells and other epithelial cells.
These techniques have allowed us to discover previously un-described subcellular organelles in neoplastic tuft cells, including nucleus-associated lipid droplets.