Developing more efficient methods to prevent, diagnose, and cure human diseases requires a deeper understanding of how the complex architecture of distinct organs is established, and how tissue-specific cellular diversity is generated. Our lab investigates the molecular bases of pancreas and liver development in health and disease. Using mouse models, in silico approaches, imaging techniques, organ explants, and iPS/ESC methods, we study the interrelation between cell fate specification and tissue morphogenesis in the embryonic hepatopancreas, and the role that specific transcription factors play in those processes. We also investigate how postnatal exocrine cells acquire plasticity and how oncogenes exploit this capacity to foster pancreas tumor formation. More recently, we began exploring how genomic instability contributes to pancreatic cancer.
Drosos Y, Neale G, Ye J, Paul L, Kuliyev E, Maitra A, Means AL, Washington MK, Rehg J, Finkelsiein DB, Sosa-Pineda B. Prox1-heterozygosis sensitizes the pancreas to oncogenic Kras-induced neoplastic transformation. [February 2016, accepted in Neoplasia].
Seth A, Ye J, Yu N, Guez F, Bedford DC, Neale GA, Cordi S, Brindle PK, Lemaigre FP, Kaestner KH, and Sosa-Pineda B. Prox1 ablation in hepatic precursors causes defective hepatocyte specification and increases biliary cell commitment. Development. 141(3):538-47, 2014. PMCID: PMC3899812
Westmoreland JJ, Kilic G, Sartain C, Sirma S, Blain J, Rehg J, Harvey N, Sosa-Pineda B. Pancreas-specific deletion of Prox1 affects development and disrupts homeostasis of the exocrine pancreas. Gastroenterology. 142(4):999-1009, 2012. PMCID: PMC3398795.