Thesis supervisor: Eszter Hegyi
Location of studies (in Hungarian): PTE ÁOK Pécs, Szigeti u. 12. Abbreviation of location of studies: ÁOK
Description of the research topic:
Chronic pancreatitis is a progressive inflammatory disease of the pancreas leading to irreversible morphological changes and impairment of both exocrine and endocrine functions. Genetic susceptibility plays an important role in the pathogenesis of chronic pancreatitis, especially in children. Over the past 20 years the role of genetic factors in the etiology of chronic pancreatitis has been extensively studied and a mechanistic model in which premature trypsinogen activation plays a central pathogenic role has been established. More recently, an alternative pathomechanism unrelated to accelerated intrapancreatic trypsinogen activation has been revealed, in which mutation-induced misfolding and consequent ER stress lead to acinar cell damage and pancreatitis. Using animal models of genetically determined chronic pancreatitis we aim to study both pathomechanisms, the trypsin-dependent and the ER stress related pathways in vivo. Moreover, we also focus on the identification of new genetic risk factors in chronic pancreatitis using candidate gene association studies.