PMON230 Pancreatic Exocrine Cells are Altered during the Progression of Ovarian Cancer-Driven Cachexia in Female Mice

Abstract Cancer-associated cachexia (CAC) is a progressive debilitating syndrome that frequently complicates metabolic function in body vital organs and subsequently causes high mortality rate cancer patients. However, the underlying mechanisms functional consequences of dysfunction during CAC are not fully elucidated. Recently, we have developed preclinical model characterized by oocyte-specific knockin for constitutively active Pi3k (Pik3ca*) which induces ovarian granulosa cell tumor (GCT) mimics stagewise progression humans. Here, aim to characterize pathophysiological effect on pancreatic investigate potential role pancreas development complication transgenic female mice with cancer. Notably, found cachectic showed drastic loss volume (PV) before death. Histological morphometric assays revealed exocrine acinar atrophy (PAA) PIK3CA* mice. The appeared an increased number stellate-shaped cells between acini. No significant changes were observed morphology endocrine islets. Immunohistochemical assay confirmed level TNF-a atrophied tissue decreased intensity amylase cytoplasm cells. Additionally, moderate fibrosis was also wall ducts blood vessels, but Masson trichrome histochemical staining expression extracellular matrix proteins including collagen I, II, IV, -smooth muscle actin vessel walls. Overall, our preliminary findings this novel mouse strongly suggest signs exhausted cancer-driven cachexia. This line could be ideal aid clarifying molecular mediators pathophysiology CAC. Keywords: Ovarian cachexia, pancreas, atrophy, amylase. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30