M1977 The Role of Inflammation in Patients With Intraductal Mucinous Tumors of the Pancreas and in Those With Pancreatic Adenocarcinoma

Abstract

Background: There are very few data regarding inflammation in patients with intraductal papillary mucinous neoplasms (IPMNs) of the pancreas. Aim: To evaluate the circulating concentrations of placental growth factor (PlGF), transforming growth factor-alpha (TGF-α), transforming growth factor-beta1 (TGF-β1), tumour necrosis factor receptor 1 (TNF-R1) and matrix metalloproteinase-2 (MMP-2) in patients with IPMNs and in those with pancreatic adenocarcinomas. Patients and Methods: Sixty-nine patients were enrolled: 23 (33.3%) had IPMNs and 46 (66.7%) had histologically confirmed pancreatic adenocarcinomas. Thirteen healthy subjects were also studied. PlGF, TGF-α, TGF-β1, TNF-R1 and MMP-2 were determined using commercially available kits. Results: TNF-R1 (p=0.003) was the only protein significantly different among the three groups. Conclusion: Serum TNF-R1 was elevated in patients with IPMNs and in those with pancreatic adenocarcinomas, suggesting a high apoptotic activity in both groups of patients studied. Intraductal papillary mucinous neoplasms (IPMNs) of the pancreas have received much clinical attention in the last decade because they are slow-growing tumours which may be cured surgically in most patients (1). However, there are only few data regarding inflammation processes associated with this disease. In contrast, there is notably more information available about ductal adenocarcinomas of the exocrine pancreas. Among the causes of the aggressive behaviour of IPMNs, several passive and active strategies appear to be adopted by tumour cells to circumvent antitumour immune defenses. They include altered expression of major histocompatibility complex (MHC) class I and II antigens (2), which may impair interaction between malignant cells and potential tumour cytotoxic T lymphocytes (CTLs), and resistance to apoptosis through the Fas receptor pathway coupled with aberrant expression of the ligand, which may be considered part of the 'counterattack' of the tumour cells against the immune effector cells (3-5). Pancreatic carcinoma cells have also been shown to spontaneously secrete immunosuppressive cytokines, such as