Abstract. Synthesis of extracellular matrix components is enhanced in the rat pancreas during regeneration from caerulein-induced pancreatitis. To study the involvement of transforming growth factor , 131 (TGFPI), one of the most potent modulators of the extracellular matrix, in the process of pancreatic regeneration we examined the expression of this gene on the transcript and protein level. Pancreatic RNA was extracted from rats killed Oh, 12h, 24h, 2, 3 and 7 days after induction of caerulein pancreatitis. Transcript levels for TGFPl were measured by slot-blot analysis and mRNA in situ hybridization. Total amount of TGFPl-protein was measured using a radioligand binding assay. TGFPI protein was increased twofold after 24 h and 48 h and returned to control values 7 days after induction of pancreatitis, TGFPl -mRNA reached maximal values (3-fold over controls) after 2 days. The largest amount of TGFPImRNA was found in pancreatic acinar cells and in stromal cells. In summary, expression of TGFPl in acinar and stromal cells of the rat pancreas is enhanced during regeneration from caerulein-induced pancreatitis, whch may indicate an involvement of TGFPl in the regulation of extracellular matrix regeneration in the rat pancreas after caerulein-induced pancreatitis.
To evaluate p-cell function in patients with pancreatic cancer, the glucagon stimulation test was performed in seven patients with pancreatic adenocarcinoma, seven patients with type I diabetes mellitus, seven patients with type I1 diabetes mellitus, and in seven healthy controls. C-peptide serum levels were determined before and after a 1-mg i.v. glucagon injection. Basal C-peptide values were normal or slightly increased in pancreatic cancer and type I1 diabetic patients and low in type I diabetic patients. Following glucagon stimulation, no significant increase was observed in C-peptide values of type I diabetics and pancreatic cancer patients, whereas significant increases occurred in controls and type I1 diabetics. It is concluded that the altered p-cell function found in pancreatic cancer patients may lead to hyperglycemia, which is frequently associated with this tumor type.
The aims of this study were to (1) evaluate the diagnostic utility of a new tumor marker, TPS, with respect to TPA and CA 19-9 in patients with pancreatic cancer; (2) ascertain the reliability of the markers in predicting survival, and (3) evaluate the effect of liver dysfunction on the results. CA 19-9, TPA and TPS were measured in the serum of 19 control subjects, 42 patients with pancreatic cancer, 29 with chronic pancreatitis, and 52 with extrapancreatic diseases. CA 19-9 was confirmed to be the best serological indicator of pancreatic cancer, while TPA and TPS lacked both sensitivity and specificity. Pancreatic cancer patients with liver metastases had higher mean C A19-9 and TPA, but not TPS, values than pancreatic cancer patients without metastases. A shorter survival time was associated with the presence of liver metastases and with higher serum tumor marker levels. CA 19-9, TPA and TPS were found to be correlated with liver function test results (ALT, ALP and bilirubin). In conclusion: (1) TPS adds no significant information to that obtained using CA 19-9 in the diagnosis of pancreatic cancer; (2) CA 19-9 and TPA, but not TPS, are influenced by the presence of liver metastases; (3) the main factor to influence survival is advanced disease, which is in turn associated with higher tumor marker levels, and (4) liver dysfunction can influence not only CA 19-9 and TPA, as already described, but also TPS.
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