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Pancreatic Pathology (pancreatic + pathology)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Broad tumor spectrum in a mouse model of multiple endocrine neoplasia type 1

INTERNATIONAL JOURNAL OF CANCER, Issue 2 2007
Kelly A. Loffler
Abstract Multiple endocrine neoplasia type 1 (MEN1) is an inherited cancer predisposition syndrome typified by development of tumors in parathyroid, pituitary and endocrine pancreas, as well as less common sites including both endocrine and nonendocrine organs. Deletion or mutation of the tumor suppressor gene MEN1 on chromosome 11 has been identified in many cases of MEN1 as well as in sporadic tumors. The molecular biology of menin, the protein encoded by MEN1, remains poorly understood. Here we describe a mouse model of MEN1 in which tumors were seen in pancreatic islets, pituitary, thyroid and parathyroid, adrenal glands, testes and ovaries. The observed tumor spectrum therefore includes types commonly seen in MEN1 patients and additional types. Pancreatic pathology was most common, evident in over 80% of animals, while other tumor types developed with lower frequency and generally later onset. Tumors of multiple endocrine organs were observed frequently, but progression to carcinoma and metastasis were not evident. Tumors in all sites showed loss of heterozygosity at the Men1 locus, though the frequency in testicular tumors was only 36%, indicating that a different molecular mechanism of tumorigenesis occurs in those Leydig tumors that do not show loss of the normal Men1 allele. Menin expression was below the level of detection in ovary, thyroid and testis, but loss of nuclear menin immunoreactivity was observed uniformly in all pancreatic islet adenomas and in some hyperplastic islet cells, suggesting that complete loss of Men1 is a critical point in islet tumor progression in this model. © 2006 Wiley-Liss, Inc. [source]

Intramedullary fat necrosis, polyarthritis and panniculitis with pancreatic tumor: a case report

INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 4 2010
Vivek VASDEV
Abstract Acute polyarthritis can occur in non-rheumatic systemic illnesses, presenting a diagnostic dilemma. We present an extremely rare case presenting as acute polyarthritis, panniculitis and medullary fat necrosis with underlying pancreatic pathology. This case report describes a young woman presenting with panniculits, pancreatic tumour, polyarthritis and intra-osseus fat necrosis with a fatal outcome. The medical fraternity needs to be aware of this potentially fatal albeit rare musculoskeletal complication secondary to a pancreatic pathology. [source]

Cholinergic Mediation of Alcohol-Induced Experimental Pancreatitis

ALCOHOLISM, Issue 10 2010
Aurelia Lugea
Objectives:, The mechanisms initiating pancreatitis in patients with chronic alcohol abuse are poorly understood. Although alcohol feeding has been previously suggested to alter cholinergic pathways, the effects of these cholinergic alterations in promoting pancreatitis have not been characterized. For this study, we determined the role of the cholinergic system in ethanol-induced sensitizing effects on cerulein pancreatitis. Methods:, Rats were pair-fed control and ethanol-containing Lieber-DeCarli diets for 6 weeks followed by parenteral administration of 4 hourly intraperitoneal injections of the cholecystokinin analog, cerulein at 0.5 ,g/kg. This dose of cerulein was selected because it caused pancreatic injury in ethanol-fed but not in control-fed rats. Pancreatitis was preceded by treatment with the muscarinic receptor antagonist atropine or by bilateral subdiaphragmatic vagotomy. Measurement of pancreatic pathology included serum lipase activity, pancreatic trypsin, and caspase-3 activities, and markers of pancreatic necrosis, apoptosis, and autophagy. In addition, we measured the effects of ethanol feeding on pancreatic acetylcholinesterase activity and pancreatic levels of the muscarinic acetylcholine receptors m1 and m3. Finally, we examined the synergistic effects of ethanol and carbachol on inducing acinar cell damage. Results:, We found that atropine blocked almost completely pancreatic pathology caused by cerulein administration in ethanol-fed rats, while vagotomy was less effective. Ethanol feeding did not alter expression levels of cholinergic muscarinic receptors in the pancreas but significantly decreased pancreatic acetylcholinesterase activity, suggesting that acetylcholine levels and cholinergic input within the pancreas can be higher in ethanol-fed rats. We further found that ethanol treatment of pancreatic acinar cells augmented pancreatic injury responses caused by the cholinergic agonist, carbachol. Conclusion:, These results demonstrate key roles for the cholinergic system in the mechanisms of alcoholic pancreatitis. [source]