Pancreatic tumors acinar cell

Rats fed diets containing 30 or 300ppm ammonium perfluorooctanoate for 2 years had increased liver weights with occasional necrosis and an apparent dose-dependent increase in Leydig cell adenomas, but there was no evidence of an increased incidence of hepatocellular carcinoma. In a follow-up study in male mice, 300ppm in the diet for 2 years caused increases in liver, Leydig cell, and pancreatic acinar cell tumors that may have been associated with the peroxisome-proliferating capabilities of the compound. Ammonium perfluorooctanoate also produced sustained increases in serum estradiol concentrations. ... 

Pancreatic effect. Cigarette smoke, administered to anesthetized rats alone or in combination with iv ethanol infusion, reduced pancreatic blood flow temporarily and increased leukocyte-endothelium interaction (roller p < 0.001, sticker p < 0.01 vs baseline). Cigarette smoke potentiated the impairment of pancreatic capillary perfusion caused by ethanol, and both the number of rolling leukocytes and myeloperoxidase activity levels were increased compared with ethanol or nicotine administration alone h Tobacco-specific nitrosamines, administered to rats, induced pancreatic acinar cell and ductal cell neoplasms. One of the tumors had a mixed ductal-squamous-islet cell components . 

G10. Gukovskaya, A. S., Gukovsky, I., Zaninivic, V., Song, M., Sandoval, D., and Gukovsky, S., Pancreatic acinar cells produce, release, and respond to tumor necrosis factor a. J. Clin. Invest. 

In addition to fiver tumors, many PPARa activators also induce testicular Leydig cell tumors as well as pancreatic acinar cell tiunors in rats but not mice (also known as the tumor triad ). Little progress has been made to refine the proposed modes of action for the pancreatic and testicular rat tumors as detailed in Klaunig et al. (2003). As such, the present chapter will focus on the mode of action of PPARa activator-induced fiver tumors. 

Morohoshi T, Kanda M, Horie A, et al. Immunocytochemi-cal markers of uncommon pancreatic tumors. Acinar cell carcinoma, pancreatoblastoma, and solid cystic (papillary-cystic) tumor. Cancer. 1987 59 739-747. 

Yantiss RK, Chang HK, Farraye FA, et al. Prevalence and prognostic significance of acinar cell differentiation in pancreatic endocrine tumors. Am J Surg Pathol. 2002 26 893-901. 

The biological functions of the lipo-gastrin and lipo-CCK peptides were analyzed on these two receptors of known sequence using rat pancreatic acinar cells and the tumoral rat pancreatic acinar cell line AR42J. The CCK-A receptor has been thoroughly characterized in the rat pancreatic acinar cells (140-142) and in its... 

In the pediatric population, pancreatic tumors are very unusual entities. They account for less than 5% of all malignancies in children. These tumors may arise from the exocrine or endocrine pancreas. Exocrine neoplasias include ductal adenocarcinoma, acinar adenocarcinoma, pancreaticoblastoma, or infantile adenocarcinoma. Endocrine tumors or islet cell tumors are named after the hormone produced, with insulinoma being the most common in children (Walker 1996). 

In the rat and hamster models, enhanced cell proliferation by promoters leads to an increase in pancreatic tumors. The exact mechanisms involved are not known, but stimulation of cell turnover by elevated dietary fat or stimulation of regenerative hyperplasia, or by a hormonal mechanism involving cholecystokinin could result in the observed enhancement. Very limited information is available on induction of enzymes involved in cell proliferation for both ductal and acinar cells, and it is not clear which compounds are capable of promotion. Future areas of research should focus on mechanistic aspects of promotion that may lead to an understanding of pancreatic tumor promotion in humans. 

DAs are typically negative for pancreatic enzymes such as trypsin, chymotrypsin, and lipase °76 unless there is a mixed acinar component, which is uncommon. They also fail to label with endocrine markers however, in 30% of DAs there are scattered, possibly non-neoplastic, endocrine cells in close association with the neoplastic cells, which can be highlighted with immunostains for chromogranin A, synaptophysin, and NSE.2 2 77-79 latter two markers can occasionally show more diffuse expression, which should not be regarded as evidence of neuroendocrine differentiation if the tumor is an otherwise conventional adenocarcinoma. 

Pancreatic endocrine neoplasm versus ACC Scattered endocrine cells or a focal endocrine component are common in ACC however, diffuse and strong reactivity for the endocrine markers (chromogranin and synaptophysin) throughout the tumor is characteristic of PENs. Additionally, PENS do not show immunoreactivity for acinar markers. 

Focal endocrine differentiation, especially in the form of scattered cells, is quite common in pancreatic neoplasia of ductal and acinar nature and is of no known biologic significance. However, if a tumor is predominantly composed of cells with endocrine lineage, it is classified as endocrine. ... 

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