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PubMed1993

Stimulation of pancreatic growth by cholecystokinin is mediated by high affinity receptors on rat pancreatic acinar cells.

Pancreatic acinar cells possess both high low affinity receptors for cholecystokinin. The cholecystokinin analog caerulein, which exerts a trophic effect on the rat pancreas, acts as an agonist at both types of receptors. In contrast, the synthetic analog CCK-JMV-180, which also acts as an agonist at high affinity receptors, opposes the action of caerulein on the low affinity receptors. We report that infusion of either caerulein or CCK-JMV-180 into rats increases [3H]-thymidine incorporation into pancreatic DNA and causes the pancreatic weight as well as content of DNA, RNA, and protein to increase. CCK-JMV-180 also stimulates in-vitro incorporation of [3H]-thymidine into DNA of cultured rat acini. The finding that both caerulein and CCK-JMV-180 exert the same trophic effect on pancreatic acinar cells indicates that this effect is mediated via high affinity acinar cell cholecystokinin receptors.

Animals↗
PubMed1976

Effects of ions on amylase release by dissociated pancreatic acinar cells.

Dissociated acinar cells prepared from guinea pig and mouse pancreas were intact on the basis of structure, ion content, and their ability to increase release of amylase in response to bethanechol and the calcium ionophore A23187. Guinea pig but not mouse acinar cells increased amylase release in response to caerulein. An increase in the concentration of K+ in the medium, which increases amylase release from whole pancreas, did not increase release. The effect of varying the ionic content of the medium on basal and stimulated amylase release was studied. Bethanechol and caerulein were still able to stimulate amylase release when Ca2+ was omitted from the medium, whereas stimulation induced by A23187 was abolished. Elevation of the concentration of Mg2+ did not affect basal or stimulated amylase release. Removal of Na+ from the medium initially had no effect on amylase release although bethanechol-stimulated release by mouse cells was inion of the HCO3- or Cl- content of the medium did not affect cholinergic stimulation of secretion. It is concluded that stimulated amylase release by isolated acinar cells is relatively independent of the ionic constituency of the bathing medium.

Amylases↗
PubMed1994

Correlation between nucleolar organizer regions and cell proliferation in pancreatic acinar cell proliferative lesions in rats.

The numbers of nucleolar organizer regions (NORs) stained by the one-step silver (Ag) colloid method were measured in rat pancreatic basophilic foci, eosinophilic foci, and acinar cell adenomas induced by 4-hydroxyaminoquinoline 1-oxide (HAQO) followed by crude soybean trypsin inhibitor (SBTI) treatments and compared with values for bromodeoxyuridine (BrdU)-incorporating cells and nuclear DNA contents. Both numbers of AgNORs and BrdU-labeling indices showed stepwise increases from normal pancreatic acinar cells through eosinophilic foci to adenomas, and a good correlation was found between cell proliferation and mean numbers of AgNORs. Microspectrometry of nuclear DNA contents revealed a wide range of values in basophilic and eosinophilic foci and acinar cell adenomas as compared with normal acinar cells, but there was no significant difference in the profile of DNA content among these three proliferative lesions. The present results suggest that mean numbers of AgNORs may reflect cellular kinetics in rat pancreatic acinar cell lesions.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1989

Density gradient separation of two populations of lysosomes from rat parotid acinar cells.

Exocrine acinar cells possess two cytochemically distinct populations of secondary lysosomes. One population is Golgi associated and has demonstrable acid phosphatase (AcPase) activity, whereas the second is basally located and lacks AcPase activity but has trimetaphosphatase (TMPase) activity. The basal lysosomes are tubular in shape and rapidly label with horseradish peroxidase (HRP) after intravenous injection. In the present study using isolated rat parotid acinar cells, the two lysosomal populations were separated by cell fractionation on Percoll density gradients and were analyzed biochemically and by EM cytochemistry. On 35% Percoll gradients, two peaks of AcPase and beta-hexosaminidase, both lysosomal marker enzymes, and succinic dehydrogenase, an enzyme marker for mitochondria, could be resolved. The major peaks of beta-hexosaminidase and succinic dehydrogenase and the minor peak of AcPase corresponded with the dense lysosome fraction. The major peak of AcPase and the minor peaks for beta-hexosaminidase and succinic dehydrogenase coincided with the light membrane fraction. Galactosyl transferase (a marker enzyme for Golgi saccules) and 5'-nucleotidase (a plasma membrane marker) were also associated with this fraction. By electron microscopy, the light membrane fraction was seen to contain tubular elements, multivesicular bodies (MVB), Golgi saccules, GERL, immature secretory granules, and some mitochondria. Electron microscopic cytochemical examination showed that these tubular structures were lysosomes. The dense lysosome fraction contained lysosomes positive for both AcPase and TMPase. After continuous incubation of isolated acinar cells with HRP, reaction product was rapidly localized to the light membrane fraction (greater than 2 min), where it was found in vesicles and tubular lysosomes. By 10 min it was present in MVB and tubular lysosomes, but by 60 min no HRP reaction product had appeared in the dense lysosomes. These results demonstrate that the tubular lysosomes are separable from dense lysosomes, typical secondary lysosomes, and are involved in the initial stages of endocytosis.

Acid Anhydride Hydrolases↗
PubMed1995

Cross-talk between calcium and cAMP-dependent intracellular signaling pathways. Implications for synergistic secretion in T84 colonic epithelial cells and rat pancreatic acinar cells.

Treatment of various cells with combinations of agents that increase either cAMP or cytosolic calcium can lead to synergistic responses. This study examined interactions, or cross-talk, between these two intracellular messengers and its implication for signaling in two secretory cell types, T84 human colonic epithelial cells and rat pancreatic acinar cells. T84 cell chloride secretion was measured in Ussing chambers. Acinar cell activation was monitored as amylase secretion. Cytosolic calcium was assessed via fura-2 microfluorimetry. A cell-permeant analogue of cAMP synergistically enhanced secretory responses to calcium-mobilizing hormones in both cell types, but paradoxically reduced overall calcium mobilization. The reduction in calcium mobilization could be attributed to an inhibition of calcium influx in T84 cells, although a different mechanism likely operates in acinar cells. The effects of the cAMP analogue were reproduced by other agents that increase cAMP. Furthermore, econazole, an inhibitor of calcium influx, potentiated secretory responses to calcium-dependent stimulation in T84 cells without itself inducing secretion. We conclude that there is cross-talk between calcium and cAMP-dependent signaling pathways at the level of second messenger generation in two secretory cell types. This cross-talk appears to regulate the extent of secretory responses.

Amylases↗
PubMed1995

Increased DT-diaphorase activity in transformed and tumorigenic pancreatic acinar cells.

Pancreatic acinar cells from rats treated in vitro with 5-azacytidine and/or transfected with an activated c-H-ras demonstrated transformation and tumorigenic phenotypes. DT-diaphorase (NAD(P)H:quinone oxidoreductase) activity was determined in these non-tumorigenic (3AP) and tumorigenic cells (T3AP and T5AM). T5AM cells were those treated with 5-azacytidine and further treated with N'-methyl-N'-nitro-nitrosoguanidine. Higher levels of enzyme activity were found in transformed cells when compared to that in control cells (> 15-fold, 3AP cells; > 40-fold, T3AP cells; > 20-fold T5AM cells). In contrast, NADPH-cytochrome c reductase activity was decreased in transformed cells (> 10-fold, 3AP cells; > 20-fold, T3AP cells; > 10-fold, T5AM cells). These studies demonstrated that pancreatic acinar cells are capable of undergoing alterations in enzyme activity patterns when transformed and that DT-diaphorase may be a good marker for malignant transformation.

Animals↗
PubMed2004

Aberrant acinar cell CA 19-9 expression and peri-insular acinar cell alterations in an adult human pancreas.

We herein report on a 23-year-old female patient who suffered from Crohn's disease and anorexia nervosa and died after long-term malnutrition and a perforated colitis. At autopsy, her pancreas displayed two peculiar findings. First, there was a constant and aberrant expression of CA 19-9 in the acinar cells. The expression of the carbohydrate antigen CA 19-9 is normally confined to duct-like epithelia, including centroacinar cells, while islet and acinar cells have repeatedly been reported to be immunohistochemically negative. Thus, to the best of our knowledge, our case is the first to show aberrant acinar CA 19-9 expression, and its potential meaning is discussed. Second, the pancreas showed a heterogeneity in acinar morphology, with peri-insular acini being considerably larger than tele-insular acini. The existence of enlarged peri-insular acini, mainly in animals, has occasionally been reported. Its origin, however, is still unclear. Some authors have proposed an influence of high insulin concentrations, exerted via the insulo-acinar capillary axis. We agree with the concept of an islet-derived mechanism. However, as we have observed a similar heterogeneity in streptozotocin- and autoimmune-diabetic rats, we presume that other islet hormones, in particular glucagon, might be more important for this phenomenon in the animals, as well as in the present case.

Adult↗
PubMed2006

DNA repair Ku proteins in gastric cancer cells and pancreatic acinar cells.

The DNA repair protein Ku acts as a heterodimer of Ku70 and Ku80 that binds to the DNA ends, nicks, or single-to-double-strand transition. It has a crucial role for DNA double-strand-break repair. Either Ku70 or Ku80 itself may have a unique function that is independent of the other Ku subunit. In this review, the role of Ku on cell proliferation and apoptosis will be discussed. Ku acts as a regulator of transcription by interacting with the recombination signal binding protein Jkappa and the NF-kappaB p50 homodimer to up-regulate p50 expression, which may regulate the proliferation of gastric cancer cells. Both Ku70 and Ku80 expressions are mediated by constitutively activated NF-kappaB and constitutively expressed cyclooxygenase-2 in gastric cancer cells, which may be related to gastric cell proliferation and carcinogenesis. In addition, nuclear loss of Ku may underlie the mechanism of apoptosis in pancreatic acinar cells after oxidative stress.

Animals↗
PubMed2006

Effects of the cholecystokinin A receptor antagonist loxiglumide on the proliferation and cell cycle time of pancreatic acinar cells in rats.

OBJECTIVES: Prior studies have indicated that endogenous or exogenous cholecystokinin (CCK) induces transient acinar cell proliferation at about 24 hours after its stimulation. The aims of the present study were to determine the time point when the administration of the CCK-A-receptor antagonist loxiglumide had its maximal suppressive effect on the proliferation of pancreatic acinar cells and to investigate the effects of loxiglumide on the cell cycle time of pancreatic acinar cells during transient acinar cell proliferation induced by endogenous or exogenous CCK. METHODS: Eight-week-old Wistar rats were divided into the following groups: preadministration of loxiglumide (40 mg/kg) intravenously at 120, 60, and 0 minutes before endogenous CCK stimulation induced by a single oral administration of camostat (50 mg/kg) or exogenous CCK stimulation by a subcutaneous injection of CCK-8 (6 g/kg body weight). For the controls, intravenous saline was used instead of loxiglumide (n = 7 in each group). The proliferative activity of pancreatic acinar cells at 24 hours after CCK stimulation and the cell cycle time of these proliferating pancreatic acinar cells were studied using an immunohistochemical technique. RESULTS: The most significant suppression of the proliferation of the acinar cells was observed in those groups which received loxiglumide 60 minutes before CCK stimulation (P < 0.016), but preadministration of loxiglumide had no effect on the cell cycle time of the proliferating acinar cells (not significant). CONCLUSION: CCK antagonist loxiglumide is expected as an excellent clinical applicable agent for acute pancreatitis. Previous researches suggest that CCK is an aggravating factor during the acute phase of acute pancreatitis, but CCK may be a healing factor during the recovery period. From the results of the present study, it can be said that the excess chronic administration of CCK antagonists during the acute phase of acute pancreatitis may prevent any regrowth of pancreatic cells during the healing period of acute pancreatitis.

Animals↗
PubMed1989

Epidermal growth factor inhibits rat pancreatic cell proliferation, causes acinar cell hypertrophy, and prevents caerulein-induced desensitization of amylase release.

The in vivo effects of epidermal growth factor (EGF) on pancreatic growth and digestive enzyme concentrations were compared with the actions of the pancreatic secretagogue caerulein in the adult rat. EGF (10 micrograms/kg BW) did not alter pancreatic weight or protein content. However, this concentration of EGF inhibited [3H]thymidine incorporation into DNA by 44%, decreased DNA content by 20%, and increased the concentrations of amylase, chymotrypsinogen, and protein by 106%, 232%, and 42%, respectively. Pancreatic acini prepared from EGF-treated rats exhibited a characteristic secretory response to caerulein that was superimposable to that obtained in acini from saline-treated rats. In both groups of acini half-maximal and maximal stimulation of amylase release occurred at approximately 5 pM and 50 pM caerulein, respectively. In contrast to EGF, caerulein (1 microgram/kg BW) increased pancreatic weight by 29% and protein content by 59%, and enhanced [3H]thymidine incorporation into DNA by 70%. Although caerulein increased the concentrations of pancreatic amylase and chymotrypsinogen by 38% and 297%, respectively, pancreatic acini prepared from caerulein-treated rats were less sensitive to the actions of caerulein in vitro when compared with acini from control rats. Indeed, the EC50 was shift from 4.8 pM to 9.8 pM after 4 days of treatment. EGF potentiated the actions of caerulein on pancreatic weight, protein content, and chymotrypsinogen concentration, and prevented the caerulein-induced alteration in the secretory responsiveness of the acinar cell. Conversely, caerulein reversed the inhibitory effect of EGF on thymidine incorporation. These findings suggest that EGF may modulate the trophic effects of certain gastrointestinal hormones, and may participate in the regulation of pancreatic exocrine function in vivo.

Amylases↗
PubMed1991

Oscillations of cytosolic sodium during calcium oscillations in exocrine acinar cells.

In acinar cells from rat salivary glands, cholinergic agonists cause oscillations in cytoplasmic free calcium concentration, which then drive oscillations of cell volume that reflect oscillating cell solute content and fluid secretion. By quantitative fluorescence ratio microscopy of an intracellular indicator dye for sodium, it has now been shown that large amplitude oscillations of sodium concentration were associated with the calcium and cell volume oscillations. Both calcium and sodium oscillations were dependent on the continued presence of calcium in the extracellular medium and were abolished by the specific sodium-potassium adenosine triphosphatase inhibitor ouabain. Thus, calcium oscillations in salivary acinar cells, by modulating the activities of ion transport pathways in the plasma membrane, can cause significant oscillations of monovalent ions that may in turn feed back to regulate calcium oscillations and fluid secretion.

Animals↗
PubMed1977

Development of acinar cells in the rat submandibular gland.

Three types of cells - terminal tubule cells, proacinar cells and acinar cells - have been observed during the development of acini in the rat submandibular gland. The terminal tubules are lined by terminal tubule cells which show PAS-positive, dark granules. From the terminal tubules pouches develop which are lined by similar cells to those lining the terminal tubules. These pouches give rise to the next generation of terminal tubules. The last generation of terminal tubules, whose cells lose their dark, PAS-positive granules, develop into secondary tubules lined by proacinar cells. At 14 days of age large coarse granules appear in the cytoplasm of the proacinar cells lining the secondary tubules as well as in the cells of intercalated ducts. These granules are discharged into the lumen of the tubule and the proacinar cells become foamy-looking acinar cells, while the secondary tubule becomes an acinus. Thus the terminal tubule cells give rise to proacinar cells which become acinar cells and cells to the intercalated duct cells. The development of acini in the rat submandibular gland thus takes place in three stages: (1) development of terminal tubules by continuing pouch formation up to 12 days of age, (2) conversion of terminal tubules into secondary tubules tined by proacinar cells from 6 to 12 days of age, and (3) development of large coarse granules in proacinar cells and their excretion into the lumen of tubules, resulting in the transformation of proacinar cells into acinar cells between 14 and 21 days.

Age Factors↗
PubMed1983

Characterization of basal lysosomes in exocrine acinar cells.

Exocrine acinar cells possess a unique system of basally located lysosomes. Cytochemically, these lysosomes do not contain acid phosphatase, but react positively for trimetaphosphatase (C Oliver: J Histochem Cytochem 28:78, 1980). The present study extends the morphological and cytochemical characterization of these lysosomes in pancreatic, parotid, and exorbital lacrimal acinar cells from Sprague-Dawley rats and National Institutes of Health Swiss mice. The basal lysosomes are highly pleomoric in nature, and frequently appear as a system of anastomosing tubules of varying width. The lysosomes have a close morphological relationship with both the rough endoplasmic reticulum and mitochondria. In addition to trimetaphosphatase activity, the lysosomes are reactive for aryl sulfatase B, thiolacetic acid esterase, and cholinesterase. Since the cholinesterase activity could not be inhibited by specific inhibitors, this activity is most likely due to the presence of nonspecific esterases. The results of this study confirm the lysosomal nature of the basal lysosomes and underscore the necessity of using multiple enzyme activities to identify and characterize lysosomes.

Acid Anhydride Hydrolases↗
PubMed1985

Activation of Ca2+-dependent Cl- and K+ conductances in rat and mouse parotid acinar cells.

Isolated acinar cells from rat and mouse parotid glands were studied with patch-clamp whole-cell current recordings. Acetylcholine (ACh) stimulation caused a transient inward current at a membrane potential of -70 mV, and a sustained outward current at a membrane potential of 0 mV, in quasi physiological Na+, K+ ion gradients, except the zero-Cl- ion gradient condition across the membrane. The reversal potential obtained from the ACh-evoked steady current was about -75 mV, in this ionic condition. When major Cl- ions of both the pipette and the bath solution were replaced, either by glutamate or by sulphate, only a large outward current was observed, at a membrane potential of -60 mV, in the presence of ACh. The addition of Ca2+-ionophore A23187 caused responses similar to those evoked by ACh. The reversal potential of A23187-induced current was close to the K+ equilibrium potential of -90 mV, in a Cl- -free condition. When K+-free NaCl solution was used in the pipette and the bath, A23187 caused only a large inward current, at a membrane potential of -60 mV. The reversal potential of A23187-evoked current was about -15 mV, in a symmetrical K+-free, NaCl condition. These results suggest that the ACh and A23187 activate Cl- as well as K+ conducting pathways via an increase in [Ca2+]i in the parotid acinar cells. The A23187-evoked large K+ current could not be explained solely by a rise in open probability of the channels.

Acetylcholine↗
PubMed1998

Growth factor regulation of the amylase promoter in a differentiating salivary acinar cell line.

Salivary glands contain two major epithelial cell types: acinar cells which produce the primary salivary secretion, including amylase, and ductal cells which reabsorb electrolytes but also secrete kallikrein. Here we investigated salivary acinar cell differentiation in vitro using the activity of the salivary amylase and tissue kallikrein promoters as markers of acinar cell and ductal cell differentiation, respectively. Each of the promoter sequences was cloned into a replication-deficient adenoviral vector containing the luciferase reporter gene. Previous studies showed that a human submandibular gland cell line (HSG) differentiated into acinar cells when cultured on a reconstituted basement membrane matrix (Matrigel). The luciferase activity of the amylase promoter vector (AdAMY-luc) was low in HSG cells cultured on plastic, where they grow as an epithelial monolayer. The promoter activity increased approximately tenfold when HSG cells were cultured on Matrigel and developed an acinar phenotype. Under the same conditions, the luciferase activity of the kallikrein promoter (AdKALL-luc) was not induced. Because HSG cells demonstrate acinar cell morphology, but not amylase gene expression, when cultured on laminin-1, certain soluble components of Matrigel were tested for their ability to induce the amylase promoter during in vitro differentiation of acinar cells. We find that epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha), which are present in the basement membrane, and hepatocyte growth factor (HGF) increase activity of the amylase promoter. Other basement membrane-derived growth factors such as TGF-beta, basic fibroblast growth factor (bFGF), and platelet-derived growth factor (PGDF), as well as tumor necrosis factor (TNF-alpha), keratinocyte growth factor (KGH), nerve growth factor (NGF) and interferon gamma (IFN-gamma) were inactive. This system will be further exploited to study the mechanisms by which extracellular matrix molecules and growth factors regulate salivary acinar cell differentiation.

Amylases↗
PubMed1996

Imaging of intracellular calcium stores in individual permeabilized pancreatic acinar cells. Apparent homogeneous cellular distribution of inositol 1,4,5-trisphosphate-sensitive stores in permeabilized pancreatic acinar cells.

Several lines of evidence suggest that the existence of a heterogeneous population of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3)-sensitive Ca2+ stores underlies the polarized agonist-induced rise in cytosolic Ca2+ concentration ([Ca2+]i) in pancreatic acinar cells (Kasai, H., Li, Y. X., and Miyashita, Y. (1993) Cell 74, 669-677; Thorn, P., Lawrie, A. M., Smith, P. M., Gallacher, D. V., and Petersen, O. H. (1993) Cell 74, 661-668). To investigate whether the apical pole of acinar cells contains Ca2+ stores which are relatively more sensitive to Ins(1,4,5)P3 than those in basolateral areas, we studied Ca2+ handling by Ca2+ stores in individual streptolysin O (SLO) permeabilized cells using the low affinity Ca2+ indicator Magfura-2 and an in situ imaging technique. The uptake of Ca2+ by intracellular Ca2+ stores was ATP-dependent. A steady-state level was reached within 10 min, and the free Ca2+ concentration inside loaded Ca2+ stores was estimated to be 70 microM. Ins(1,4,5)P3 induced Ca2+ release in a dose-dependent, "quantal" fashion. The kinetics of this release were similar to those reported for suspensions of permeabilized pancreatic acinar cells. Interestingly, the permeabilized acinar cells showed no intercellular variation in Ins(1,4,5)P3 sensitivity. Although SLO treatment is known to result in a considerable loss of cytosolic factors, permeabilization did not result in a redistribution of zymogen granules, as judged by electron microscope analysis. These results suggest that Ins(1,4,5)P3-sensitive Ca2+ stores are unlikely to be redistributed as a result of SLO treatment. The effects of Ins(1,4,5)P3 were therefore subsequently studied at the subcellular level. Detailed analysis demonstrated that no regional differences in Ins(1,4,5)P3 sensitivity exist in this permeabilized cell system. Therefore, we propose that additional cytosolic factors and/or the involvement of ryanodine receptors underlie the polarized pattern of agonist-induced Ca2+ signaling in intact pancreatic acinar cells.

Adenosine Triphosphate↗
PubMed2002

Transporter-mediated bile acid uptake causes Ca2+-dependent cell death in rat pancreatic acinar cells.

BACKGROUND & AIMS: The mechanism by which cholelithiasis increases the risk of acute pancreatitis remains obscure. Because bile acids can enter the pancreas either by luminal diffusion or by interstitial leakage during gallstone impaction and pancreatitis is associated with impaired Ca(2+) signaling, we examined the effect of bile acids on pancreatic acinar cell signaling and the associated intracellular events. METHODS: Rat pancreatic acinar cells were isolated by collagenase digestion and the effects of bile acids on [Ca(2+)](i) signaling, cell survival, inflammatory signals, and the molecular and functional expressions of bile uptake transporters were analyzed. RESULTS: Bile acids specifically inhibited the sarco/endoplasmic reticulum Ca(2+) ATPase pump to chronically deplete part of the Ca(2+) stored in the endoplasmic reticulum. This in turn led to the activation of capacitative Ca(2+) entry and a chronic [Ca(2+)](i) load. The increase in [Ca(2+)](i) and Ca(2+) load activated the inflammation-associated signals of c-Jun amino-terminal kinases and NF-kappaB and led to cell death, which was inhibited by buffering [Ca(2+)](i) with 1,2-bis(2-aminophenoxy)ethane-N,N,N,N'-tetraacetic acid. A comprehensive molecular analysis of bile acid transporters revealed that pancreatic acinar cells express the bile uptake transporters Na(+)-taurocholate co-transporting polypeptide and organic anion transporting polypeptide in the luminal and basolateral membranes, respectively. Bile acid uptake into acinar cells was in part Na(+)-dependent and in part Na(+)-independent, suggesting that both transporters contribute to bile acid influx into acinar cells. CONCLUSIONS: These results suggest that bile acids can be transported into pancreatic acinar cells through specific membrane transporters and induce cell death by impairing cellular Ca(2+) signaling.

Animals↗
PubMed1997

Comparative cytologic features of pancreatic acinar cell carcinoma and islet cell tumor.

Acinar cell carcinoma (ACC) and islet cell tumor (ICT), both rare pancreatic neoplasms, can be diagnosed accurately and rapidly with the use of imaging-guided fine-needle aspiration biopsies. The specific cytologic features of these tumors are described in a series of 17 patients, and histologic and immunocytochemical correlations are discussed. Important cytologic findings in ACC are loosely cohesive clusters with cells having uniform nuclei and prominent nucleoli, cytoplasm is finely granular and eosinophilic. Islet cell tumors show many single cells, occasional rosettes, uniform nuclei, sometimes binucleate, dense basophilic cytoplasm. Chromogranin is often positive (80%) in ICT. Trypsin and chymotrypsin were often positive (71%) in ACC. Histology was confirmatory in all cytology cases. The recognition of cytologic features in conjunction with immunocytochemical studies can increase the diagnostic sensitivity for these two rare tumors.

Adenoma, Islet Cell↗