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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acinar cell carcinoma is a rare pancreatic neoplasm that may contain scattered endocrine cells in as many as 40% of cases. In addition, unusual tumors exist in which the acinar and endocrine components each constitute a significant proportion (> 25%) of the neoplasm; we propose to designate them as "mixed acinar-endocrine carcinomas." In a study of five such cases, we found one case with segregated areas of acinar and endocrine cells that were identifiable in routinely stained sections and four cases with morphologically uniform cell populations where the divergent differentiation was only detected immunohistochemically. The tumors occurred in adults (age range, 48-81; mean, 68); there were two men and three women. None of the patients presented with symptoms related to either enzyme or hormone liberation. Histologically, the tumors were very cellular; various combinations of solid, trabecular, acinar, and glandular growth patterns were noted. The cells contained d-PAS-positive granules and showed immunohistochemical positivity for pancreatic enzymes (trypsin, chymotrypsin, and lipase) and endocrine markers (chromogranin and synaptophysin); specific endocrine hormones were found in two cases. Double immunohistochemical staining for acinar and endocrine markers showed that most cells expressed only one line of differentiation. Ultrastructural study of two cases showed two populations of granules. Two of the patients died of their tumors (mean survival, 10.5 months), one with widespread metastases. Two patients were alive with disease at 12 months after diagnosis, and one patient was lost to follow-up after 3 months. This rare type of pancreatic neoplasm provides further evidence of the close histogenetic relationship between the exocrine and endocrine components of this organ.
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PMID:Mixed acinar-endocrine carcinomas of the pancreas. 803 90

Phospholipase C (PLC) activity and its response to stimulation by bile acids was assayed in cellular extracts from 16 primary human colon tumors of various Duke's stages and paired adjacent normal mucosal samples. In the absence of bile acid, there was negligible degradation of phosphatidylinositol (PI) 1-stearoyl-2-[14C]-arachiodonoyl by tumor or normal tissue, but the addition of deoxycholic acid (DCA) or taurocholic acid (TCA) resulted in concentration-dependent and time-dependent stimulation of diacylglycerol (DAG) formation at optimal concentrations of 2 mM DCA and 4 mM TCA. Triton X-100 (0.125-1.0%) inhibited rather than enhanced the PI-degrading activity of these extracts, indicating that the stimulatory effects of DCA and TCA were not simply due to a detergent effect. Under the same assay conditions there was only a small amount of labeled monoacylglycerol or free arachidonic acid produced by extracts incubated in the absence or presence of DCA or TCA. No major differences in DAG production from PI were seen between paired samples of normal colon mucosa and primary colon tumors, in assays done in the presence of 2 mM TCA. Extracts from tumors in the distal part of the colon had higher activity than those from the proximal colon. This was also true for the extent of release of free arachidonic acid from labeled PI. Under the same conditions, labeled phosphatidylcholine or phosphatidylethanolamine did not serve as substrates for the colon mucosa or tumor extracts. Nor was there significant hydrolysis of the labeled DAG (1-stearoyl-2-14C-arachidonoylglycerol) by normal colon mucosa or tumor extracts, in the absence or presence of DCA or TCA. On the other hand, a low level of DAG lipase activity was detected in the presence of Triton X-100. These findings provide the first evidence that normal human colon mucosa and primary colon tumors contain a PI-specific PLC activity that is markedly stimulated by bile acids. Our results also suggest that bile acids may enhance colon carcinogenesis by acting on this enzyme system, thereby influencing signal transduction pathways in the target cells.
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PMID:The effects of bile acids on phospholipase C activity in extracts of normal human colon mucosa and primary colon tumors. 814 13

Cystic islet-cell tumors are rare neoplasms that may be confused with more familiar cystic pancreatic lesions, such as pseudocysts, serous cystadenoma, and mucinous tumors. Analysis of aspirated cyst fluid for tumor markers (carcinoembryonic antigen [CEA], CA-125, and CA-15.3), enzymes (amylase and lipase), viscosity, and cytology has been proposed as an aid to preoperative differential diagnosis. These tests will distinguish mucinous from nonmucinous cysts and usually help in determining malignancy. However, cyst fluid parameters from rarer types of pancreatic cystic tumors have not been described. We report the clinical and pathologic features of two cystic islet-cell tumors including cyst fluid parameters in one of the cases. Two cases of cystic islet-cell tumors were identified by clinical history, histopathologic, and immunohistochemical techniques. Cyst fluid was aspirated intraoperatively from one case and analyzed for CEA, CA-125, CA 15.3, insulin, amylase, viscosity, and cytology. Cyst fluid analysis showed low values for CEA, CA-125, and CA-15.3, low viscosity, and variable amylase content. This spectrum of findings is similar to that of serous cystadenomas. Cyst fluid cytologic examination was positive for neuroendocrine-type epithelial cells and insulin levels were elevated, observations indicative of an islet-cell tumor. Analysis of fluid from cystic islet-cell tumors may aid in the preoperative differentiation of these tumors from more common pancreatic cystic lesions. These findings represent the first report of the characteristics of the fluid in these uncommon tumors.
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PMID:Pancreatic cystic islet-cell tumors. Clinical and pathologic features in two cases with cyst fluid analysis. 819 44

In a series of 22 pancreatic acinar cell carcinomas, including two acinar cystadenocarcinomas, cellular differentiation was analyzed by immunocytochemistry and electron microscopy. In addition, overexpression of p53 protein and Ki-ras codon 12 mutation was studied. Four of the 20 noncystic acinar cell carcinomas showed a pure acinar pattern, nine an acinar-solid, and seven a solid pattern. All tumors stained for at least one of the following pancreatic acinar markers: trypsin (21 of 22), lipase (19 of 22), chymotrypsin (13 of 22), phospholipase A2 (nine of 22), and pancreatic stone protein (19 of 22). One-third of the tumors expressed neuroendocrine markers (synaptophysin, eight of 22; chromogranin A, six of 21) and duct cell markers (CA19.9, nine of 21; B72.3, six of 21). Cellular coexpression of trypsin and synaptophysin was demonstrated in one tumor. Electron microscopy revealed zymogen granules (nine of nine). In only one of 16 tumors a Ki-ras mutation at codon 12 was found, whereas in none of 19 tumors could overexpression of p53 protein be demonstrated. The results suggest that acinar cell carcinomas show obvious capacity to differentiate into several directions, but nevertheless constitute an entity different from ductal adenocarcinomas or endocrine tumors.
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PMID:Pancreatic acinar cell carcinoma. An analysis of cell lineage markers, p53 expression, and Ki-ras mutation. 836 71

The medical records of 101 dogs with acute pancreatitis, diagnosed on the basis of medical histories of acute vomiting, with serum lipase or amylase activity greater than the reference range, or with gross signs of pancreatitis at surgery or histopathologic evidence at necropsy, were evaluated to identify potential risk factors for the development of acute pancreatitis. Age, sex, and breed of dogs with acute pancreatitis were compared with those from a reference population of 100 dogs admitted for other medical emergencies during the same period. Analysis of multiple regression models indicated that dogs > 7 years old were at increased risk for acute pancreatitis. Spayed dogs and castrated male dogs had an increased risk, compared with that of sexually intact males. Similarly, terrier and nonsporting breeds appeared to be at higher risk of developing acute pancreatitis than were other breed types. Most dogs in this study (63/101) had intercurrent diseases, including diabetes mellitus (n = 14), hyperadrenocorticism (n = 12), chronic renal failure (n = 8), neoplasia (n = 17), congestive heart failure (n = 6), and autoimmune disorders (n = 5). Fourteen dogs had undergone anesthesia or surgery in the week before admission; only 3 had undergone abdominal procedures. Recent medication use was listed in 52 of 101 cases. Antibiotics (n = 18) and corticosteroids (n = 18) were most frequently described. Anticancer chemotherapeutic agents (n = 5) and organophosphate insecticides (n = 5) also were listed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Risk factors associated with acute pancreatitis in dogs: 101 cases (1985-1990). 840 36

Pancreatic cystic lesions include inflammatory pseudocysts, benign serous tumors, and mucinous neoplasms, some of which are malignant. Clinical and radiologic indices are often inadequate to discriminate reliably among these possibilities. In an attempt to develop new preoperative diagnostic criteria to assist in decisions regarding therapy, the authors have performed cyst fluid analysis for tumor markers (carcinoembryonic antigen: CEA, CA 125, and CA 19.9), amylase content, amylase isoenzymes, relative viscosity, and cytology on 26 pancreatic cysts. The cases included nine pseudocysts, five serous cystadenomas, 4 mucinous cystic neoplasms, 7 mucinous cystadenocarcinomas, and one mucinous ductal adenocarcinoma with cystic degeneration. Carcinoembryonic antigen levels were high (> 367) in all benign and malignant mucinous cysts, but were low (< 23) in the pseudocysts and benign serous cystadenomas, an indication that CEA discriminates between mucinous and nonmucinous cysts (p < 0.0001). Values for CA 125 were high in all malignant cysts, low in pseudocysts, and variable in mucinous cystic neoplasms and serous cystadenomas. Levels of Ca 19.9 were nondiscriminatory. Cyst fluid amylase and lipase content were variable but were generally high in pseudocysts and low in cystic tumors. Amylase isoenzyme analysis was useful to differentiate pseudocysts from cystic tumors. Measurement of the relative viscosity in cyst fluid showed high (> serum viscosity) values in 89% of mucinous tumors and low values (< serum) in all pseudocysts and serous cystadenomas (p < 0.01). Cytologic analysis of cyst fluids was of limited value in differentiating pseudocysts from serous cystadenoma, but in seven of eight mucinous tumors provided useful diagnostic information and correctly classified three of five malignant tumors. The authors conclude that cyst fluid analysis can provide a preoperative classification of these diagnostically difficult lesions. The combination of viscosity, CEA, CA 125, and cytology can reliably distinguish malignant cystic tumors and potentially premalignant mucinous cystic neoplasms from pseudocysts and serous cystadenomas. Amylase content with isoenzyme analysis is useful to identify pseudocysts.
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PMID:Cyst fluid analysis in the differential diagnosis of pancreatic cysts. A comparison of pseudocysts, serous cystadenomas, mucinous cystic neoplasms, and mucinous cystadenocarcinoma. 842 99

To establish a suitable control for pancreatic tumor cell lines, we have isolated and cultured primary human pancreatic duct cells from transplant donors. Duct cells were isolated by dissecting the main pancreatic duct and first-degree branches and enzymatic digestion. Aggregates of cells were cultured for 1 up to 5 weeks and monitored for changes in morphology and growth by phase contrast microscopy. Contaminating fibroblasts were mechanically removed from day 4 on and by cloning of epithelial cells. Cultured cells were characterized by phase contrast microscopy, electron microscopy, and immunofluorescence with antibodies against intermediate filaments (cytokeratins, vimentin, desmin), mucins (Du-Pan-2, CA 19-9), carbonic anhydrase II, acinar cell enzymes (amylase, lipase, trypsin), and islet cells. About 90% of the cultured cells could be identified as ductal epithelial cells by their expression of cytokeratins, mucins, and carbonic anhydrase II. These cells showed the ultrastructural features of duct cells. After 3-5 weeks of culture, most of the cultured cells showed co-expression of cytokeratins and vimentin in addition to duct cell markers. About 10% of cells were contaminating fibroblasts (vimentin positive, cytokeratin negative). The cultured normal human duct cells as the postulated cells of origin of the pancreatic adenocarcinoma may serve as a useful control for cultured pancreatic tumor cell lines.
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PMID:Isolation, culture, and characterization of human pancreatic duct cells. 846 98

Current evidences clearly point out that an increase in lipid peroxidation influences lipid metabolism in cancer patients. Several investigations recognize selenium as a potent antioxidant, as well as an anticarcinogen, in both animal and human systems. Selenium was administered to Wistar rats bearing mammary tumor induced by 7,12-dimethylbenz(a)anthracene (DMBA) to study alterations in the concentration of lipid profiles and in the activities of some lipid metabolising enzymes. Control and tumor-bearing rats administered with selenium, were fed 5 mg sodium selenite/kg diet from the day of tumor induction. Plasma total lipids, total cholesterol, free fatty acids, triglycerides, phospholipids, VLDL and LDL cholesterol were significantly lower in selenium-treated rats bearing tumors, whereas, plasma ester cholesterol and HDL cholesterol were significantly greater due to selenium administration in DMBA induced-tumor rats. Total lipase and lecithin: cholesterol acyltransferase registered greater activities in plasma of selenium administered rats with tumor, while the activity of preheparin lipoprotein lipases in plasma of rats bearing tumors was lower due to selenium administration. These observations clearly indicate the effect of selenium in correcting the abnormalities of lipid metabolism in tumor-induced rats.
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PMID:Effect of selenium on lipids and some lipid metabolising enzymes in DMBA induced mammary tumor rats. 853 19

A 51-year-old man developed a large retroperitoneal tumor with liver and lymph node metastases; there was no radiological evidence of pancreatic involvement. Despite the progression of disease, results of laboratory tests, notably serum amylase, were normal except for minor increases in aspartate aminotransferase and gamma-glutamyltransferase and a marked increase in lipase. The increased lipase was not attributable to formation of macroenzyme. To determine the source of the lipase, we fractionated serum and a tumor biopsy homogenate, using electrophoresis. The lipase pattern obtained from the patient's serum differed from that seen in serum from a patient with acute pancreatitis. Additionally, the lipase pattern obtained from a homogenate of biopsy sample from the retroperitoneal tumor did not match the pattern observed for normal pancreas. Apparently, the source of this increased serum lipase activity was the nonpancreatic tumor.
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PMID:Chronic increased serum lipase without evidence of pancreatitis: tumor-derived lipase? 859 14

We report at unique, previously unreported pancreatic tumor occurring in a 60-year-old woman who was preoperative diagnosed on cytoaspiration as having clear cell carcinoma. The resected tumor consisted of a population of large epithelioid cells with clear or eosinophilic, granular cytoplasm, rich in glycogen, with nuclear pleomorphism and no mitotic activity. In spite of the epithelioid appearance, the tumor cells were negative for epithelial (CAM 5.2, KL1, AE1-AE3), endocrine (neuron-specific enolase [NSE], chromogranin A), and acinar (lipase, amylase) markers and positive for actin and melanogenesis-related marker HMB 45. Ultrastructurally, the neoplastic cells showed membrane-bound granules; no evidence of either epithelial or melanocytic differentiation was present. These morphophenotypic features have never been reported in a pancreatic tumor and overlap those of clear cell "sugar" tumor of the lung. The same morphophenotypic features are observed in a family of lesions characterized by the presence of the perivascular epithelioid cell that also includes lymphangiomyomatosis and angiomyolipoma. The present case may be considered a novel member of this family of lesions. We propose this new entity be named clear cell "sugar" tumor of the pancreas.
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PMID:Clear cell "sugar" tumor of the pancreas. A novel member of the family of lesions characterized by the presence of perivascular epithelioid cells. 865 52


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