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At least 19 recordsLinked to original sources
PubMed1996

Fine-needle aspiration cytology of islet cell tumors.

Islet cell tumors of the pancreas are neuroendocrine neoplasms whose biologic behavior has been well characterized. Frequently, these tumors produce one or more hormones which may strongly affect the patients' clinical presentation. In this study, we have examined fine-needle aspirates (FNA) from 13 islet cell tumors and have summarized their cytomorphologic appearances. The smears prepared from aspirates of the islet cell tumors displayed loose cellular arrangements and numerous single cells, with most cases demonstrating a predominance of single cells over the loose groups. An important diagnostic feature was the uniform appearance of the neoplastic cells. Nuclei were small to moderate in size, always round to oval in shape, and frequently contained small nucleoli. In 11 cases, the nuclear chromatin pattern was finely granular and evenly-distributed while in two cases the chromatin was coarser. Eccentrically located nuclei were commonly found and binucleated cells were seen in one-half of the aspirates. At least a moderate amount of finely granular cytoplasm was always identifiable. Immunocytochemical stains for neuron-specific enolase were positive in all five of our cases in which staining for this marker was attempted and chromogranin was positive in five of six cases. Generally, our cytomorphologic observations were supported by the findings of other investigators as reported in the cytology literature. The cytomorphologic characteristics of islet cell tumors are distinctive, and appropriate ancillary studies can be used to support the FNA diagnosis of this entity.

Adenoma, Islet Cell↗
PubMed1990

Binding of [3H]cytochalasin B to tumoral islet cells.

Tumoral pancreatic islet cells of the RINm5F line are equipped with two classes of [3H]cytochalasin B binding sites with respective Kd of 0.4 and 7 microM. The binding of the fungal metabolite and its dissociation from the binding sites display rapid time courses. The binding is inhibited by D-glucose, more than by L-glucose, by phlorizin and by cytochalasin E. These findings are considered in the light of the dual action of cytochalasin B upon hexose transport and motile activity in islet cells.

Adenoma, Islet Cell↗
PubMed2000

Ultrasound-guided laparoscopic resection of pancreatic islet cell tumors.

Pancreatic islet cell tumors represent a diverse group of neuroendocrine lesions. These tumors may be singular or multiple, benign or malignant, sporadic, or part of the constellation of multiple endocrine neoplasia type 1. Tumors such as insulinomas and gastrinomas produce gastrointestinal peptides that lead to diagnosis. Nonfunctioning lesions may be found incidentally or by screening patients at high risk for such tumors. Successful management of patients with pancreatic islet cell tumors relies on accurate localization and sound operative technique. With proper preoperative localization, advanced laparoscopic methods can be used to manage patients with these pancreatic neoplasms. Preoperative localization of pancreatic islet cell tumors was difficult in the past. Standard imaging and localizing modalities, such as computed tomography scanning, magnetic resonance imaging, angiography, transabdominal sonography, and portal venous sampling, yield only 24% to 75% accuracy. Consequently, many biochemically suspected lesions cannot be imaged with current techniques. Decreased tactile sensation of laparoscopy adds complexity to intraoperative identification. Endoscopic sonography and laparoscopic sonography provide accurate preoperative and intraoperative localization to enhance laparoscopic and open resection. The authors treated two patients with islet cell neoplasms using endoscopic sonography to preoperatively visualize the tumors and laparoscopic sonography to guide laparoscopic enucleation. Their approach and difficulties are discussed.

Adenoma, Islet Cell↗
PubMed1995

Clinical review 72: diagnosis and management of functioning islet cell tumors.

Functional islet cell tumors cause recognizable clinical syndromes based on the peptide products they secrete (Table 1). Frequently, the diagnosis of these tumors is delayed. A high index of suspicion coupled with the use of appropriate biochemical and provocative tests should lead to earlier diagnosis. A suggested management plan for patients suspected of having an islet cell tumor is shown in Fig. 1. Earlier diagnosis coupled with advances in preoperative and intraoperative localization techniques have resulted in an increased number of patients being cured.

Adenoma, Islet Cell↗
PubMed1987

Radiotherapy in the management of pancreatic islet cell tumors.

Malignant islet cell tumors are commonly treated with surgical resection. Chemotherapy is reserved for residual, unresectable, or metastatic disease. The role for radiotherapy has not been clearly defined. This article describes three cases of advanced islet cell tumors treated effectively with radiotherapy. This experience, in addition to that from other published reports, suggests that radiotherapy is a useful mode for treating advanced islet cell carcinoma.

Adenoma, Islet Cell↗
PubMed1997

Gelatinases and inhibitors of gelatinases in pancreatic islets and islet cell tumors.

Pancreatic islets contain trace amounts of zinc to form insulin dimer, and matrix metalloproteinases (MMPs) are single-chain zinc-containing metallo-enzymes. By immunocytochemically staining pancreatic tissue, which contained exocrine duct adenocarcinoma, normal islets were incidentally found positive for gelatinase-A (MMP-2) and gelatinase-B (MMP-9), and for tissue inhibitor of metalloproteinase 1 and 2 (TIMP-1 and TIMP-2). Normal islets from five pancreata were exclusively stained for two each of gelatinases and TIMPs. Twenty-two islet cell tumors were also stained for pancreatic hormones, gelatinases, and TIMPs, which included insulinomas, gastrinomas, glucagonomas, pancreatic polypeptide-omas (PPomas), and nonfunctioning tumor. In general, islet cell tumors were weakly stained for gelatinases and TIMPs, compared with normal islets in the adjacent pancreatic tissue. No clear difference in staining intensity among five kinds of islet cell tumors was observed. The selective immunolocalization of gelatinases and TIMPs in islet cells and islet cell tumors may suggest possible a structure-function relationship among zinc, gelatinases-TIMPs, and pancreatic hormones.

Adenocarcinoma↗
PubMed2002

New markers for pancreatic islets and islet cell tumors.

Islets of Langerhans account for 2 g of endocrine tissue in the pancreas, comprising approximately one million islets, with each containing 1000 endocrine cells. The major hormone secreted from the islets is insulin, which regulates blood glucose, the main fuel of the body. Islets also secrete glucagon, somatostatin and pancreatic polypeptide and all are involved in the paracrine mechanism. Islet cells can be stained immunohistochemically for the general endocrine markers, chromogranin A, synaptophysin, neuron-specific enolase and Leu7. Beta islet cells are well equipped with glucose transporter 2, which binds to glucose and regulates diffusion of glucose through the beta cell membrane. As all four islet hormones are initially synthesized as prohormones, all islet cells are equipped with prohormone convertase 1/3 and 2. In addition, islet cells also contain zinc-containing matrix metalloproteinases and their inhibitors, metallothionein, cyclin-dependent kinases and insulin-like growth factors, and many more hormones, peptides and enzymes. Thus, islets not only secrete insulin and other pancreatic hormones but are a complex organ whose major function is glucose homeostasis.

Adult↗
PubMed1987

Fructose metabolism via the pentose cycle in tumoral islet cells.

In tumoral islet cells (RINm5F line) the phosphorylation of D-fructose is catalyzed by hexokinase rather than fructokinase. Fructose 6-phosphate appears to be preferentially channelled into the pentose cycle, as suggested by a ratio of D-[1-14C]fructose/D-[U-14C]fructose oxidation close to 2.7, the failure to generate 14C-labelled lactate from D-[1-14C]fructose and a poor metabolic response to menadione. When the islet cells are exposed to both D-fructose and D-glucose, however, the metabolism of the former hexose is dramatically modified, fructose 6-phosphate being now formed at a lower rate and preferentially channelled into the glycolytic pathway. These findings illustrate the existence of regulatory steps in fructose catabolism located distally to its site of phosphorylation.

Adenoma, Islet Cell↗
PubMed1994

Is there a prognostic difference between functional and nonfunctional islet cell tumors?

BACKGROUND: Pancreatic islet cell tumors are categorized as either functioning or nonfunctioning. Functioning islet cell tumors (FIT) elaborate a variety of hormones, producing dramatic symptoms, while the initial presentation of non-functioning islet cell tumors (NIT) is commonly an abdominal mass or symptom complex related to invasion of adjacent structures. As a result, NIT are purported to present at a later stage, with lower resectability rates, and an overall poorer prognosis, when compared to FIT. In addition, a number of reports have indicated that the incidence of NIT has increased significantly in recent years. PATIENTS AND METHODS: Twenty-eight patients were studied retrospectively. All had islet cell tumors of the pancreas and were seen at the University of Nebraska Medical Center and affiliated Nebraska Methodist Hospital during a 19-year period. RESULTS: There were 9 patients (32%) in the NIT group and 19 (68%) in the FIT group. The mean ages at presentation were 61 years for the NIT and 52 years for the FIT group. In the NIT group, all presented with either abdominal pain (n = 7) or jaundice (n = 2). In contrast, over 90% of the patients with FIT had symptoms referable to the specific hormone elaborated by the tumor. Primary tumor size for NIT was 4.1 +/- 0.7 cm versus 5.0 +/- 0.6 cm for the FIT group. No significant difference was found for NIT versus FIT with respect to the incidence of metastatic disease at presentation (44% versus 53%), resectability rate with curative intent (44% versus 53%), or disease-free survival at 2 years (67% versus 40%). CONCLUSIONS: This series, in contrast to earlier reports, suggests that nonfunctioning islet cell tumors do not present at a more advanced stage, have lower resectability rates, or an overall poorer long-term prognosis when compared to functioning tumors.

Adenoma, Islet Cell↗
PubMed1981

Nonfunctioning islet cell tumors.

In nonfunctioning islet cell tumors of the pancreas, hormone production is not clinically evident. This type of tumor constituted 15% of all islet cell tumors seen at the Mayo Clinic from 1960 through 1978. Although identical to functioning islet cell tumors embryologically and histologically, the nonfunctioning tumors differ in presentation, location, size, and rate of malignancy. At admission to the hospital, patients often have pain or jaundice due to a large, solid, solitary lesion that occurs most commonly in the head of the pancreas. Extended survival is not excluded by the high malignancy rate (92%) of these slow-growing tumors. The survival rates at three and five years were 60% and 44%, respectively, even though most patients had metastatic disease at the time of exploration.

Adenoma, Islet Cell↗
PubMed1983

Clonal analysis of insulin and somatostatin secretion and L-dopa decarboxylase expression by a rat islet cell tumor.

A cell line, RIN-m, established from a transplantable rat islet cell tumor secretes insulin (IRI) and somatostatin (SRIF) and expresses high levels of the key amine precursor uptake and decarboxylation (APUD) cell enzyme L-dopa-decarboxylase (DDC). Conditioned medium from a rat pituitary tumor line GH3, secreting GH and PRL, improved the cloning efficiency of RIN-m cells 24-fold and enabled the isolation and establishment of a large number of primary and secondary clones. These clones were used to study clonal relationships between peptide hormone secretion and APUD features of an endocrine cell. All the primary and secondary clonal derivatives, irrespective of whether they secreted peptide hormones, maintained high levels of DDC activity. In contrast, IRI and SRIF secretion patterns of the primary clones were highly variable. Selective recloning of primary clones resulted in the isolation of subclones which produced either no hormones or high levels of either IRI or SRIF, but no clone that continuously secreted high levels of both IRI and SRIF. We conclude that: 1) the rat pituitary tumor line GH3 produces a factor(s), possibly GH and/or PRL, which dramatically affects the growth and cloning efficiency of rat islet tumor cells; 2) in contrast to the variability in hormone secretion patterns, DDC activity was consistently expressed in all clones and subclones; and 3) although wide fluctuation in hormone secretion levels occurred among the primary clones, subclones were obtained which revealed that IRI and SRIF can be expressed independently. The subclones of RIN-m developed should be useful for the analyses of factors influencing the synthesis, storage, and secretion of IRI and SRIF. The persistence of high DDC activity in the primary and secondary clones suggests that the APUD property of this endocrine cell may be a primitive differentiation feature closely related to the stem cell; in contrast, peptide hormone production may be associated with more terminal differentiation events.

Adenoma, Islet Cell↗
PubMed1989

Glucagon storage, release and degradation by tumoral islet cells (RINm5F line).

Tumoral islet cells of the RINm5F line contain and release glucagon. Over 90 min incubation, the secreted hormone represents about 50% of the final cell content (1.4 +/- 03 fg/cell). L-arginine augments modestly glucagon release, the relative magnitude of such an effect being inversely related to the concentration of D-glucose. The immunoreactive material secreted by the cells consists of both true glucagon (59-64%) and larger peptides. The RINm5F cells also release a proteolytic factor able to degrade exogenous glucagon or insulin. These results reveal that glucagon producing tumoral cells display several abnormal features in their secretory behaviour.

Adenoma, Islet Cell↗
PubMed1975

Islet cell tumors in childhood.

Islet cell tumors in children are briefly reviewed. Three of the total of 53 children reported in the literature are described in detail. Special emphasis is directed to localization of the tumor by angiography. The difficulties of localizing the tumor in neonates is discussed. Treatment consists in excision of the insulinoma or, if it is not possible to localize the tumor, in subtotal or total pancreatectomy.

Adenoma, Islet Cell↗
PubMed1986

[Carcinoid of ectopic pancreas tissue--islet cell tumor].

A case of islet cell tumor--carcinoid of the ectopic pancreas is reported. The patient had been operated six times because of recurrent abdominal tumor mass and intermittent hypoglycemic coma. The first five operations were done with the diagnosis of mesotheliosarcoma by pathology. The last operation was done in our hospital with the final diagnosis of carcinoid--islet cell tumor. In addition to the light microscopic view, several diagnostic features were observed as follows: Under electron microscopy, membrane bound secretive granules were present in the tumor cytoplasm. Neither brush-like microvilli nor lumen formation of the mesothelioma were found. By immunohistochemistry, positive granules to immunoperoxidase stain of insulin were observed in some tumor cytoplasm. By laboratory test, levels of blood 5-hydroxytryptamine and urinary 5-hydroxyindolacetic acid were elevated. Sometimes it is difficult to differentiate carcinoid from islet cell tumor only by morphology, because both are derived from the same origin during the embryonic development which is probably related to the endocrine system from the embryonic foregut. The latter arises from the neuro-ectoderm and belongs to APUD system.

Abdominal Neoplasms↗
PubMed1985

Pancreatic polypeptide in islet cell tumors. Morphologic and functional correlations.

Twelve islet cell tumors and one islet cell hyperplasia were studied with immunocytochemical and radioimmunoassay methods. With immunocytochemical staining, all six insulinomas, one mixed insulinoma-glucagonoma, and four gastrinomas were positive for insulin, insulin and glucagon, and gastrin, respectively. Pancreatic polypeptide (PP) was positive in three insulinomas and one mixed insulinoma-glucagonoma. All of the tumors were positive for neuron-specific enolase (NSE). Radioimmunoassays of tissue extracts further disclosed that all functioning tumors contained more than one pancreatic hormone. PP concentrations of two insulinomas and one mixed insulinoma-glucagonoma were higher than that of normal control pancreases. A study of protein meal-stimulated PP secretion revealed that three of the insulinoma cases and two gastrinoma cases exhibited higher plasma PP levels than the age-matched controls. The findings suggest that: both functioning and nonfunctioning islet cell tumors derive from neuroendocrine cells positive for NSE; all functioning islet cell tumors appear to contain PP in the tumor tissue as a minor component; as many as 70% of the patients with islet cell tumors present with abnormally higher plasma PP levels after protein meals; and a study of meal-stimulated PP secretion may well be used as a marker for the presence of functional islet cell tumors.

Adenoma, Islet Cell↗
PubMed1986

Cloned cell lines from a transplantable islet cell tumor are heterogeneous and express cholecystokinin in addition to islet hormones.

A liver metastasis (MSL) with a remarkable in vitro proliferation potential has been identified in an NEDH rat carrying a transplantable x-ray-induced islet cell tumor. Two insulin-secreting cell lines, MSL-G and MSL-H, with doubling times of 3-5 d were established by repeated limiting dilution cloning. In vivo inoculation of MSL-G cells induced severe hypoglycemia caused by a small but highly heterogeneous tumor as revealed by immunocytochemistry. Whereas most cells stained for the islet hormones, insulin, glucagon, and somatostatin, clustered cells were discovered to contain cholecystokinin (CCK). Additional in vitro-limiting dilution cloning, followed by immunocytochemical characterization, clearly demonstrated the capacity of single cell clones to simultaneously express the same four hormones. Radioimmunoassays with a panel of site-specific antisera of culture supernatants and purified cell extracts showed the MSL-G2 cells to produce, store, and secrete readily detectable amounts of processed and unprocessed CCK. Gastrin was not detected while coexpression of glucagon and CCK were demonstrated. Mutant clones selected for resistance to 6-thioguanine (frequency, 2 X 10(-7] and checked for HAT (hypoxanthine, aminopterin, thymidine) sensitivity retained the capacity for multi-hormone expression. We propose that the MSL tumor contains pluripotent endocrine stem cells. The MSL tumor and the MSL-G2 cells in particular will allow studies of not only CCK biosynthesis and processing but also of mechanisms involved in tumor and islet cell differentiation.

Adenoma, Islet Cell↗