Immunoexpression of Villin in Neuroendocrine Tumors and Its Diagnostic Implications

1999 ◽  
Vol 123 (9) ◽  
pp. 812-816
Author(s):  
Paul J. Zhang ◽  
Kenneth R. Harris ◽  
Bachir Alobeid ◽  
John J. Brooks
Keyword(s):  
Neuroendocrine Tumors ◽  
Brush Border ◽  
Islet Cell ◽  
Intestinal Tract ◽  
Small Cell ◽  
Merkel Cell ◽  
Round Cell ◽  
Islet Cell Tumors ◽  
Microfilament Bundles ◽  
Different Origins

Abstract Background.—Villin, a 95-kd cytoskeletal protein associated with axial microfilament bundles of brush border microvilli, is mostly restricted to intestinal glandular tumors. Villin immunoexpression was recently observed in a small number of carcinoids of the intestinal tract and lung, but its significance in a broad category of neuroendocrine tumors has not been evaluated. Design.—A total of 114 neuroendocrine tumors of different origins were tested for villin expression. They included gastrointestinal carcinoids (n = 30), lung carcinoids (n = 15), small cell carcinomas of the lung (n = 24), small cell carcinomas of other sites (n = 15), islet cell tumors (n = 8), Merkel cell carcinomas (n = 6), paragangliomas (n = 6), and others (n = 10). Nine round cell sarcomas were tested as well. Results.—Villin immunoreactivity was present in 85% of gastrointestinal carcinoids and small cell carcinomas, but was found in only 40% of lung carcinoids. Other tumors tested were virtually negative for villin. In general, while cytoplasmic reactivity was most common, a characteristic apical membranous pattern simulating brush border was seen in 76% of the gastrointestinal carcinoids and in 50% of the lung carcinoids. Conclusions.—We found that villin was predominantly restricted to gastrointestinal neuroendocrine tumors (excluding islet cell tumors), although a small number of bronchial carcinoids may be positive as well. These results suggest a role for villin in the differential diagnosis of neuroendocrine tumors.

Nuclear Localization of E-Cadherin Expression in Merkel Cell Carcinoma

2000 ◽  
Vol 124 (8) ◽  
pp. 1147-1151 ◽  
Author(s):  
Aaron C. Han ◽  
Alejandro Peralta Soler ◽  
Chik-Kwun Tang ◽  
Karen A. Knudsen ◽  
Hernando Salazar
Keyword(s):  
Cell Carcinoma ◽  
Merkel Cell Carcinoma ◽  
Neuroendocrine Tumors ◽  
Nuclear Localization ◽  
Critical Role ◽  
Immunohistochemical Analysis ◽  
Cell Types ◽  
Small Cell ◽  
Merkel Cell ◽  
E Cadherin

Abstract Context.—Cadherins are cell-cell adhesion proteins that act as tumor suppressor genes and have a critical role in cell sorting and tissue formation during organogenesis. The pattern of cadherin expression constitutes a useful diagnostic and prognostic tool in the evaluation of tumors and for determining the histogenesis of tumor cells. We have previously characterized the cell types of several tumors based on the expression of individual cadherins. Objective.—To investigate the expression of cadherins in Merkel cell carcinomas. Design.—Paraffin immunohistochemical analysis of the 3 best-studied cadherins was performed on 35 cases of Merkel cell carcinoma. Results.—E-cadherin was expressed in 34 (97%) of 35 Merkel cell carcinomas examined, N-cadherin was expressed in 22 (63%) of 35 cases, and P-cadherin was expressed in 15 (43%) of 35 cases. This frequency of cadherin expression was similar to a group of small cell and neuroendocrine tumors from other primary sites. Interestingly, the localization of E-cadherin expression was unique in Merkel cell carcinomas compared with other primary neuroendocrine tumors. Merkel cell carcinomas showed marked preference for nuclear versus membrane localization, whereas small cell tumors from other sites showed fewer cases of nuclear E-cadherin expression. The nuclear localization of E-cadherin did not correlate with cadherin-associated protein β-catenin nuclear expression. Conclusions.—Our findings show that E-cadherin is the most frequently expressed cadherin in Merkel cell carcinoma, followed in frequency by N-cadherin then P-cadherin. The pattern of nuclear E-cadherin expression is more frequent for Merkel cell carcinoma than small cell tumors of other primary sites. These observations suggest that E-cadherin expression and function are altered in Merkel cell carcinoma, and this finding has potential use in the differential diagnosis of these tumors.

Ulcerogenic Tumors of the Pancreas

1968 ◽  
Vol 26 ◽  
pp. 186-187
Author(s):  
J. C. Garancis ◽  
J. F. Kuzma ◽  
S. D. Wilson ◽  
E. H. Ellison
Keyword(s):  
Endoplasmic Reticulum ◽  
Tumor Cells ◽  
Islet Cell ◽  
Disease Process ◽  
Central Core ◽  
Islet Cell Tumors ◽  
Opaque Zone ◽  
Granular Form ◽  
Zollinger Ellison Syndrome

It has been proposed that a gastrin-like hormone elaborated by non-beta islet tumors of the pancreas may be responsible for a fulminating ulcer diathesis. Subsequently, a potent gastric secretagogue was isolated from ulcerogenic tumors of the pancreas. This disease process is known now as “Zollinger-Ellison syndrome”.In our studies of two cases of Zollinger-Ellison syndrome, pancreatic lesions were identified as alpha islet cell tumors (Fig. 1). Tumor cells were fairly uniform. The sizes of the alpha granules were not significantly different, but their number and distribution varied greatly from one cell to another. Each granule consisted of a round, highly dense central core, separated from the limiting membrane by an opaque zone. The granular form of the endoplasmic reticulum was particularly prominent. Numerous mitochondria, round or elongated, were dispersed throughout the cytoplasm. Individual or clusters of lysosomes were observed in the majority of cells.

Islet Cell Tumors of the Pancreas

1994 ◽  
Vol 23 (1) ◽  
pp. 53-65 ◽  
Author(s):  
Rena Vassilopoulou-Sellin ◽  
Jaffer Ajani
Keyword(s):  
Islet Cell ◽  
Islet Cell Tumors

Diarrhea associated with pancreatic islet-cell tumors

1964 ◽  
Vol 9 (2) ◽  
pp. 97-108 ◽  
Author(s):  
Julien Deleu ◽  
Hendrik Tytgat ◽  
Guy E. Goidsenhoven
Keyword(s):  
Pancreatic Islet ◽  
Islet Cell ◽  
Islet Cell Tumors ◽  
Pancreatic Islet Cell ◽  
Pancreatic Islet Cell Tumors

scholarly journals Non-Islet Origin of Pancreatic Islet Cell Tumors

2004 ◽  
Vol 89 (4) ◽  
pp. 1934-1938 ◽  
Author(s):  
Alexander O. Vortmeyer ◽  
Steve Huang ◽  
Irina Lubensky ◽  
Zhengping Zhuang
Keyword(s):  
Pancreatic Islet ◽  
Islet Cell ◽  
Islet Cell Tumors ◽  
Pancreatic Islet Cell ◽  
Pancreatic Islet Cell Tumors

scholarly journals Immunohistochemistry of Pancreatic Islet Cell Tumors in the Ferret (Mustela putorius furo)

1997 ◽  
Vol 34 (5) ◽  
pp. 387-393 ◽  
Author(s):  
G. A. Andrews ◽  
N. C. Myers ◽  
C. Chard-Bergstrom
Keyword(s):  
Pancreatic Islets ◽  
Pancreatic Islet ◽  
Pancreatic Polypeptide ◽  
Islet Cell ◽  
Islet Cells ◽  
Neuron Specific Enolase ◽  
Islet Cell Tumors ◽  
Pancreatic Islet Cell ◽  
Formalin Fixed Paraffin Embedded ◽  
Pancreatic Islet Cell Tumors

Twenty-two pancreatic islet cell tumors and normal pancreatic islets from ferrets were evaluated by immunohistochemistry for expression of the peptide hormones insulin, somatostatin, glucagon, and pancreatic polypeptide (PP) and the neuroendocrine markers chromogranin A (CgA) and neuron-specific enolase (NSE). In normal pancreatic islets, the majority of cells stained strongly with CgA and NSE. A cells, B cells, D cells, and PP cells stained strongly with glucagon, insulin, somatostatin, and PP, respectively. All 22 tumors stained with CgA and NSE. The proportion of cells within tumors staining for CgA was variable, but more than half of the cells stained positively in 18 of the tumors. The intensity of staining for CgA was strong (reactivity equivalent to or greater than normal islet cells in adjacent tissue) in 11 moderate in six, and weak in five of the tumors. All tumors stained for NSE, with ≥50% of the cells staining in 21 of the tumors, and the intensity of staining was strong in 18 of the tumors. Twenty of 22 tumors stained positively for insulin, with ≥50% of the cells staining in 19 of them. The intensity of staining for insulin was strong in 12, moderate in seven, and weak in one of the tumors. Approximately ≤1% of the cells in 15 of 22 tumors stained for somatostatin, five tumors stained for pancreatic polypeptide, and three tumors stained for glucagon. These data indicate that the majority of islet cell tumors of ferrets express immunohistochemically detectable insulin. CgA and NSE are both useful general markers for such tumors, including those that are insulin negative. Commercially available antisera to CgA, NSE, insulin, glucagon, somatostatin, and PP work well in formalin-fixed, paraffin-embedded tissue for immunophenotyping islet cell tumors in the ferret.

Tailored imaging of islet cell tumors of the pancreas amidst increasing options

2012 ◽  
Vol 82 (2) ◽  
pp. 213-226 ◽  
Author(s):  
Helle-Brit Fiebrich ◽  
Sophie J. van Asselt ◽  
Adrienne H. Brouwers ◽  
Hendrik M. van Dullemen ◽  
Milan E.J. Pijl ◽  
...  
Keyword(s):  
Islet Cell ◽  
Islet Cell Tumors

Insulin and glucagon in rats with Islet cell tumors Induced by small doses of streptozofoclii

1981 ◽  
Vol 59 (8) ◽  
pp. 818-823 ◽  
Author(s):  
Gen Yoshino ◽  
Tsutomu Kazumi ◽  
Soichiro Morita ◽  
Shighaki Baba
Keyword(s):  
Plasma Glucose ◽  
Islet Cell ◽  
Insulin Response ◽  
Oral Glucose ◽  
Islet Cell Tumors ◽  
Glucose Levels ◽  
Tumor Bearing ◽  
Small Doses ◽  
Wet Weight ◽  
Glucose Plasma

Plasma insulin and glucagon responses to oral glucose loading were examined in rats with islet cell tumors induced by a single intravenous injection of streptozotocin (30 or 40 mg/kg body weight). Twenty-four macroscopic and six microscopic tumors occurred in 21 rats. In 15 of 21 tumor-bearing rats, there was exaggerated insulin release in response to oral glucose. Plasma glucose levels did not rise with the oral glucose load and were comparable to those seen in normal animals. Hence these rats are described as having "responsive tumors." In six rats with "nonresponsive tumors" there was no insulin response and the plasma glucose levels rose. No significant differences in plasma glucagon levels were observed between the two groups. Nonresponsive tumors as well as responsive tumors contained a significant amount of extractable insulin (17.68 ± 8.60 and 35.07 ± 10.05 mg/g wet weight, respectively) and detectable amounts of immunoreactive glucagon (1.47 ± 0.61 and 2.24 ± 0.67 μg/g wet weight, respectively).These results suggest that a small dose of streptozotocin produces two types of islet cell tumors. One is insulin producing and insulin secreting whereas the other is insulin producing but not insulin secreting.

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