Ulcerogenic Tumors of the Pancreas

Author(s):  
J. C. Garancis ◽  
J. F. Kuzma ◽  
S. D. Wilson ◽  
E. H. Ellison

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.

1968 ◽  
Vol 115 (2) ◽  
pp. 177-184 ◽  
Author(s):  
James C. Thompson ◽  
Frank M. Hirose ◽  
Carlos A.E. Lemmi ◽  
Warren D. Davidson

1997 ◽  
Vol 33 (6) ◽  
pp. 524-527 ◽  
Author(s):  
RA Green ◽  
CL Gartrell

Islet-cell tumors of the pancreas, such as gastrinoma, are rare in veterinary medicine. Patients with gastrinoma or Zollinger-Ellison syndrome have elevated serum gastrin levels which ultimately cause gastrointestinal ulcerations. Due to their small size, gastrinomas are a challenge to localize prior to surgery. In veterinary medicine, exploratory surgery with biopsy for histopathology confirms the diagnosis of gastrinoma. This is a retrospective study of four dogs with gastrinoma.


Author(s):  
John R. Palisano

Although confronting cistemae (CC) have been observed in a variety of tumor cells and normal fetal rat, mouse, and human epithelial tissues, little is known about their origin or role in mitotic cells. While several investigators have suggested that CC arise from nuclear envelope (NE) folding back on itself during prophase, others have suggested that CC arise when fragments of NE pair with endoplasmic reticulum. An electron microscopic investigation of 0.25 um thick serial sections was undertaken to examine the origin of CC in HeLa cells.


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

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

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

1997 ◽  
Vol 34 (5) ◽  
pp. 387-393 ◽  
Author(s):  
G. A. Andrews ◽  
N. C. Myers ◽  
C. Chard-Bergstrom

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.


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