Pseudoneoplastic proliferation of endocrine cells in pancreatic fibrosis

Bartow, Sue A.; Mukai, Kiyoshi; Rosaí, Juan

doi:10.1002/1097-0142(19810601)47:11<2627::aid-cncr2820471118>3.0.co;2-c

Cited by 59 publications

(14 citation statements)

References 23 publications

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“…If clinical symptoms and laboratory findings indicate the presence of an islet cell tumor, the differential diagnosis from focal pancreatitis can become difficult not only by means of radiologic [13,19,20] but sometimes also by histologic study because of the relative increase in the number and size of the islets of Langerhans. In rare instances, proliferated insular cells can be in direct contact with nerve fibers or may even enter into the perineural space, giving the impression of early invasive carcinoma [1,21,22]. Rarely, an inflammatory mass shown by angiography or CT can be caused by a penetrating gastric or duodenal ulcer [13,23,24].…”

Section: Discussionmentioning

confidence: 99%

Pseudotumorous pancreatitis

Lämmer

Herlinger

Zalaudek

et al. 1985

Gastrointest Radiol

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Chronic pancreatitis can occasionally present as a focal, noncalcified mass, indistinguishable from carcinoma. Radiologic studies in 21 such patients were considered to show carcinoma in 16 and an islet cell tumor in 5 patients. Seventeen of the patients came to laparotomy when a palpable mass was found in each; 9 of the patients had a partial pancreatectomy, and multiple biopsy specimens were taken in 8 patients. Four patients did not come to surgery; in them the diagnosis was based on examination of percutaneous biopsy specimens and follow-up. In all patients the histologic diagnosis was chronic relapsing pancreatitis.

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Section: Discussionmentioning

confidence: 99%

Pseudotumorous pancreatitis

Lämmer

Herlinger

Zalaudek

et al. 1985

Gastrointest Radiol

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“…Furthermore, in chronic pancreatitis there is aggregation of islets as the exocrine elements atrophy, resulting in nodular collections of distorted islets and simulating a neoplasm. 8 Non-neoplastic islets retain their heterogeneous population of different peptide cell types, and immunohistochemical labeling of non-neoplastic islets for the normal islet peptides (insulin, glucagon, somatostatin, and pancreatic polypeptide (PP)) reveals the presence of all cell types, in roughly normal numbers and distribution.…”

Section: Pancreatic Endocrine Neoplasmsmentioning

confidence: 99%

Nonductal neoplasms of the pancreas

2007

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Although the majority of pancreatic neoplasms are infiltrating ductal adenocarcinomas or other neoplasms with ductal differentiation, neoplasms with acinar, endocrine, mixed, or uncertain differentiation constitute a diverse and distinctive group. The most common and best-characterized nonductal neoplasms are pancreatic endocrine neoplasm, acinar cell carcinoma, pancreatoblastoma, and solid pseudopapillary neoplasm. This review details the clinical and pathologic features of these nonductal neoplasms, highlighting diagnostic criteria including the use of specific immunohistochemical stains to define the cellular differentiation of the neoplasms. Modern Pathology (2007) 20, S94-S112.

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“…ation with ductal complexes in pancreatic duct obstruction and pancreatitis in humans [7,8]. The formation of ductal complexes in the pancreas is at least partially caused by a transdifferentiation of acinar to duct cells [9] which illustrates the remarkable differentiation plasticity of acinar cells.…”

mentioning

confidence: 91%

Modulation of rat pancreatic acinoductal transdifferentiation and expression of PDX-1 in vitro

Rooman¹,

Heremans²,

Heimberg³

et al. 2000

Diabetologia

177

180

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Regeneration, or neogenesis, of beta cells in adult pancreas is an important research issue because it could find applications in the restoration of the normal beta-cell mass in diabetic patients. In vitro neogenesis might be a means of generating additional beta cells intended for transplantation, as the number of beta cells that can be isolated from organ donors is very limited. Neogenesis can be induced in vivo in several ways [1] but the identity of the beta-cell precursors is not clear. Several lines of evidence suggest that, in addition to duct cells, exocrine acinar cells could be able to transdifferentiate into beta cells [2]. In several experimental models and pathological conditions, islet neogenesis is accompanied by the transformation of the normal exocrine tissue into ductal complexes, a process called acinoductal metaplasia. This is seen in the model of pancreatic duct ligation [3], transforming growth factor-alpha transgenic mice [4,5] and interferon-gamma transgenic mice [6]. Islet neogenesis has also been observed in associ- Diabetologia (2000) Abstract Aims/hypothesis. In adult pancreatic regeneration models exocrine acini are found to transdifferentiate to duct-like complexes. This has also been associated with the formation of new endocrine islet cells. We aimed to establish an in vitro model in which this transdifferentiation process is characterised and can be modulated. Methods. Purified rat pancreatic acini were cultured in suspension. Differentiation was analysed by immunocytochemistry, electron microscopy, western blotting and RT-PCR.Results. During culture acinar cells directly transdifferentiated without dividing, the cells lost their acinar phenotype and started to express cytokeratins 20 and 7 and fetal liver kinase-1 (Flk-1) receptors for vascular endothelial growth factor. Expression of the acinar pancreatic exocrine transcription factor (PTF-1) remained and the pancreatic duodenal homeoboxcontaining transcription factor (PDX-1) was induced. When transdifferentiation was completed, the cells started to express protein gene product 9.5, a panneuroendocrine marker. By combining these features, the transdifferentiated cells show similar characteristics to precursor cells during active beta-cell neogenesis. We were able to modulate the differentiation state by addition of nicotinamide or sodium butyrate, agents which are known to stimulate endocrine differentiation in other models. Conclusion/interpretation. Here, we present an in vitro system in which the cellular differentiation of putative pancreatic endocrine precursor cells and their PDX-1 expression can be modulated, thereby providing a possible model for the study of beta-cell transdifferentiation. [Diabetologia (2000) Corresponding author: L. Bouwens, VUB-Department of Experimental Pathology, Laarbeeklaan 103, B-1090 Brussels, Belgium Abbreviations: BrdU, Bromodeoxyuridine; CK7, cytokeratin 7; CK20, cytokeratin 20; Flk-1, fetal liver kinase-1; PDX-1, pancreatic duodenal homeodomain containing transcription factor; PGP9.5, ...

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Pseudoneoplastic proliferation of endocrine cells in pancreatic fibrosis

Cited by 59 publications

References 23 publications

Pseudotumorous pancreatitis

Pseudotumorous pancreatitis

Nonductal neoplasms of the pancreas

Modulation of rat pancreatic acinoductal transdifferentiation and expression of PDX-1 in vitro

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