Disturbed intestinal movement, bile reflux to the stomach, and deficiency of c-kit-expressing cells in WsWs mutant rats

Isozaki, Koji; Hirota, Seiichi; Nakama, Akihiro; Miyagawa, Jun‐ichiro; Shinomura, Yasuhisa; Xu, Zhao‐Dong; Nomura, Shosaku; Kitamura, Yukihiko

doi:10.1016/0016-5085(95)90333-x

Cited by 164 publications

(129 citation statements)

References 40 publications

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“…The interaction between the kinase receptor and its ligand is essential for the development of melanocytes, erythrocytes, germ cells, mast cells and interstitial cells of Cajal. [12][13][14][15][16] Gain-offunction mutations of the c-kit gene lead to stem cell factor-independent activation of intracytoplasmic signal transduction and finally tumor growth and differentiation. c-kit mutations have been found in mast cell tumors 17 and gastrointestinal stromal tumors (GISTs), 18 which are classified on the basis of About two-thirds of GISTs coexpress CD34 19,20 and/or bcl-2.…”

Section: Resultsmentioning

confidence: 99%

Cellular hamartoma resembling gastrointestinal stromal tumor: a solid tumor of the pancreas expressing c-kit (CD117)

et al. 2005

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Solid tumors of the pancreas are usually neoplastic. We report on two adult patients, each with a solid tumor of the pancreas that presented with an unusual histology and seemed to follow a benign course. The tumors, one located in the body and one in the tail, were well demarcated and composed of irregularly arranged but welldifferentiated acini and small intralobular and interlobular ducts embedded in predominantly hypocellular fibrotic tissue that contained fascicles of cytologically bland spindle cells. Islets were lacking, but immunohistochemical staining for chromogranin A and insulin revealed individual scattered insulin-producing cells distributed between acinar and ductal cells. The spindle cell component tissue showed coexpression of CD34, c-kit (CD117) and bcl-2. The follow-up (2 and 4 years) of the patients was uneventful. We propose to designate the tumors as 'cellular hamartoma resembling gastrointestinal stromal tumor.' Modern Pathology ( Keywords: pancreatic tumor; hamartoma; c-kit; CD34; bcl-2; differential diagnosis Well-demarcated tumor-like lesions in the pancreas are uncommon. They have been described under the term pseudotumor 1 or inflammatory pseudotumor. 2 Recently, we described a tumorous lesion that we termed pancreatic solid and cystic hamartoma. 3 Here we report on two further solid pancreatic tumors that have features in common with both hamartomas and gastrointestinal stromal tumors. Patients, materials and methodsThe cases were collected from the consultation files of the Department of Pathology of the University of Kiel, to which they had been submitted by the Department of Pathology in Dinslaken, Germany (case 1), and the Department of Pathology of the University of Coimbra, Portugal (case 2).In the first case, a 51-year-old man without clinical symptoms had a routine check-up, during which a mass, 3 cm in diameter, was detected by ultrasonography in the tail of the pancreas next to the splenic artery. This finding was confirmed by endosonography and CT. Laboratory tests were normal. As a result of the unclear nature of the tumor, abdominal surgery was performed with resection of the tumor.In the second case, a 54-year-old woman with slight abdominal discomfort was examined by ultrasonography, which revealed a well-demarcated tumor, 2 cm in diameter, in the body of the pancreas. A left-sided pancreatic resection was performed to remove the tumor. Both patients had an uncomplicated postoperative course and so far (2 and 4 years, respectively) have relapse-free follow-up.Representative 4 mm sections of formalin-fixed, paraffin-embedded tissue from both specimens were stained with hematoxylin and eosin (H&E) and periodic acid-Schiff. Immunohistochemical staining was performed using the standard avidinbiotin method against following antibodies: cytokeratin 8 (CAM 5

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Section: Resultsmentioning

confidence: 99%

Cellular hamartoma resembling gastrointestinal stromal tumor: a solid tumor of the pancreas expressing c-kit (CD117)

et al. 2005

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“…16,17 Enhanced duodeno-gastric reflux is also a feature in W s /W s rat that suffers a 12 base-pair deletion in its c-kit gene and lacks a functional c-kit receptor. 18,19 These differences in the gastric phenotype of nNOS −/− and W/W v mice may be related, at least in part, to the differences in pyloric function.…”

Section: Introductionmentioning

confidence: 99%

Pyloric Sphincter Dysfunction in nNOS−/− and W/Wv Mutant Mice: Animal Models of Gastroparesis and Duodenogastric Reflux

2008

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“…[28][29][30] Moreover, the secretory response of After ultraviolet cross-linking, the filters were hybridized with apthe intestinal epithelium induced by cholera toxin has been propriate probes at 60ЊC. Blots were washed twice each with 11 shown to depend upon SCF/c-kit signal transduction.…”

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confidence: 99%

Expression of α-fetoprotein and stem cell factor/c-kit system in bile duct ligated young rats

et al. 1997

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ported by the finding that the early population of oval cells, The existence of a facultative hepatic stem cell comwhich represent the progeny of the hepatic stem cell compartpartment in bile ductules that participates in the rement, are both phenotypically similar to bile ductular cells newal process of epithelial cell populations in the liver and indeed may at least at an early stage be anatomically is well documented. The present study was undertaken connected to the bile tree. 3 The differentiation of oval cells to determine whether the immature bile epithelium reinto hepatocytes has now been shown in several experimental sponds differently to growth stimulus induced by bile models in which normal liver regeneration was impaired bestasis to that seen in the adult animal. In addition, the cause of the inability of hepatocytes to enter the cell cycle. 9-11 possible involvement of the growth factor/receptor sys-The most common experimental model used to induce extems associated with early activation of hepatic stem tensive and prolonged proliferation of bile epithelial cells in cells in bile duct proliferation was also examined. Bile duct ligation was used to induce the proliferation of bile the adult rat is the ligation of the common bile duct. 12 The epithelial cells. The expression of full-length alpha-feto-results from these experiments have shown that proliferation protein (AFP) was used as an indicator for activation of of bile-like cells are derived from existing biliary epithelium the stem cell compartment. AFP was highly and selec-and retain its characteristics; that bile duct cells divide irretively expressed in small bile ducts 7 days after bile duct spective of size of the ducts in which they are located, and ligation in immature rats up to 5 weeks of age. Although retain a lumen that is continuous with the preexisting biliary no significant increase in the expression of stem cell fac-tree. 13 Furthermore, no indications of a functioning stem cell tor (SCF) c-kit, hepatocyte growth factor (HGF), and compartment for the proliferation of either biliary epithelium transforming growth factor-a (TGF-a) was observed 7 or other cell lineages have been observed in any particular days after bile duct ligation in adult rats, the expression duct size or within the periportal connective tissue. 13 These of all these growth factors was increased in bile duct data suggest that the bile epithelium, and in particular the ligated rats up to 5 weeks of age. These results suggest bile ductular epithelium responds in a dramatically different that the bile ductular epithelium in the young rats re-way to growth stimulation induced by the ligation of the comsponds to bile stasis in a fashion that is phenotypically mon bile duct to that observed in the experimental models in similar to that seen during early activation of hepatic which oval cell proliferation occurs. Because the development stem cells in adult liver. (HEPATOLOGY 1997;25:1115-1122.) and maturation of the biliary system extends well into the perinatal period...

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Disturbed intestinal movement, bile reflux to the stomach, and deficiency of c-kit-expressing cells in WsWs mutant rats

Cited by 164 publications

References 40 publications

Cellular hamartoma resembling gastrointestinal stromal tumor: a solid tumor of the pancreas expressing c-kit (CD117)

Cellular hamartoma resembling gastrointestinal stromal tumor: a solid tumor of the pancreas expressing c-kit (CD117)

Pyloric Sphincter Dysfunction in nNOS−/− and W/Wv Mutant Mice: Animal Models of Gastroparesis and Duodenogastric Reflux

Expression of α-fetoprotein and stem cell factor/c-kit system in bile duct ligated young rats

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