Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10721 (c-kit)
 6,575 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of somatostatinoma of the papilla of Vater with multiple gastrointestinal stromal tumors in a patient with von Recklinghausen's disease (VRD). A 64-year-old woman who had had recurrent attacks of acute pancreatitis and cholangitis was found, on gastroduodenal endoscopy, to have a tumor of the papilla of Vater and multiple submucosal tumors of the stomach and duodenum. Numerous submucosal tumors were observed in the stomach, duodenum, and jejunum, and total excision of the papilla of Vater and resection of the duodenal and jejunal submucosal tumors was performed. The tumor of the papilla of Vater showed the histologic appearance of a dense proliferation of tumor cells in acinar form, from the duodenal mucosa to the muscle layer, and psammoma bodies were revealed within the tumor. Immunohistologically, the tumor cells were intensely positive for somatostatin. The submucosal tumors of the duodenum and jejunum were negative for smooth muscle actin, s-100, and neuron-specific enolase (NSE), and positive for CD34 and c-kit, and they were diagnosed as gastrointestinal stromal tumors (GISTs) according to the strict definition. The only 25 cases of papilla of Vater somatostatinoma associated with VRD to have been reported in the English-language literature since 1982 are reviewed, as well as our own case.
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PMID:Somatostatinoma of the papilla of Vater with multiple gastrointestinal stromal tumors in a patient with von Recklinghausen's disease. 1248 51

This study investigated the role of adult islet-derived stem cells in repairing islet damage. Using intraperitoneal injection of cerulein, a rat model of acute pancreatitis was induced in an experimental group. The expression of the protein c-kit, a pancreatic stem cell marker, was observed using immunohistochemistry at set intervals following successful model preparation. Pathological changes in pancreatic tissues were also observed using routine hematoxylin and eosin staining. Cells with positive c-kit staining were rarely observed in normal tissues. At all observation intervals after the induction of acute pancreatitis, c-kit staining was restricted to the islets. Over the course of observations, staining changed from low to high intensity, and then back to low intensity again. The primary pathological manifestation in the experimental group was edematous pancreatic tissues with local necrotic lesions. These findings suggested that c-kit positive cells are likely to be a type of pancreatic progenitor cell that is involved only in the self-repair of islet damage and does not migrate.
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PMID:Islet-derived stem cells from adult rats participate in the repair of islet damage. 2297 33

Pazopanib is an oral angiogenesis inhibitor targeting vascular endothelial growth factor receptors, platelet-derived growth factor receptors, and c-Kit approved for the treatment of renal cell carcinoma and soft tissue sarcoma. Nonselective kinase inhibitors, such as sunitinib and sorafenib, are known to be associated with acute pancreatitis. There are few case reports of severe acute pancreatitis induced by pazopanib treatment. We present a case of severe acute pancreatitis caused by pazopanib treatment for cutaneous angiosarcoma. The patient was an 82-year-old female diagnosed with cutaneous angiosarcoma. She had been refractory to docetaxel treatment and began pazopanib therapy. Three months after pazopanib treatment, CT imaging of the abdomen showed the swelling of the pancreas and surrounding soft tissue inflammation without abdominal pain. After she continued pazopanib treatment for 2 months, she presented with nausea and appetite loss. Abdominal CT showed the worsening of the surrounding soft tissue inflammation of the pancreas. Serum amylase and lipase levels were 296 and 177 IU/l, respectively. She was diagnosed with acute pancreatitis induced by pazopanib treatment and was managed conservatively with discontinuation of pazopanib, but the symptoms did not improve. Subsequently, an abdominal CT scan demonstrated the appearance of a pancreatic pseudocyst. She underwent endoscopic ultrasound-guided pseudocyst drainage using a flared-end fully covered self-expandable metallic stent. Then, the symptoms resolved without recurrence. Due to the remarkable progress of molecular targeted therapy, the oncologist should know that acute pancreatitis was recognized as a potential adverse event of pazopanib treatment and could proceed to severe acute pancreatitis.
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PMID:Pazopanib-Induced Severe Acute Pancreatitis. 2646 70