neurokinin-a and Pancreatic-Neoplasms
neurokinin-a has been researched along with Pancreatic-Neoplasms* in 3 studies
Reviews
1 review(s) available for neurokinin-a and Pancreatic-Neoplasms
Article | Year |
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The importance of the measurement of circulating markers in patients with neuroendocrine tumours of the pancreas and gut.
The measurement of general and specific biochemical markers in patients with neuroendocrine tumours assists with diagnosis and gives an indication of the effectiveness of treatment and they may be used as prognostic indicators. There is much agreement that chromogranin A is the most universally helpful marker; it is found to be elevated in the circulation of about 90% of patients with metastatic neuroendocrine tumours and there are several excellent commercially available kits which give reliable estimations. Specific markers are useful for diagnosis also, and are helpful indicators of the effectiveness of treatment, particularly where tumour bulk may not change as much as tumour activity. Sporadic pancreatic neuroendocrine tumours may secrete more than one peptide and this indicates a worsening prognosis. Because of the wide variation in the progression of neuroendocrine tumours, a prognostic indicator gives a significant advantage to the clinician in order to facilitate optimum treatment at the optimum stage of disease. Both chromogranin A and neurokinin A have been used as powerful prognostic indicators for midgut carcinoid tumours. Topics: Biomarkers, Tumor; Chromogranin A; Chromogranins; Disease Progression; Gastrointestinal Neoplasms; Humans; Neuroendocrine Tumors; Neurokinin A; Pancreatic Neoplasms; Prognosis | 2003 |
Other Studies
2 other study(ies) available for neurokinin-a and Pancreatic-Neoplasms
Article | Year |
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Signaling pathways via NK1 receptors and their desensitization in an AR42J cell line.
Substance P (SP) has been shown to induce phosphatidylinositol (PI) hydrolysis and Ca2+ mobilization in AR42J cells. In this study, we confirmed the expression of NK1 but not NK2 or NK3 receptors in this cell line, and further investigated signaling pathways via NK1 receptors and their desensitization. The activation of NK1 receptors by SP affected neither basal cyclic AMP level nor cyclic AMP accumulation induced by secretin and forskolin, although it stimulated PI hydrolysis. Furthermore, SP induced Ca2+ mobilization even in the absence of extracellular Ca2+, though maximal response was reduced. U73122, a phospholipase C (PLC) inhibitor, nearly abolished Ca2+ response to SP. In addition, SP-induced Ca2+ signaling and PI hydrolysis rapidly desensitized following short exposure to SP, which did not affect the Ca2+ amount in intracellular Ca2+ stores or Ca2+ responses to carbachol and gastrin releasing peptide-10. These findings suggested that NK1 receptors do not couple to adenylate cyclase, although they induce PI response, and that NK1 receptors induce both intracellular Ca2+ release and Ca2+ influx through PLC activation. Ca2+ signaling and PI hydrolysis through NK1 receptors desensitized rapidly after the stimulation, maybe dependent on the modification of NK1 receptors. Topics: Animals; Calcium Signaling; Carcinoma, Acinar Cell; Cyclic AMP; Desensitization, Immunologic; Hydrolysis; Neurokinin A; Neurokinin B; Pancreatic Neoplasms; Phosphatidylinositols; Rats; Receptors, Neurokinin-1; Signal Transduction; Substance P; Tumor Cells, Cultured | 1998 |
Investigations of the expression and post-translational processing of the preprotachykinin-I (PPT-I) gene by rat pancreatic, insulin-producing tumor cell-lines.
Topics: 8-Bromo Cyclic Adenosine Monophosphate; Animals; Gene Expression; Insulin; Insulinoma; Neurokinin A; Pancreatic Neoplasms; Protein Precursors; Protein Processing, Post-Translational; Radioimmunoassay; Rats; Substance P; Tachykinins; Tumor Cells, Cultured | 1993 |