Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphogenesis and growth of the endocrine pancreas has not been well investigated in man although it represents an important issue in diabetology. We examined human fetal pancreas from 12 to 41 weeks of gestation immunocytochemically to evaluate proliferative activity with the Ki-67 marker, and cytodifferentiation with cytokeratin 19 (ductal cells), synaptophysin (all endocrine cells), and insulin, glucagon, somatostatin and pancreatic polypeptide (islet cell types). Ki-67 labelling was found in all these cell types but was much higher in ductal cells than in islet cells. An intermediate population expressed synaptophysin but lacked islet hormones. With increasing gestational age the Ki-67 labelling index decreased from 17 to 4% in ductal cells, from 9 to 1% in synaptophysin-positive cells, and from 3 to 0.1% in insulin- or glucagon-positive cells. From 12 to 16 weeks, all epithelial cells including the endocrine islet cells expressed cytokeratin 19. Thereafter cytokeratin 19 expression decreased and eventually disappeared from most islet cells, whereas strong expression remained in the ductal cells. We show that differentiated human islet cells have only very limited proliferative capacity, and we demonstrate the existence of transitional differentiation stages between ductal and islet cells.
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PMID:Proliferation and differentiation in the human fetal endocrine pancreas. 911 16

In the early human embryonic/fetal pancreas, we studied 1) the ontogenetic pattern of the endocrine cells and the evolution of the endocrine mass, and 2) the morphogenetic pattern of development and, more precisely, the complex relationship of the epithelial mass with the surrounding mesenchyme. We studied 15 pancreases between 7 and 11 weeks of development (WD) by double immunohistochemistry. Epithelial cells in these pancreatic anlage were detected by cytokeratin staining, and differentiated endocrine cells were detected by insulin, glucagon, somatostatin, and pancreatic polypeptide staining. Proliferation was quantified using a nuclear marker, the Ki-67 antibody. At this early stage, the pancreas is made up of an epithelial mass composed of central ducts intermingled with a loose mesenchyme and peripheral ducts surrounded by a dense peripancreatic mesenchyme. Hormone-containing cells appear in the epithelium at 8 WD. Newly differentiated endocrine cells coexpress insulin, glucagon, and somatostatin; endocrine differentiation starts within the central ducts of the epithelial mass, at a distance from the dense peripancreatic surrounding mesenchyme. The fraction of the primitive endocrine cells undergoing proliferation is low (5% of the insulin cells at 8 WD, 3% at 11 WD), which is in favor of massive differentiation as the major mechanism for increasing endocrine mass. By contrast, the nonendocrine epithelial cells have a higher rate of proliferation; the epithelial cells in contact with the dense peripancreatic surrounding mesenchyme show more proliferation activity than those within the central part of the epithelial mass (at 11 WD, labeling index: periphery 65% vs. center 15%, P < 0.001). In conclusion, the patterns of endocrine differentiation and epithelial proliferation observed within the human pancreas early in development suggest that the mesenchyme plays a role in these phenomena.
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PMID:Early pattern of differentiation in the human pancreas. 1086 39

Neuroendocrine tumors are rare neoplasms. In most cases conventional imaging techniques (US,CT,RMN) are not able to identify primitive tumors. This fact conditions the approach to the treatment of these tumors. 111In-Pentetreotide scintigraphy (Octreoscan) permits to visualize occult primary tumor by somatostatin receptors, changing the clinical history of patients. This method can be used in guided surgery with a hand-held gamma probe allowing to improve the detection of occult tumor (inverse square law), giving to the patient further possibilities of survival. Intraoperative gamma probe was still utilized with success in the management of other tumors, as relapsed colorectal cancer, while reports about gamma probe in neuroendocrine tumors are poor because of the rarity of disease. In two cases we have utilized a gamma probe (ORIS model 2) in neuroendocrine tumors: in a case we have observed liver recurring localizations originating from pancreas, with high proliferative index (Ki-67 = 2033 x 10 HPF), and in a case liver metastatic carcinoid of lung. The difference between tumor and background counts was significant exceeds 2 standard deviation count rate. Gamma probe permits a radical cure in many cases and completes intraoperative ultrasound in order to provide the surgeon with other information on the intraoperative staging of the patient.
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PMID:[Radioguided surgery in the treatment of gastro-entero-pancreatic neuroendocrine tumors] . 1114 Jan 6

In TT cells, originating from medullary carcinoma of the human thyroid, the presence of receptors for somatostatin was demonstrated at the ultrastructural level. Inhibitory effect of octreotide (a somatostatin analogue) was observed on proliferation of in vitro cultured TT cells and confirmed by evaluating levels of PCNA and Ki-67 proliferation-associated antigens and examining the extent of DNA damage using the comet assay. Our studies indicate a potential for application of somatostatin analogues to diagnosis and adjunct treatment in thyroid medullary carcinomas.
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PMID:Effect of octreotide on proliferation of in vitro cultured thyroid medullary carcinoma cells. 1137 17

We report an autopsy case of pancreatic and ectopic nesidioblastosis. A five-month-old Japanese girl was born at 35 weeks gestation, and showed clinical symptoms of hyper-insulinemic hypoglycemia before death. At autopsy a tumorous nodule was observed at the portion of the jejunum, 90 cm from Treitz's ligament. The nodule measured 30 x 20 x 20 mm. The ectopic pancreas, also revealed nesidioblastosis histologically. Immunohistologically, both nesidioblastoses were stained positive for chromogranin A, insulin, glucagon and somatostatin. The proliferating cell nuclear antigen (PCNA) and Ki-67 indices were less than 4% in the nesidioblastosis. To our knowledge, this is the first reported case of nesidioblastosis demonstrating proliferating activity with PCNA and Ki-67, and is the third reported case of nesidioblastosis arising in the pancreas and ectopic pancreas.
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PMID:An autopsy case of pancreatic and ectopic nesidioblastosis. 1142 96

Immunohistochemistry is part of the routine diagnosis of the neuroendocrine tumors. In our study, we included 52 paragangliomas with various localizations by routine histology and immunohistochemistry. In order to increase the diagnostic specificity, a complex immunohistochemistry panel has been performed consisting of Bcl-2, Ki-67, Bax and Pituitary Adenylate Cyclase-Activating Peptide (PACAP), somatostatin, VIP and Calcitonin Gene Related Peptide (CGRP). After heat induced antigen retrieval, the immunostaining was performed by StreptABC using DAB as a chromogen. We were the first to demonstrate the presence of Bax and PACAP in paragangliomas. Some of the used markers are of prognostic value. The relationship between Bcl-2 and Bax is decisive in generating the final response to the input apoptotic signals. The Ki-67 antigen staining has gained wide acceptance in prognostic evaluation of other tumor types. We noted a small number of Ki-67 positive cases, which signifies a low mitotic activity of these tumors and a relatively high number of Bax positivities (32.9%) and the much lower number of Bcl-2 positivities (11.39%), and could explain the benign behaviour of paragangliomas.
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PMID:Immunohistochemical features of paragangliomas. 1206 90

Although non-functional islet cell tumor (NFICT) and solid and papillary neoplasm (SPN) share similar clinical and pathological features, the outcome of each is different. Because NFICT often follow a malignant course and SPN are usually benign, the correct differential diagnosis is very important. We investigated the clinical and pathological findings in 10 cases of NFICT and 12 cases of SPN, including immunohistochemical analysis for chromogranin, vimentin, neuron-specific enolase, somatostatin, alpha-1-antitrypsin, estrogen receptor, progesterone receptor, CD99, p21 and Ki-67. The current study shows that chromogranin is the most valuable marker in differentiating between the tumors (P < 0.01). In contrast to previous reports stating that SPN express the progesterone and/or estrogen receptors, which are absent in other pancreatic tumors, our results show that one-third of SPN were positive for the progesterone receptor. Downregulation of p21 was found more frequently in NFICT (40%) than SPN (17%). The mean value of the Ki-67 proliferation index for NFICT (2.77% +/- 2.53%) was significantly higher than that for SPN (0.94% +/- 0.89%; P = 0.043). These results are consistent with NFICT having more malignant behavior than SPN.
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PMID:Comparative study of non-functional islet cell tumors and pancreatic solid and papillary neoplasms: biological behavior and immunohistochemistry. 1210 May 18

With the aim to investigate histopathological changes and proliferative and apoptotic activity in GH-secreting adenomas we compared 14 cases pre-treated with somatostatin analogues before surgery with a reference group of 17 un-pretreated ones. Besides routine histology, immunocytochemical detection of all pituitary hormones, caspase-3, cytokeratin-18, and "M30 antigen", its apoptosis-specific fragment was performed. Proliferation activity of the tumour was determined by the Ki-67 antigen expression. In treated adenomas more prominent regressive changes were found accompanied by compensatory increase in perivascular fibrosis. The Ki-67 labelling index was lower in treated group (mean 2.5, median 1.6 per mille) than in untreated patients (mean 9.4, median 5.0 per mille). The difference was statistically significant (p=0.049 using Mann-Whitney Rank Sum Test). Apoptosis was detected in only 2 of the 14 pre-treated adenomas, and it was more frequent (9/17) and more prominent in the untreated group.
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PMID:The influence of treatment with somatostatin analogues on morphology, proliferative and apoptotic activity in GH-secreting pituitary adenomas. 1285 83

The aim of the study was to investigate the mechanism of action of somatostatin analogues (SSA), ionizing radiation, and their combination on pituitary adenoma cells with special emphasis on proliferative and apoptotic activity. In the 14 GH-secreting adenomas pretreated with SSA before surgery, more prominent regressive changes were found accompanied by compensatory increase in perivascular fibrosis than in the reference group of 17 unpretreated adenomas. The proliferative Ki-67 labeling index was significantly lower in the treated group (median 1.6 per 1000) than in the untreated patients (median 5.0 per 1000). Apoptosis was detected in only 2 of the 14 pretreated adenomas, and it was more frequent (9/17) and more prominent in the untreated group. In cell lines, the SSA had minimal antiproliferative effect, and they were unable to induce apoptosis. Ionizing radiation at doses of 5-20 Gy induced apoptosis in the corticotroph cell line AtT20 with no cell-cycle block. In the somatotroph GH3 cell line, the early (premitotic) apoptosis was detectable using only a high dose of 200 Gy; after irradiation with doses of 20-50 Gy, apoptosis appeared with the latency of 48-72 hours, and was preceded by cell-cycle arrest in the G(2)/M phase. The treatment with somatostatin-14 during irradiation increased the percentage of apoptotic cells in culture 10 days after irradiation (11% versus 3% using 20 Gy).
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PMID:The role of apoptosis in pituitary adenomas in the field of conventionally used therapeutic approaches. 1503 83

Somatostatin analogs are effective in inhibiting growth of human breast cancer cell lines. These antiproliferative effects are mediated by specific receptors located on cell membranes. The somatostatin receptor subtype 2 (sst2) is the principal mediator of somatostatin effects in normal and cancer cells, and its presence has already been demonstrated in breast cancer. The purpose of our study was to evaluate the clinical relevance of the expression of sst2 by quantifying its mRNA in a large group of infiltrating breast cancers and their corresponding normal tissues. The expression of sst2 mRNA was measured with quantitative real time RT-PCR in 169 breast cancers and in their corresponding unaffected tissues. We evaluated the association of sst2 expression with the commonest clinical-pathologic features of breast cancer. The correlation with a marker of cell proliferation (Ki-67) and with receptor concentration was also evaluated. In cancer tissues, we found that the absolute concentrations of sst2 mRNA were significantly higher in estrogen receptor (ER)-positive samples (P=0.002) as well as in lymph-node-negative cancers (P=0.04) (Student's t-test or one-way ANOVA). In addition, sst2 mRNA was significantly higher in breast cancers than in corresponding unaffected tissues (P=0.0002). However, when the clinical-pathologic parameters were considered, this gradient maintained its statistical significance only in tumors expressing positive prognostic markers, such as the presence of ER (P=0.0005) and progesterone receptors (PgR) (P=0005), and the lack of lymph-node involvement (P=0.0003). The same difference was also significant in postmenopausal women (P=0.001) and in T1 patients (P=0.001). In addition, sst2 mRNA expression was significantly higher (P=0.008) in low-proliferating breast cancers. Finally, we found that the quantitative expression of sst2 mRNA was directly related to the PgR concentration in breast cancer tissues (P<0.001). Our data seem to indicate that an upregulation of sst2 gene expression is a common feature of breast cancers which, on the basis of conventional predictive parameters, are expected to have a better prognosis. Featuring a possible role of somatostatin analogs in combined endocrine therapies for breast cancer, our results seem to confirm that the sst2 status of the tumor should be previously investigated.
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PMID:Measurement of somatostatin receptor subtype 2 mRNA in breast cancer and corresponding normal tissue. 1516 7


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