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6. Fiskesund R, Abeyama K, Yoshinaga K, Abe J, Yuan Y, Yu S: 1,5-anhydro-D-fructose and its derivatives: biosynthesis, preparation and potential medical applications. Planta Med; 2010 Oct;76(15):1635-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The genes coding for the enzymes in this pathway have been cloned, enabling the large-scale production of AF and related products in a cell-free reactor.
  • AG also stimulates insulin secretion in insulinoma cell lines. in vivo, APP has been shown to lengthen the life span of cancer-afflicted mice.
  • It interferes with tumor growth and metastasis by its cidal effects on fast multiplying cells.
  • [MeSH-minor] Animals. Anti-Infective Agents / chemistry. Anti-Infective Agents / metabolism. Anti-Infective Agents / pharmacology. Antineoplastic Agents / chemistry. Antineoplastic Agents / metabolism. Antineoplastic Agents / pharmacology. Antioxidants / chemistry. Antioxidants / metabolism. Antioxidants / pharmacology. Carbohydrate Metabolism. Dental Caries / prevention & control. Humans. Insulin / secretion. Ketoses / metabolism. Ketoses / pharmacology. Mice. Protective Agents / chemistry. Protective Agents / metabolism. Protective Agents / pharmacology. Rats

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  • [Copyright] © Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20645241.001).
  • [ISSN] 1439-0221
  • [Journal-full-title] Planta medica
  • [ISO-abbreviation] Planta Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / Insulin; 0 / Ketoses; 0 / Protective Agents; 0 / microthecin; 30237-26-4 / Fructose; 75414-43-6 / 1,5-anhydrofructose
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7. Kim EK, Song MY, Hwang TO, Kim HJ, Moon WS, Ryu DG, So HS, Park R, Park JW, Kwon KB, Park BH: Radix clematidis extract protects against cytokine- and streptozotocin-induced beta-cell damage by suppressing the NF-kappaB pathway. Int J Mol Med; 2008 Sep;22(3):349-56
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  • [Title] Radix clematidis extract protects against cytokine- and streptozotocin-induced beta-cell damage by suppressing the NF-kappaB pathway.
  • In the present study, we demonstrated that Radix clematidis extract (RCE) could prevent cytokine-induced beta-cell damage and streptozotocin (STZ)-induced diabetes in mice.
  • Treatment of RINm5F insulinoma cells with interleukin-1beta and interferon-gamma reduced cell viability; however, RCE protected the cells from this cytokine-mediated viability reduction in a concentration-dependent manner.
  • Furthermore, RCE abolished the cytokine-induced increases in NF-kappaB binding activity and p65 subunit levels in the nucleus, as well as IkappaBalphadegradation in the cytosol when compared to unstimulated cells.
  • The protective effect of RCE was further demonstrated by the observed suppression of NF-kappaB-dependent iNOS expression and normal insulin secreting responses to glucose in cytokines-treated islets.
  • [MeSH-major] Cytokines / pharmacology. Gastropoda / chemistry. Insulin-Secreting Cells / drug effects. Insulin-Secreting Cells / metabolism. NF-kappa B / metabolism. Signal Transduction / drug effects. Streptozocin / pharmacology
  • [MeSH-minor] Animals. Cell Survival / drug effects. Cells, Cultured. Cytoprotection / drug effects. Glucose / pharmacology. Insulin / secretion. Male. Nitric Oxide / biosynthesis. Nitric Oxide Synthase Type II / metabolism. Rats. Rats, Sprague-Dawley

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  • (PMID = 18698494.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cytokines; 0 / Insulin; 0 / NF-kappa B; 31C4KY9ESH / Nitric Oxide; 5W494URQ81 / Streptozocin; EC 1.14.13.39 / Nitric Oxide Synthase Type II; IY9XDZ35W2 / Glucose
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8. Brand MD, Parker N, Affourtit C, Mookerjee SA, Azzu V: Mitochondrial uncoupling protein 2 in pancreatic β-cells. Diabetes Obes Metab; 2010 Oct;12 Suppl 2:134-40
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  • [Title] Mitochondrial uncoupling protein 2 in pancreatic β-cells.
  • Pancreatic β-cells have remarkable bioenergetics in which increased glucose supply upregulates the cytosolic ATP/ADP ratio and increases insulin secretion.
  • This arrangement allows glucose-stimulated insulin secretion (GSIS) to be regulated by the coupling efficiency of oxidative phosphorylation.
  • Importantly, however, the enhancement of GSIS is robustly recapitulated with acute UCP2 knockdown in INS-1E insulinoma cells.
  • UCP2 protein level in these cells is dynamically regulated, over at least a fourfold concentration range, by rapid proteolysis (half-life less than 1 h) opposing regulated gene transcription and mRNA translation.
  • Evidence for proteasomal turnover of UCP2 includes sensitivity of degradation to classic proteasome inhibitors in cells, and reconstitution of degradation in vitro in mitochondria incubated with ubiquitin and the cytosolic 26S proteasome.
  • These dynamic changes in UCP2 content may provide a fine level of control over GSIS in β-cells.
  • [MeSH-major] Energy Metabolism / physiology. Insulin / secretion. Insulin-Secreting Cells / metabolism. Ion Channels / physiology. Mitochondrial Proteins / physiology

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 21029310.001).
  • [ISSN] 1463-1326
  • [Journal-full-title] Diabetes, obesity & metabolism
  • [ISO-abbreviation] Diabetes Obes Metab
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / P01AG025901; United States / NIA NIH HHS / AG / P30 AG025708; United States / NIA NIH HHS / AG / PL1AG032118; United States / NIA NIH HHS / AG / R01 AG033542; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Insulin; 0 / Ion Channels; 0 / Mitochondrial Proteins; 0 / Reactive Oxygen Species; 0 / mitochondrial uncoupling protein 2; IY9XDZ35W2 / Glucose
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9. d'Annunzio G, Giannattasio A, Poggi E, Castellano E, Calvi A, Pistorio A, Barabino A, Lorini R: Beta-cell autoimmunity in pediatric celiac disease: the case for routine screening? Diabetes Care; 2009 Feb;32(2):254-6
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  • [Title] Beta-cell autoimmunity in pediatric celiac disease: the case for routine screening?
  • OBJECTIVE: To evaluate the prevalence of beta-cell autoimmunity and the usefulness of a type 1 diabetes screening in patients with celiac disease.
  • RESEARCH DESIGN AND METHODS: We measured GAD antibodies (GADAs), insulinoma-associated protein 2 antigens (IA-2As), and insulin autoantibodies (IAAs) in 188 young Italian patients with celiac disease (66 male [35.1%]).
  • Mean age at celiac disease diagnosis was 5.4 years (0.5-17.1), and mean celiac disease duration was 4.2 years (0-28.8).
  • Celiac disease was diagnosed by jejunal biopsy after positivity for endomysial and tissue transglutaminase antibody was confirmed.
  • There was no significant association among beta-cell autoimmunity and sex, age, pubertal stage, family history, or coexistence of other autoimmune disorders; compliance to a gluten-free diet was confirmed.
  • CONCLUSIONS: Our results showed a low prevalence of beta-cell autoimmunity and do not support a precocious screening for beta-cell autoimmunity in young celiac disease patients.
  • [MeSH-major] Autoimmune Diseases / epidemiology. Celiac Disease / immunology. Insulin-Secreting Cells / immunology
  • [MeSH-minor] Adolescent. Age of Onset. Autoantibodies / blood. Autoimmunity. Child. Child, Preschool. Female. Humans. Infant. Insulin Antibodies / blood. Italy. Male

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  • [Cites] Horm Res. 1999;52(3):119-24 [10725775.001]
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  • (PMID = 19017767.001).
  • [ISSN] 1935-5548
  • [Journal-full-title] Diabetes care
  • [ISO-abbreviation] Diabetes Care
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / ICA512 autoantibody; 0 / Insulin Antibodies
  • [Other-IDs] NLM/ PMC2628689
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10. Tomita T: Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors. Pancreas; 2007 Nov;35(4):e18-22
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  • [Title] Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors.
  • OBJECTIVES: Immunocytochemical staining for lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) is able to recognize lymphatic vessel endothelium and pancreatic endocrine cells (PETs).
  • Pancreatic endocrine tumors were studied for LYVE-1 immunocytochemical staining compared with normal pancreatic islets to detect possible presence of LYVE-1 in PETs.
  • METHODS: Twenty-five cases of primary and metastatic PETs were immunocytochemically stained for LYVE-1, including insulinomas, glucagonomas, somatostatinoma, pancreatic polypeptidomas, gastrinomas, and nonfunctioning tumors.
  • RESULTS: All normal pancreatic islet cells were positive for LYVE-1, whereas 2 cases of 25 PETs, 1 each of gastrinoma and nonfunctioning tumor, were positive for LYVE-1, retaining immunocytochemical reactivity of islet cells.
  • CONCLUSIONS: Normal pancreatic islets were positive for LYVE-1, whereas only 2 of 25 PETs were positive, suggesting that most PETs lost LYVE-1 or contained below detectable levels of LYVE-1.
  • The presence of LYVE-1 in pancreatic islets and in some PETs may suggest structure-function relationship of LYVE-1/lymphatic vessel in hormone synthesis and secretion.
  • [MeSH-major] Gastrinoma / chemistry. Glucagonoma / chemistry. Immunohistochemistry. Insulinoma / chemistry. Islets of Langerhans / chemistry. Pancreatic Neoplasms / chemistry. Somatostatinoma / chemistry. Vesicular Transport Proteins / analysis

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  • (PMID = 18090227.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LYVE1 protein, human; 0 / Vesicular Transport Proteins
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11. Gartner W, Koc F, Nabokikh A, Daneva T, Niederle B, Luger A, Wagner L: Long-term in vitro growth of human insulin-secreting insulinoma cells. Neuroendocrinology; 2006;83(2):123-30
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  • [Title] Long-term in vitro growth of human insulin-secreting insulinoma cells.
  • OBJECTIVE: Long-term in vitro maintenance of human insulin-secreting insulinoma cells. METHODS:.
  • (1) Cell culture of ex vivo-derived insulinoma cell suspensions from 8 individual human donors, using various cell culture medium supplementations;.
  • (2) determination of insulin synthesis and secretion using immunocytochemistry and insulin and pro-insulin radioimmunoassays;.
  • (3) nestin-immunostaining of long-term in vitro grown insulinoma cell suspensions, and (4) phase-contrast light microscopy for analyzing the in vitro growth characteristics of the insulinoma cells. RESULTS:.
  • (1) Parallel persistence of in vitro insulinoma cell proliferation as well as insulin-synthesizing and -secreting capacity depended on both the co-culture of insulinoma cells with human fibroblasts and the supplementation of the cell culture medium with tissue culture supernatant derived from the rodent pituitary adenoma cell line GH-3;.
  • (2) immunostaining for insulin and secretagogin confirmed the neuroendocrine origin of the insulinoma cells grown in vitro;.
  • (3) insulin secretion capability persisted up to an observation period of 25 weeks;.
  • (4) insulin secretion rates after 6 weeks of in vitro growth ranged from 3.5 to 83.3 muU/ml/h/60,000 cells plated, and (5) after long-term in vitro growth of insulinoma-derived cell suspensions with persistent insulin-secreting capacity, nestin staining was observed predominantly in co-cultured fibroblasts.
  • CONCLUSION: Our data describe for the first time the long-term in vitro culture of insulin-secreting human insulinomas and highlight the importance of beta-cell trophic factors for insulinoma cell growth.
  • [MeSH-major] Insulin / secretion. Insulin-Secreting Cells / physiology. Insulinoma / pathology
  • [MeSH-minor] Adult. Cell Culture Techniques / methods. Cell Proliferation. Coculture Techniques / methods. Culture Media, Conditioned / pharmacology. Female. Fibroblasts / physiology. Humans. Immunohistochemistry / methods. Intermediate Filament Proteins / metabolism. Male. Middle Aged. Nerve Tissue Proteins / metabolism. Nestin. Radioimmunoassay / methods. Time Factors. Tumor Cells, Cultured

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  • (PMID = 16888402.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Insulin; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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12. Ceteci F, Ceteci S, Karreman C, Kramer BW, Asan E, Götz R, Rapp UR: Disruption of tumor cell adhesion promotes angiogenic switch and progression to micrometastasis in RAF-driven murine lung cancer. Cancer Cell; 2007 Aug;12(2):145-59
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  • [Title] Disruption of tumor cell adhesion promotes angiogenic switch and progression to micrometastasis in RAF-driven murine lung cancer.
  • Progression of non-small-cell lung cancer (NSCLC) to metastasis is poorly understood.
  • Two genetic approaches were used to evaluate the role of adherens junctions in a C-RAF driven mouse model for NSCLC: conditional ablation of the cdh1 gene and expression of dominant-negative (dn) E-cadherin.
  • Vascularized tumors grew more rapidly, developed invasive fronts, and gave rise to micrometastasis. beta-catenin was identified as a critical effector of E-cadherin disruption leading to upregulation of VEGF-A and VEGF-C.
  • In vivo, lung tumor cells with disrupted E-cadherin expressed beta-catenin target genes normally found in other endodermal lineages suggesting that reprogramming may be involved in metastatic progression.
  • [MeSH-major] Adenocarcinoma / secondary. Cadherins / metabolism. Carcinoma, Non-Small-Cell Lung / secondary. Cell Adhesion. Lung Neoplasms / blood supply. Neovascularization, Pathologic / pathology. Proto-Oncogene Proteins c-raf / physiology
  • [MeSH-minor] Adenoma / etiology. Adenoma / pathology. Adherens Junctions. Animals. Apoptosis. Biomarkers / metabolism. Cells, Cultured. Disease Progression. Endoderm / metabolism. Endothelium, Vascular / cytology. Endothelium, Vascular / metabolism. Endothelium, Vascular / pathology. Fluorescent Antibody Technique. Genes, Dominant. Immunoblotting. Immunoprecipitation. In Situ Nick-End Labeling. Luciferases / metabolism. Mice. Mice, Knockout. Mice, Transgenic. Neoplasm Invasiveness. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism. beta Catenin / genetics. beta Catenin / metabolism


13. Herzig M, Savarese F, Novatchkova M, Semb H, Christofori G: Tumor progression induced by the loss of E-cadherin independent of beta-catenin/Tcf-mediated Wnt signaling. Oncogene; 2007 Apr 5;26(16):2290-8
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  • [Title] Tumor progression induced by the loss of E-cadherin independent of beta-catenin/Tcf-mediated Wnt signaling.
  • E-cadherin-mediated cell-cell adhesion is frequently lost during the development of malignant epithelial cancers.
  • Employing a transgenic mouse model of beta-cell carcinogenesis (Rip1Tag2) we have previously shown that the loss of E-cadherin is a rate-limiting step in the progression from adenoma to carcinoma.
  • However, the mere loss of cell adhesion may not be sufficient and additional signals are required to cause tumor cells to permeate the basal membrane and to invade surrounding tissue.
  • Besides being an important component of the E-cadherin cell-adhesion complex, beta-catenin plays a critical role in canonical Wnt signaling.
  • We report here that beta-catenin-mediated Wnt signaling does not contribute to tumor progression in Rip1Tag2 mice.
  • E-cadherin downregulates beta-catenin/Tcf-mediated transcriptional activity by sequestrating beta-catenin into E-cadherin cell-adhesion complexes even in the presence of activated Wnt signaling.
  • Upon loss of E-cadherin expression, beta-catenin is degraded and Tcf/beta-catenin-mediated transcriptional activity is not induced.
  • Moreover, forced expression of constitutive-active beta-catenin or genetic ablation of Tcf/beta-catenin transcriptional activity in tumor cells of Rip1Tag2 transgenic mice does not affect tumor progression.
  • Together, the data indicate that signals other than beta-catenin/Tcf-mediated Wnt signaling are induced by the loss of E-cadherin during tumor progression in Rip1Tag2 transgenic mice.
  • [MeSH-major] Adenoma / pathology. Cadherins / genetics. Lymphoma / pathology. TCF Transcription Factors / physiology. Wnt Proteins / physiology. beta Catenin / physiology
  • [MeSH-minor] Animals. DNA Primers. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Insulinoma. Mice. Mice, Transgenic. Neoplasm Invasiveness. Pancreatic Neoplasms. Polymerase Chain Reaction. Transcription, Genetic

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  • (PMID = 17043652.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; 0 / DNA Primers; 0 / TCF Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin
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4. Jasinski JM, Eisenbarth GS: Insulin as a primary autoantigen for type 1A diabetes. Clin Dev Immunol; 2005 Sep;12(3):181-6
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  • [Title] Insulin as a primary autoantigen for type 1A diabetes.
  • Type 1A diabetes mellitus is caused by specific and progressive autoimmune destruction of the beta cells in the islets of Langerhans whereas the other cell types in the islet (alpha, delta, and PP) are spared.
  • The autoantigens of Type 1A diabetes may be divided into subgroups based on their tissue distributions: Beta-cell-specific antigens like insulin, insulin derivatives, and IGRP (Islet-specific Glucose-6-phosphatase catalytic subunit Related Peptide); neurendocrine antigens such as carboxypeptidase H, insulinoma-associated antigen (IA-2), glutamic acid decarboxylase (GAD65), and carboxypeptidase E; and those expressed ubiquitously like heat shock protein 60 (a putative autoantigen for type 1 diabetes).
  • This review will focus specifically on insulin as a primary autoantigen, an essential target for disease, in type 1A diabetes mellitus.
  • In particular, immunization with insulin peptide B:9-23 can be used to induce insulin autoantibodies and diabetes in animal models or used to prevent diabetes.
  • Genetic manipulation of the insulin 1 and 2 genes reciprocally alters development of diabetes in the NOD mouse, and insulin gene polymorphisms are important determinants of childhood diabetes.
  • We are pursuing the hypothesis that insulin is a primary autoantigen for type 1 diabetes, and thus the pathogenesis of the disease relates to specific recognition of one or more peptides.

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  • (PMID = 16295523.001).
  • [ISSN] 1740-2522
  • [Journal-full-title] Clinical & developmental immunology
  • [ISO-abbreviation] Clin. Dev. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI95380; United States / NIDDK NIH HHS / DK / DK32493; United States / NIDDK NIH HHS / DK / DK32083; United States / NIDDK NIH HHS / DK / DK50970; United States / NCRR NIH HHS / RR / M01 RR00051; United States / NIDDK NIH HHS / DK / DK55969; United States / NIDDK NIH HHS / DK / P30 DK57516; United States / NIDDK NIH HHS / DK / DK62718; United States / NIAID NIH HHS / AI / AI46374; United States / NCRR NIH HHS / RR / M01 RR00069; United States / NIAID NIH HHS / AI / AI39213; United States / NIAID NIH HHS / AI / AI50864
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Autoantigens; 0 / Epitopes; 0 / Insulin; 0 / Protein Precursors; 61116-24-3 / preproinsulin; 9035-68-1 / Proinsulin
  • [Number-of-references] 58
  • [Other-IDs] NLM/ PMC2275421
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15. Marsh V, Winton DJ, Williams GT, Dubois N, Trumpp A, Sansom OJ, Clarke AR: Epithelial Pten is dispensable for intestinal homeostasis but suppresses adenoma development and progression after Apc mutation. Nat Genet; 2008 Dec;40(12):1436-44
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  • [Title] Epithelial Pten is dispensable for intestinal homeostasis but suppresses adenoma development and progression after Apc mutation.
  • PTEN acts as a tumor suppressor in a range of tissue types and has been implicated in the regulation of intestinal stem cells.
  • We show that Pten loss specifically within the adult or embryonic epithelial cell population does not affect the normal architecture or homeostasis of the epithelium.
  • We conclude that Pten is redundant in otherwise normal intestinal epithelium and epithelial stem cells but, in the context of activated Wnt signaling, suppresses progression to adenocarcinoma through modulation of activated Akt levels.
  • [MeSH-major] Adenoma / genetics. Adenomatous Polyposis Coli Protein / genetics. Intestinal Neoplasms / genetics. Intestine, Small / pathology. PTEN Phosphohydrolase / genetics
  • [MeSH-minor] Animals. Gene Deletion. Mice. Tamoxifen. beta-Naphthoflavone

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  • (PMID = 19011632.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0301154; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 094ZI81Y45 / Tamoxifen; 6051-87-2 / beta-Naphthoflavone; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.1.3.67 / Pten protein, mouse
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16. Fukazawa K, Kayanuma H, Kanai E, Sakata M, Shida T, Suganuma T: Insulinoma with basal ganglion involvement detected by magnetic resonance imaging in a dog. J Vet Med Sci; 2009 May;71(5):689-92
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  • [Title] Insulinoma with basal ganglion involvement detected by magnetic resonance imaging in a dog.
  • Suspecting a metabolic disorder, an abdominal ultrasonography was performed, and a tumor was found in the pancreas.
  • The pancreatic tumor was surgically removed based on suspicion that it had induced the brain damage.
  • The resected tumor was histopathologically diagnosed as an insulinoma.
  • Consequently, the tumor was thought to have induced the lesion in the basal ganglion, and this was verified by MRI.

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  • (PMID = 19498303.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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17. L'Amoreaux WJ, Cuttitta C, Santora A, Blaize JF, Tachjadi J, El Idrissi A: Taurine regulates insulin release from pancreatic beta cell lines. J Biomed Sci; 2010;17 Suppl 1:S11
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  • [Title] Taurine regulates insulin release from pancreatic beta cell lines.
  • BACKGROUND: Pancreatic beta-cells release insulin via an electrogenic response triggered by an increase in plasma glucose concentrations.
  • The critical plasma glucose concentration has been determined to be approximately 3 mM, at which time both insulin and GABA are released from pancreatic beta-cells.
  • Taurine, a beta-sulfonic acid, may be transported into cells to balance osmotic pressure.
  • The taurine transporter (TauT) has been described in pancreatic tissue, but the function of taurine in insulin release has not been established.
  • Uptake of taurine by pancreatic beta-cells may alter membrane potential and have an effect on ion currents.
  • If taurine uptake does alter beta-cell current, it might have an effect on exocytosis of cytoplasmic vesicle.
  • We wished to test the effect of taurine on regulating release of insulin from the pancreatic beta-cell.
  • METHODS: Pancreatic beta-cell lines Hit-TI5 (Syrian hamster) and Rin-m (rat insulinoma) were used in these studies.
  • Cells were grown to an 80% confluence on uncoated cover glass in RPMI media containing 10% fetal horse serum.
  • The cells were then adapted to a serum-free, glucose free environment for 24 hours.
  • At that time, the cells were treated with either 1 mM glucose, 1 mM taurine, 1 mM glucose + 1 mM taurine, 3 mM glucose, or 3 mM glucose + 1 mM taurine.
  • The cells were examined by confocal microscopy for cytoplasmic levels of insulin.
  • RESULTS: In both cell lines, 1 mM glucose had no effect on insulin levels and served as a control.
  • Cells starved of glucose had a significant reduction (p<0.001) in the level of insulin, but this level was significantly higher than all other treatments.
  • As expected, the 3 mM glucose treatment resulted in a statistically lower (p<0.001) insulin level than control cells.
  • Interestingly, 1 mM taurine also resulted in a statistically lower level of insulin (p<0.001) compared to controls when either no glucose or 1 mM glucose was present.
  • Cells treated with 1 mM taurine plus 3 mM glucose showed a level of insulin similar to that of 3 mM glucose alone.
  • CONCLUSIONS: Taurine administration can alter the electrogenic response in beta-cell lines, leading to a change in calcium homeostasis and a subsequent decrease in intracellular insulin levels.
  • The consequence of these actions could represent a method of increasing plasma insulin levels leading to a decrease in plasma glucose levels.
  • [MeSH-major] Insulin / secretion. Insulin-Secreting Cells. Taurine / pharmacology
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Line. Cricetinae. Glucose / pharmacology. Membrane Glycoproteins / metabolism. Membrane Transport Proteins / metabolism. Rats. gamma-Aminobutyric Acid / metabolism

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  • (PMID = 20804585.001).
  • [ISSN] 1423-0127
  • [Journal-full-title] Journal of biomedical science
  • [ISO-abbreviation] J. Biomed. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Membrane Glycoproteins; 0 / Membrane Transport Proteins; 148686-53-7 / taurine transporter; 1EQV5MLY3D / Taurine; 56-12-2 / gamma-Aminobutyric Acid; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2994409
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18. Mziaut H, Kersting S, Knoch KP, Fan WH, Trajkovski M, Erdmann K, Bergert H, Ehehalt F, Saeger HD, Solimena M: ICA512 signaling enhances pancreatic beta-cell proliferation by regulating cyclins D through STATs. Proc Natl Acad Sci U S A; 2008 Jan 15;105(2):674-9
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  • [Title] ICA512 signaling enhances pancreatic beta-cell proliferation by regulating cyclins D through STATs.
  • Changes in metabolic demands dynamically regulate the total mass of adult pancreatic beta-cells to adjust insulin secretion and preserve glucose homeostasis.
  • Glucose itself is a major regulator of beta-cell proliferation by inducing insulin secretion and activating beta-cell insulin receptors.
  • Here, we show that islet cell autoantigen 512 (ICA512)/IA-2, an intrinsic tyrosine phosphatase-like protein of the secretory granules, activates a complementary pathway for beta-cell proliferation.
  • On granule exocytosis, the ICA512 cytoplasmic domain is cleaved and the resulting cytosolic fragment (ICA512-CCF) moves into the nucleus where it enhances the levels of phosphorylated STAT5 and STAT3, thereby inducing insulin gene transcription and granule biogenesis.
  • We now show that knockdown of ICA512 decreases cyclin D1 levels and proliferation of insulinoma INS-1 cells, whereas beta-cell regeneration is reduced in partially pancreatectomized ICA512-/- mice.
  • Conversely, overexpression of ICA512-CCF increases both cyclin D1 and D2 levels and INS-1 cell proliferation.
  • Up-regulation of cyclin D1 and D2 by ICA512-CCF is affected by knockdown of STAT3 and STAT5, respectively, whereas it does not require insulin signaling.
  • These results identify ICA512 as a regulator of cyclins D and beta-cell proliferation through STATs and may have implication for diabetes therapy.
  • [MeSH-major] Cyclins / biosynthesis. Gene Expression Regulation. Insulin-Secreting Cells / metabolism. Receptor-Like Protein Tyrosine Phosphatases, Class 8 / physiology. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism
  • [MeSH-minor] Animals. Cell Proliferation. Cyclin D. Cyclin D2. Diabetes Mellitus / drug therapy. Diabetes Mellitus / metabolism. Humans. Insulin / metabolism. Models, Biological. Phosphorylation. Rats. Regeneration. Signal Transduction


19. Leow MK, Wyckoff J: Under-recognised paradox of neuropathy from rapid glycaemic control. Postgrad Med J; 2005 Feb;81(952):103-7
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  • Insulin induced neuropathy has been reported previously in people with diabetes treated with insulin, and subsequently reported in patients with insulinomas.
  • [MeSH-major] Diabetic Neuropathies / chemically induced. Hemoglobin A, Glycosylated / drug effects. Hyperglycemia / drug therapy. Hypoglycemia / chemically induced. Hypoglycemic Agents / adverse effects. Insulin / adverse effects

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  • (PMID = 15701742.001).
  • [ISSN] 0032-5473
  • [Journal-full-title] Postgraduate medical journal
  • [ISO-abbreviation] Postgrad Med J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Hemoglobin A, Glycosylated; 0 / Hypoglycemic Agents; 0 / Insulin
  • [Number-of-references] 38
  • [Other-IDs] NLM/ PMC1743196
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20. Oue N, Mitani Y, Aung PP, Sakakura C, Takeshima Y, Kaneko M, Noguchi T, Nakayama H, Yasui W: Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma. J Pathol; 2005 Oct;207(2):185-98
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  • [Title] Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma.
  • Regenerating islet-derived family, member 4 (Reg IV) is a candidate marker for cancer and inflammatory bowel disease.
  • In the stomach, foveolar epithelium was negative for Reg IV, whereas goblet cells of intestinal metaplasia and neuroendocrine cells at the base of intestinal metaplasia expressed Reg IV.
  • Neuroendocrine cells of the small intestine and colon showed strong expression of Reg IV, whereas goblet cells of the small intestine and colon showed weak or no expression of Reg IV.
  • Insulin-producing beta cells of the endocrine pancreas were positive for Reg IV.
  • Among 143 gastric adenocarcinomas, Reg IV expression was detected in 42 (29.4%) and was associated with both the intestinal mucin phenotype and neuroendocrine differentiation.
  • No association was found between Reg IV expression and clinical characteristics such as tumour stage and patient prognosis.
  • Of 36 colorectal adenocarcinomas, 13 (36.1%) were positive for Reg IV, which was associated with tumour stage (p = 0.0379, Fisher's exact test).
  • Expression of Reg IV was detected in 14 (93.3%) of 15 colorectal carcinoid tumours.
  • Reg IV expression was also detected in 5 (21.7%) of 23 ductal adenocarcinomas of the pancreas.
  • This is the first immunohistochemical analysis of the expression and distribution of Reg IV protein in human tumours.
  • These data suggest that Reg IV is expressed by gastrointestinal and pancreatic tumours, including adenocarcinomas and carcinoid tumours, and that Reg IV is associated with intestinal and neuroendocrine differentiation of the stomach and gastric carcinoma.
  • [MeSH-major] Adenocarcinoma / chemistry. Lectins, C-Type / analysis. Neoplasm Proteins / analysis. Stomach Neoplasms / chemistry
  • [MeSH-minor] Adenoma / chemistry. Biomarkers, Tumor / analysis. Blotting, Western / methods. Breast Neoplasms / chemistry. Carcinoid Tumor / chemistry. Cell Differentiation / physiology. Cell Line, Tumor. Colon / metabolism. Colorectal Neoplasms / chemistry. Female. Humans. Immunohistochemistry / methods. Intestine, Small / metabolism. Lung Neoplasms / chemistry. Pancreas / metabolism. Pancreatic Neoplasms / chemistry. Phenotype. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Stomach / metabolism

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  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16086444.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Neoplasm Proteins; 0 / REG4 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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21. Jürgensen C, Schuppan D, Neser F, Ernstberger J, Junghans U, Stölzel U: EUS-guided alcohol ablation of an insulinoma. Gastrointest Endosc; 2006 Jun;63(7):1059-62
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  • [Title] EUS-guided alcohol ablation of an insulinoma.
  • BACKGROUND: Surgical resection is currently considered to be the criterion standard for treatment of insulinomas.
  • EUS-guided ethanol ablation of endocrine tumors has not been reported before.
  • INTERVENTION: A 78-year-old woman was referred with typical symptoms of an insulinoma.
  • Because of severe complications during several hypoglycemic episodes, a poor general condition, and strict refusal of surgical resection, the decision was made to ablate the insulinoma by EUS-guided alcohol injection.
  • A total of 8 mL 95% ethanol was injected into the tumor.
  • Based on clinical, morphologic, and biochemical criteria, we achieved a durable complete remission of the tumor.
  • CONCLUSIONS: EUS-guided ablation may become a minimally invasive alternative for patients with insulinomas in whom surgery is not feasible.
  • [MeSH-major] Endosonography. Ethanol / administration & dosage. Insulinoma / drug therapy. Pancreatic Neoplasms / drug therapy

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  • (PMID = 16733126.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 3K9958V90M / Ethanol
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22. Krause K, Karger S, Schierhorn A, Poncin S, Many MC, Fuhrer D: Proteomic profiling of cold thyroid nodules. Endocrinology; 2007 Apr;148(4):1754-63
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  • Cold thyroid nodules (CTNs) represent a frequent endocrine disorder accounting for up to 85% of thyroid nodules in a population living in an iodine-deficient area.
  • To obtain novel insights into their pathogenesis, protein expression profiling was performed in a series of 27 solitary CTNs (10 follicular adenoma and 20 adenomatous nodules) and surrounding normal thyroid tissues using two-dimensional gel electrophoresis combined with mass spectrometry analysis, Western blotting, and immunohistochemistry.
  • 1) thyroid cell proliferation, 2) turnover of thyroglobulin, and 3) H2O2 detoxification.
  • Furthermore, we provide preliminary evidence that up-regulation of H2O2 generation in CTNs could override the antioxidative system resulting in oxidative stress, which is suggested by the finding of raised 8-oxo-guanidine DNA adduct formation in CTNs.
  • [MeSH-minor] Adult. Aged. Amyloid beta-Protein Precursor / metabolism. Antioxidants / metabolism. Female. Humans. Male. Middle Aged. Models, Biological. Oxidative Stress / genetics. Protease Nexins. Receptors, Cell Surface / metabolism


23. Fontanière S, Casse H, Bertolino P, Zhang CX: Analysis of p27(Kip1) expression in insulinomas developed in pancreatic beta-cell specific Men1 mutant mice. Fam Cancer; 2006;5(1):49-54
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  • [Title] Analysis of p27(Kip1) expression in insulinomas developed in pancreatic beta-cell specific Men1 mutant mice.
  • Multiple Endocrine Neoplasia type 1 (MEN1) is a hereditary disease characterised by the occurrence of multiple endocrine tumours.
  • Interestingly, it has been recently reported that p27(Kip1) expression is regulated by menin and that decreased p27(Kip1) expression can be found in MEN1 insulinomas and parathyroid adenomas.
  • In order to address whether and when p27(Kip1) expression alters during insulinoma development in pancreatic beta-cell-specific Men1 mutant mice, we analysed p27(Kip1) expression in islet lesions from mutant mice at different ages.
  • Our data revealed that p27(Kip1) protein expression was reduced in 40 out of 52 (77%) insulinomas analysed, whereas the remaining 12 insulinomas (23%) did not show altered p27(Kip1) expression.
  • No difference between the insulinomas with and without decreased p27(Kip1) expression could be observed in terms of histological features or menin inactivation.
  • Furthermore, our analysis on hyperplastic and dysplastic islets developed in young mutant mice showed the lack of detectable alteration in p27(Kip1) expression, despite evident loss of menin expression in a substantial proportion of islet cells.
  • Our work confirms the altered p27(Kip1) expression reported in tumours from MEN1 patients, whereas it suggests that other molecular events may also participate in the tumorigenesis process initiated by the Men1 gene inactivation.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p27 / genetics. Gene Expression Regulation, Neoplastic. Insulinoma / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Animals. Blotting, Western. Cell Survival. Disease Models, Animal. Down-Regulation. Gene Deletion. Immunohistochemistry. Islets of Langerhans / cytology. Mice. Mice, Mutant Strains. Probability. Proto-Oncogene Proteins / genetics. Sensitivity and Specificity. Tumor Cells, Cultured


24. Paner GP, Luthringer DJ, Amin MB: Best practice in diagnostic immunohistochemistry: prostate carcinoma and its mimics in needle core biopsies. Arch Pathol Lab Med; 2008 Sep;132(9):1388-96
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  • CONTEXT: The unrelenting challenge encountered when differentiating limited-volume prostate carcinoma and sometimes subtle variants from its many morphologic mimics has increased the use of ancillary immunohistochemistry in routine prostate needle biopsies.
  • The availability of prostate cancer-associated and basal cell-associated markers has been an invaluable addition to diagnostic surgical pathology.
  • OBJECTIVE: To review commonly used immunohistochemical stains, including innovative combinations, for confirmation or differential diagnosis of prostate carcinoma, and to propose appropriately constructed panels using morphologic patterns in prostate needle biopsies.
  • CONCLUSIONS: Basal cell-associated markers p63, high-molecular-weight cytokeratin 34 beta E12, cytokeratin 5/6 or a cocktail containing p63 and high-molecular-weight cytokeratin 34 beta E12 or cytokeratin 5/6 and prostate carcinoma-specific marker alpha-methylacyl coenzyme A (coA) racemase alone or in combination are useful adjuncts in confirming prostatic carcinoma that either lacks diagnostic, qualitative or quantitative features or that has an unusual morphologic pattern (eg, atrophic, pseudohyperplastic) or is in the setting of prior treatment.
  • The combination of alpha-methylacyl coA racemase positivity with negative staining for basal cell-associated markers supports a malignant diagnosis in the appropriate morphologic context.
  • Dual chromogen basal cell- associated markers (p63 [nuclear] and high-molecular-weight cytokeratin 34 beta E12/cytokeratin 5/6 [cytoplasmic]) and alpha-methylacyl coA racemase in an antibody cocktail provide greater sensitivity for the basal cell layer, easing evaluation and minimizing loss of representation of the focal area interest because the staining is performed on one slide.
  • In the posttreatment setting, pancytokeratin facilitates detection of subtle-treated cancer cells.
  • Prostate-specific antigen and prostatic acid phosphatase markers are helpful in excluding secondary malignancies involving the prostate, such as urothelial carcinoma, and occasionally in excluding nonprostatic benign mimickers, such as nephrogenic adenoma, mesonephric gland hyperplasia, and Cowper glands.
  • [MeSH-major] Biomarkers, Tumor / analysis. Biopsy, Needle. Immunohistochemistry / methods. Prostatic Neoplasms / diagnosis

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  • (PMID = 18788849.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 47
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25. Rebouissou S, Amessou M, Couchy G, Poussin K, Imbeaud S, Pilati C, Izard T, Balabaud C, Bioulac-Sage P, Zucman-Rossi J: Frequent in-frame somatic deletions activate gp130 in inflammatory hepatocellular tumours. Nature; 2009 Jan 8;457(7226):200-4
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  • [Title] Frequent in-frame somatic deletions activate gp130 in inflammatory hepatocellular tumours.
  • Inflammatory hepatocellular adenomas are benign liver tumours defined by the presence of inflammatory infiltrates and by the increased expression of inflammatory proteins in tumour hepatocytes.
  • Here we show a marked activation of the interleukin (IL)-6 signalling pathway in this tumour type; sequencing candidate genes pinpointed this response to somatic gain-of-function mutations in the IL6ST gene, which encodes the signalling co-receptor gp130.
  • Indeed, 60% of inflammatory hepatocellular adenomas harbour small in-frame deletions that target the binding site of gp130 for IL-6, and expression of four different gp130 mutants in hepatocellular cells activates signal transducer and activator of transcription 3 (STAT3) in the absence of ligand.
  • Furthermore, analysis of hepatocellular carcinomas revealed that rare gp130 alterations are always accompanied by beta-catenin-activating mutations, suggesting a cooperative effect of these signalling pathways in the malignant conversion of hepatocytes.
  • The recurrent gain-of-function gp130 mutations in these human hepatocellular adenomas fully explains activation of the acute inflammatory phase observed in tumourous hepatocytes, and suggests that similar alterations may occur in other inflammatory epithelial tumours with STAT3 activation.


26. Vezzosi D, Bennet A, Fauvel J, Caron P: Insulin, C-peptide and proinsulin for the biochemical diagnosis of hypoglycaemia related to endogenous hyperinsulinism. Eur J Endocrinol; 2007 Jul;157(1):75-83
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  • [Title] Insulin, C-peptide and proinsulin for the biochemical diagnosis of hypoglycaemia related to endogenous hyperinsulinism.
  • OBJECTIVE: We evaluated the respective value of insulin, C-peptide and proinsulin levels in 33 patients with endogenous hyperinsulinism and in 67 controls to determine the best parameters and thresholds to make or to rule out the diagnosis of endogenous hyperinsulinism.
  • RESULTS: When blood glucose levels were below 2.5 mmol/l, insulin was <21 pmol/l in 8-35% of the patients and in all controls; C-peptide was >0.2 nmol/l in all insulinomas but not in the nesidioblastosis or in the controls; proinsulin was >5 pmol/l in all patients but not in the controls.
  • Concomitant C-peptide levels above 0.2 nmol/l also make the diagnosis of all our insulinoma patients, not the diagnosis of nesidioblastosis, while insulin levels have much less diagnostic accuracy.

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  • [ErratumIn] Eur J Endocrinol. 2007 Nov;157(5):693
  • (PMID = 17609405.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Controlled Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Blood Glucose; 0 / C-Peptide; 0 / Insulin; 9035-68-1 / Proinsulin
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27. Körner M, Waser B, Reubi JC, Miller LJ: CCK(2) receptor splice variant with intron 4 retention in human gastrointestinal and lung tumours. J Cell Mol Med; 2010 Apr;14(4):933-43
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  • [Title] CCK(2) receptor splice variant with intron 4 retention in human gastrointestinal and lung tumours.
  • The wild-type cholecystokinin type 2 (CCK(2)) receptor is expressed in many gastrointestinal and lung tumours.
  • A splice variant of the CCK(2) receptor with retention of intron 4 (CCK(2)Ri4sv) showing constitutive activity associated with increased tumour growth was described in few colorectal, pancreatic and gastric cancers.
  • Given the potential functional and clinical importance of this spliceoform, its occurrence was quantitatively characterized in a broad collection of 81 gastrointestinal and lung tumours, including insulinomas, ileal carcinoids, gastrointestinal stromal tumours (GIST), gastric, colorectal and pancreatic ductal adenocarcinomas, cholangiocellular and hepatocellular carcinomas, small cell lung cancers (SCLC), non-SCLC (nSCLC) and bronchopulmonary carcinoids, as well as 21 samples of corresponding normal tissues.
  • Wild-type CCK(2) receptor transcripts were found in the vast majority of tumours and normal tissues.
  • CCK(2)Ri4sv mRNA expression was present predominantly in insulinomas (incidence 100%), GIST (100%) and SCLC (67%), but rarely in pancreatic, colorectal and gastric carcinomas and nSCLC.
  • It was not found in wild-type CCK(2) receptor negative tumours or any normal tissues tested.
  • CCK(2)Ri4sv transcript levels in individual tumours were low, ranging from 0.02% to 0.14% of total CCK(2) receptor transcripts.
  • In conclusion, the CCK(2)Ri4sv is a marker of specific gastrointestinal and lung tumours.

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  • (PMID = 19627395.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R37 DK032878-27; United States / NIDDK NIH HHS / DK / R01 DK032878; United States / NIDDK NIH HHS / DK / R37 DK032878; United States / NIDDK NIH HHS / DK / DK032878-27; United States / NIDDK NIH HHS / DK / DK32878
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptor, Cholecystokinin B
  • [Other-IDs] NLM/ NIHMS144707; NLM/ PMC2888751
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28. Oertli D: [Current concepts in minimal invasive endocrine surgery]. Ther Umsch; 2005 Feb;62(2):90-5
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  • Prerequisits for all of these approaches are a positive preoperative localisation of the adenoma, an intraoperative parathormone testing, and the respective surgical experience in the minimal invasive technique.
  • The experience with the laparoscopic approach to endocrine pancreatic tumours is still limited.
  • Good indications are insulinomas that are located anteriorly or within the tail of the pancreatic gland.
  • Nowadays, laparoscopic enucleation of such tumours and tail resections become feasable and safe.
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / surgery. Aged. Female. Humans. Insulinoma / surgery. Length of Stay. Male. Pancreatic Neoplasms / surgery. Parathyroid Neoplasms / diagnosis. Parathyroid Neoplasms / surgery. Patient Selection. Postoperative Complications. Safety. Time Factors

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  • (PMID = 15756917.001).
  • [ISSN] 0040-5930
  • [Journal-full-title] Therapeutische Umschau. Revue thérapeutique
  • [ISO-abbreviation] Ther Umsch
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 52
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29. Ramos E, Baron S, Sentanac S, Touati G, Picherot G: [Hypoglycemia associated with oral sulfonylurea hypoglycaemic agents in an 11-year-old girl]. Arch Pediatr; 2005 Jul;12(7):1109-11
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  • [Transliterated title] Hypoglycémie liée à la prise volontaire de sulfamides hypoglycémiants chez une enfant de 11 ans.
  • CASE REPORT: We report the case of an 11-year-old girl who presented recurrent hypoglycemia with endogenous hyperinsulinism (high insulin and C-peptide concentrations).
  • The morphological investigations didn't find insulinoma.
  • CONCLUSION: The sulfonylurea drugs can mimic an endogenous hyperinsulinism and mislead the diagnostic to an insulinoma suspicion and lead to a surgical exploration.
  • [MeSH-minor] Child. Diagnosis, Differential. Female. Humans. Hyperinsulinism / diagnosis. Insulinoma / diagnosis

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  • (PMID = 15925501.001).
  • [ISSN] 0929-693X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / Sulfonylurea Compounds
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30. Kang TW, Lee KT, Ryu MK, Moon W, Lee SS, Lee SY, Hwang JY, Lee JK, Heo JS, Choi SH, Kim SH, Paik SW, Rhee JC: [Clinical features of neuroendocrine tumor of the pancreas: single center study]. Korean J Gastroenterol; 2006 Aug;48(2):112-8
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  • [Title] [Clinical features of neuroendocrine tumor of the pancreas: single center study].
  • BACKGROUND/AIMS: Pancreatic neuroendocrine tumors (PNET) are rare and manifest as functioning tumor (FT) or non-functioning tumor (NFT).
  • Although malignant changes are observed in some cases, its prognosis is better than pancreatic cancer.
  • RESULTS: PNET included 6 insulinomas, 4 gastrinomas, 1 glucagonoma, 1 somatostatinoma and 31 NFT.
  • The major clinical manifestations were neuroglycopenic symptoms (100%) in insulinoma, abdominal ulcer symptoms (75%) in gastrinoma, dermatitis (100%) in glucagonoma, steatorrhea (100%) in somatostatinoma, and abdominal discomfort or pain (45%) in NFT.
  • In the recurrent NFT, the findings of diabetes mellitus (p=0.010), abnormal pancreatic duct (p=0.026), Whipple's operation (p=0.013) and tumor emboli (p=0.03) were more common than in non-recurrent NFT.
  • [MeSH-major] Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diabetes Mellitus / pathology. Female. Humans. Male. Middle Aged. Neoplastic Cells, Circulating / pathology. Pancreatic Ducts / abnormalities. Pancreatic Ducts / pathology. Whipple Disease / complications

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  • (PMID = 16929155.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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31. Woeste G, Zapletal C, Golling M, Usadel KH, Vogl TJ, Bechstein WO, Wullstein C: Telerobotic-assisted laparoscopic spleen-preserving partial resection of the pancreatic tail for insulinoma. HPB (Oxford); 2006;8(3):233-4
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  • [Title] Telerobotic-assisted laparoscopic spleen-preserving partial resection of the pancreatic tail for insulinoma.
  • Laparoscopic pancreatic resection is rarely described.
  • Telerobotic-assisted laparoscopy may offer some advantages for resection of the pancreatic tail.
  • A 49-year-old woman was diagnosed with insulinoma located in the pancreatic tail.
  • Telerobotic-assisted laparoscopic spleen-preserving resection of the pancreatic tail was performed.
  • The previously described advantages of a telerobotic approach with extended range of motion and three-dimensional view make more complex operations like pancreatic resection possible and may offer extended indications for laparoscopic surgery.

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  • (PMID = 18333283.001).
  • [ISSN] 1365-182X
  • [Journal-full-title] HPB : the official journal of the International Hepato Pancreato Biliary Association
  • [ISO-abbreviation] HPB (Oxford)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2131675
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32. Nakajima K, Wu G, Takeyama N, Sakudo A, Sugiura K, Yukawa M, Onodera T: Insulinoma-associated protein 2-deficient mice develop severe forms of diabetes induced by multiple low doses of streptozotocin. Int J Mol Med; 2009 Jul;24(1):23-7
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  • [Title] Insulinoma-associated protein 2-deficient mice develop severe forms of diabetes induced by multiple low doses of streptozotocin.
  • Insulinoma-associated protein 2 (IA-2) is the major autoantigen that contributes to the pathogenesis of type 1 diabetes (T1D).
  • IA-2-deficient (IA-2-/-) mice showed impaired insulin secretion after intraperitoneal injection of glucose as well as elevated glucose level in a glucose tolerance test.
  • STZ injection to IA-2-/- mice caused significant elevation of blood glucose and depressed insulin concentration in the pancreas.
  • Furthermore, abnormal ultrastructure in the beta cells of the IA-2-/- mice was revealed by electron microscopy, showing a decreased number of insulin containing vesicles and dilation of the ER-Golgi complex.
  • These results demonstrated that IA-2-/- mice had higher sensitivity to STZ, suggesting a role of IA-2 not only in the secretion but also in the production of insulin.
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Insulin / blood. Insulin-Secreting Cells / metabolism. Insulin-Secreting Cells / ultrastructure. Male. Mice. Mice, Knockout

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  • (PMID = 19513530.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Blood Glucose; 0 / Insulin; 5W494URQ81 / Streptozocin; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 8
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33. Hawinkels LJ, Kuiper P, Wiercinska E, Verspaget HW, Liu Z, Pardali E, Sier CF, ten Dijke P: Matrix metalloproteinase-14 (MT1-MMP)-mediated endoglin shedding inhibits tumor angiogenesis. Cancer Res; 2010 May 15;70(10):4141-50
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  • [Title] Matrix metalloproteinase-14 (MT1-MMP)-mediated endoglin shedding inhibits tumor angiogenesis.
  • Endoglin is a transforming growth factor-beta coreceptor with a crucial role in angiogenesis.
  • Therefore, we examined the role of sEndoglin in tumor angiogenesis and the mechanism by which the extracellular domain of endoglin is released from the membrane.In colorectal cancer specimens, we observed high endothelial endoglin protein expression, accompanied with slightly lower sEndoglin levels in the circulation, compared with healthy controls.
  • Human umbilical vascular endothelial cells were found to secrete high levels of sEndoglin.
  • Using cleavage site mutants, we determined that MMP-14 cleaved endoglin at a site in close proximity to the transmembrane domain.
  • Taken together, this study shows that MMP-14 mediates endoglin shedding, which may regulate the angiogenic potential of endothelial cells in the (colorectal) tumor microenvironment.
  • [MeSH-major] Adenoma / blood supply. Antigens, CD / metabolism. Colorectal Neoplasms / blood supply. Matrix Metalloproteinase 14 / metabolism. Neovascularization, Pathologic / prevention & control. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Animals. COS Cells. Cell Membrane / metabolism. Cells, Cultured. Cercopithecus aethiops. Colon / cytology. Colon / metabolism. Endothelium, Vascular / cytology. Endothelium, Vascular / metabolism. Enzyme-Linked Immunosorbent Assay. Humans. Immunoenzyme Techniques. Matrix Metalloproteinase Inhibitors. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Rectum / cytology. Rectum / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Umbilical Veins / cytology. Umbilical Veins / metabolism

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  • [Copyright] (c)2010 AACR.
  • (PMID = 20424116.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / ENG protein, human; 0 / Matrix Metalloproteinase Inhibitors; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, Cell Surface; EC 3.4.24.80 / MMP14 protein, human; EC 3.4.24.80 / Matrix Metalloproteinase 14
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34. Doi Y, Kawamata H, Ono Y, Fujimori T, Imai Y: Expression and cellular localization of TSC-22 in normal salivary glands and salivary gland tumors: implications for tumor cell differentiation. Oncol Rep; 2008 Mar;19(3):609-16
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  • [Title] Expression and cellular localization of TSC-22 in normal salivary glands and salivary gland tumors: implications for tumor cell differentiation.
  • TGF-beta-stimulated clone-22 (TSC-22) was reported to be a differentiation-inducing factor which negatively regulates the growth of salivary gland cancer cells.
  • In the present study, we examined the expression of TSC-22 in salivary gland tumors by immunohistochemistry.
  • In pleomorphic adenoma (PA), most of the sparse myoepithelial-like tumor cells, which are considered as the differentiated cells because they produce extracellular matrix, expressed TSC-22.
  • However, only a limited number of cases of the solid myoepithelial-like tumor cells in PA, which are considered as the growing cells, expressed TSC-22.
  • In adenoid cystic carcinoma (ACC), inner ductal cells in the tubular structure, strongly expressed TSC-22, though the outer myoepithelial-like tumor cells did not express TSC-22.
  • In the cribriform structure, myoepithelial-like tumor cells did not express TSC-22.
  • Sparse type myoepithelial-like tumor cells in ACC also expressed TSC-22.
  • In mucoepidermoid carcinoma, epidermoid tumor cells and mucous-producing tumor cells in mucoepidermoid carcinoma frequently expressed TSC-22.
  • Thus, the expression of TSC-22 was frequently observed in the cells with differentiated-phenotypes, although rarely in the cells with growing potentials.
  • These results suggest that TSC-22 may play an important role in maintaining the differentiated phenotype in salivary gland tumors.
  • [MeSH-minor] Cell Differentiation. Humans. Immunohistochemistry

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  • (PMID = 18288391.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Repressor Proteins; 0 / TSC22D1 protein, human
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35. Aoyagi K, Ohara-Imaizumi M, Nishiwaki C, Nakamichi Y, Nagamatsu S: Insulin/phosphoinositide 3-kinase pathway accelerates the glucose-induced first-phase insulin secretion through TrpV2 recruitment in pancreatic β-cells. Biochem J; 2010 Dec 1;432(2):375-86
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  • [Title] Insulin/phosphoinositide 3-kinase pathway accelerates the glucose-induced first-phase insulin secretion through TrpV2 recruitment in pancreatic β-cells.
  • Functional insulin receptor and its downstream effector PI3K (phosphoinositide 3-kinase) have been identified in pancreatic β-cells, but their involvement in the regulation of insulin secretion from β-cells remains unclear.
  • In the present study, we investigated the physiological role of insulin and PI3K in glucose-induced biphasic insulin exocytosis in primary cultured β-cells and insulinoma Min6 cells using total internal reflection fluorescent microscopy.
  • The pretreatment of β-cells with insulin induced the rapid increase in intracellular Ca2+ levels and accelerated the exocytotic response without affecting the second-phase insulin secretion.
  • The inhibition of PI3K not only abolished the insulin-induced rapid development of the exocytotic response, but also potentiated the second-phase insulin secretion.
  • The rapid development of Ca2+ and accelerated exocytotic response induced by insulin were accompanied by the translocation of the Ca2+-permeable channel TrpV2 (transient receptor potential V2) in a PI3K-dependent manner.
  • Inhibition of TrpV2 by the selective blocker tranilast, or the expression of shRNA (short-hairpin RNA) against TrpV2 suppressed the effect of insulin in the first phase, but the second phase was not affected.
  • Thus our results demonstrate that insulin treatment induced the acceleration of the exocytotic response during the glucose-induced first-phase response by the insertion of TrpV2 into the plasma membrane in a PI3K-dependent manner.
  • [MeSH-major] Calcium Channels / genetics. Insulin / physiology. Insulin-Secreting Cells / physiology. TRPV Cation Channels / genetics
  • [MeSH-minor] Animals. Base Sequence. Cell Line. DNA / chemistry. DNA / genetics. DNA, Complementary / genetics. Exocytosis. Growth Hormone / secretion. Homeostasis. Humans. Male. Mice. Mice, Inbred C57BL. Molecular Sequence Data. Open Reading Frames. Phosphatidylinositol 3-Kinases / metabolism. Transfection

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  • (PMID = 20854263.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / DNA, Complementary; 0 / Insulin; 0 / TRPV Cation Channels; 0 / Trpv2 protein, mouse; 9002-72-6 / Growth Hormone; 9007-49-2 / DNA; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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36. Kim JS, Zheng H, Kim SJ, Park JW, Park KS, Ho WK, Chun YS: Role of aryl hydrocarbon receptor nuclear translocator in KATP channel-mediated insulin secretion in INS-1 insulinoma cells. Biochem Biophys Res Commun; 2009 Feb 20;379(4):1048-53
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  • [Title] Role of aryl hydrocarbon receptor nuclear translocator in KATP channel-mediated insulin secretion in INS-1 insulinoma cells.
  • Recently, it was reported that ARNT is essential for adequate insulin secretion in response to glucose input and that its expression is downregulated in the pancreatic islets of diabetic patients.
  • In the present study, the authors addressed the mechanism by which ARNT regulates insulin secretion in the INS-1 insulinoma cell line.
  • In ARNT knock-down cells, basal insulin release was elevated, but insulin secretion was not further stimulated by a high-glucose challenge.
  • Electrophysiological analyses revealed that glucose-dependent membrane depolarization was impaired in these cells.
  • Based on these results, the authors suggest that ARNT expresses K(ATP) channel and by so doing regulates glucose-dependent insulin secretion.
  • [MeSH-major] Aryl Hydrocarbon Receptor Nuclear Translocator / metabolism. Insulin / secretion. Insulin-Secreting Cells / secretion. Potassium Channels / biosynthesis. Potassium Channels, Inwardly Rectifying / biosynthesis
  • [MeSH-minor] Animals. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Line, Tumor. Gene Knockdown Techniques. Glucose / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Insulinoma. Rats

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  • (PMID = 19141293.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Hif1a protein, rat; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Insulin; 0 / Kir6.2 channel; 0 / Potassium Channels; 0 / Potassium Channels, Inwardly Rectifying; 0 / endothelial PAS domain-containing protein 1; 0 / mitochondrial K(ATP) channel; 138391-32-9 / Aryl Hydrocarbon Receptor Nuclear Translocator; IY9XDZ35W2 / Glucose
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37. Miyakoshi T, Takei M, Kajiya H, Egashira N, Takekoshi S, Teramoto A, Osamura RY: Expression of Wnt4 in human pituitary adenomas regulates activation of the beta-catenin-independent pathway. Endocr Pathol; 2008;19(4):261-73
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  • [Title] Expression of Wnt4 in human pituitary adenomas regulates activation of the beta-catenin-independent pathway.
  • A member of the Wnt family of genes, Wnt4, has been known to regulate proliferation of anterior pituitary cell types in the mouse during embryonic development.
  • In order to elucidate the roles of Wnt signaling in human pituitary adenomas, we examined the expression of Wnt4 and its putative receptor Frizzled6 (Fzd6) by immunohistochemistry in pituitary adenomas and normal pituitaries.
  • Expression of Wnt4 was higher in growth hormone-producing adenomas (GHomas), prolactin-producing adenomas (PRLomas), and thyroid-stimulating hormone-producing adenomas (TSHomas) than in the normal pituitary.
  • Fzd6 was widely expressed in GHomas, PRLomas, TSHomas, and gonadotropin subunit (GnSU)-positive adenomas.
  • In normal pituitary glands, Wnt4 and Fzd6 were colocalized predominantly in follicle-stimulating hormone-, luteinizing hormone-, and alpha-subunits of glycoprotein hormone-positive cells.
  • The canonical Wnt/beta-catenin signaling pathway was analyzed by beta-catenin immunohistochemistry. beta-Catenin was localized at the cell membrane in all pituitary adenomas, but not in the nuclei.
  • These results suggested that activation of Wnt4/Fzd6 signaling through a "beta-catenin-independent" pathway played a role in proliferation and survival of the pituitary adenoma cells.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / metabolism. Pituitary Neoplasms / metabolism. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 19034702.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / FZD6 protein, human; 0 / Frizzled Receptors; 0 / Receptors, G-Protein-Coupled; 0 / WNT4 protein, human; 0 / Wnt Proteins; 0 / Wnt4 Protein; 0 / Wnt4 protein, mouse; 0 / beta Catenin
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38. Zhang X, Sun N, Wang L, Guo H, Guan Q, Cui B, Tian L, Gao L, Zhao J: AMP-activated protein kinase and pancreatic/duodenal homeobox-1 involved in insulin secretion under high leucine exposure in rat insulinoma beta-cells. J Cell Mol Med; 2009 Apr;13(4):758-70
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  • [Title] AMP-activated protein kinase and pancreatic/duodenal homeobox-1 involved in insulin secretion under high leucine exposure in rat insulinoma beta-cells.
  • The effect of leucine on glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells is quite controversial, and mechanism involved in the effect has not been elucidated yet.
  • Consequently, we aimed to investigate effect of leucine on GSIS and its mechanism focusing on contribution of AMP-activated protein kinase (AMPK) and pancreatic/duodenal homeobox-1 (PDX-1).
  • Rat insulinoma beta-cells (INS-1, RIN m5F, DN-PDX-1#28 and PDX-1#6) were cultured with or without leucine, AICAR (AMPK agonist) or compound C (AMPK antagonist) for 48 hrs.
  • In contrast to control, AICAR treatment decreased GSIS at high glucose and insulin content, also impaired protein and mRNA expression of PDX-1 and its downstream targets, glucokinase (GCK) and glucose transporter 2 (GLUT2).
  • Chronic leucine exposure inhibited GSIS at high glucose and insulin content in a dose-dependent manner, concomitant with an increase in AMPK and a decrease in PDX-1, GCK and GLUT2.
  • Finally, the inhibition of PDX-1 could potentiate the impaired effects induced by leucine whereas overexpression of PDX-1 could protect the cell from impairment induced by leucine.
  • The study indicated that chronic leucine might result in an increase in AMPK and then a decrease in PDX-l, in turn to depress GCK and GLUT2 resulting in decreased GSIS at high glucose and insulin content.
  • [MeSH-major] AMP-Activated Protein Kinases / metabolism. Homeodomain Proteins / metabolism. Insulin / secretion. Insulin-Secreting Cells / enzymology. Insulinoma / enzymology. Leucine / pharmacology. Pancreatic Neoplasms / enzymology. Trans-Activators / metabolism
  • [MeSH-minor] Aminoimidazole Carboxamide / analogs & derivatives. Aminoimidazole Carboxamide / pharmacology. Animals. Cell Death / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Glucokinase / genetics. Glucokinase / metabolism. Glucose Transporter Type 2. Rats. Ribonucleotides / pharmacology

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  • (PMID = 19438972.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Glucose Transporter Type 2; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Ribonucleotides; 0 / Slc2a2 protein, rat; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; 360-97-4 / Aminoimidazole Carboxamide; EC 2.7.1.2 / Glucokinase; EC 2.7.11.1 / AMP-Activated Protein Kinases; F0X88YW0YK / AICA ribonucleotide; GMW67QNF9C / Leucine
  • [Other-IDs] NLM/ PMC3822882
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39. Fregeville A, Couvelard A, Paradis V, Vilgrain V, Warshauer DM: Metastatic insulinoma and glucagonoma from the pancreas responsible for specific peritumoral patterns of hepatic steatosis secondary to local effects of insulin and glucagon on hepatocytes. Gastroenterology; 2005 Oct;129(4):1150,1365
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  • [Title] Metastatic insulinoma and glucagonoma from the pancreas responsible for specific peritumoral patterns of hepatic steatosis secondary to local effects of insulin and glucagon on hepatocytes.
  • [MeSH-major] Fatty Liver / etiology. Glucagonoma / pathology. Insulinoma / pathology. Liver / pathology. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Female. Glucagon / secretion. Hepatocytes / physiology. Humans. Insulin / secretion


40. Anaye A, Mathieu A, Closset J, Bali MA, Metens T, Matos C: Successful preoperative localization of a small pancreatic insulinoma by diffusion-weighted MRI. JOP; 2009;10(5):528-31
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  • [Title] Successful preoperative localization of a small pancreatic insulinoma by diffusion-weighted MRI.
  • CONTEXT: Insulinoma is the most common functioning endocrine tumor of the pancreas responsible for fasting hypoglycemia resulting from autonomous insulin hypersecretion.
  • Most insulinomas are small and difficult to localize with conventional imaging.
  • We successfully localized a small insulinoma in our patient using diffusion-weighted magnetic resonance imaging before surgery.
  • CASE REPORT: We report the case of a female patient with a clinical suspicion of insulinoma.
  • A preoperative MR with diffusion-weighted imaging was performed and localized a small nodule in the pancreatic tail.
  • Histologic examination identified a neuroendocrine tumor compatible with an insulinoma.
  • CONCLUSION: Diffusion-weighted imaging can be useful in detecting and localizing small insulinomas, especially for those with no hypervascular pattern.
  • [MeSH-major] Diffusion Magnetic Resonance Imaging. Insulinoma / radiography. Pancreatic Neoplasms / radiography

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  • (PMID = 19734630.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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41. Saddig C, Goretzki PE, Starke AA: Differentiation of insulin secretion patterns in insulinoma. World J Surg; 2008 May;32(5):918-29
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  • [Title] Differentiation of insulin secretion patterns in insulinoma.
  • BACKGROUND: In patients with insulinoma, biochemical proof of inappropriately elevated insulin secretion during hypoglycemia is required prior to surgery.
  • Because circulating insulin levels usually vary widely, we have used the combined OGTT-fasting test to define new normative criteria for a retrospective systematic analysis.
  • METHODS: We retrospectively analyzed insulin concentrations from OGTT-fasting tests of 64 patients with surgically removed insulinomas.
  • Normative criteria were defined to obtain comparable estimates of insulin concentrations: basal, glucose-stimulated maximum, postglucose plateau, and secretory bursts.
  • RESULTS: Three types of insulin secretion patterns were identified:.
  • (1) the autonomous secretion pattern (type 1, N=17) with basal and post-OGTT plateau insulin concentrations of approximately 50 mU/L, suppression after OGTT by 41%, virtual absence of distinctive secretory bursts, and resistance to somatostatin-mediated suppression (25 %);.
  • (2) the inadequate suppression pattern (type 2, N=28) with moderately elevated basal and post-OGTT insulin concentrations of approximately 20 mU/L, suppression after OGTT by 73%, absence of secretory bursts, and incomplete somatostatin-induced suppression (56 %);.
  • (3) the late-burst secretion pattern (type 3, N=19) with similar basal and post-OGTT insulin concentrations of 17 mU/L, suppression after OGTT by 76%, true insulin bursts of Delta 13+/-11 mU/L (184%), and nearly complete somatostatin-induced suppression by 64%.
  • CONCLUSIONS: By means of a new normative analysis of the combined OGTT-fasting test, three different patterns of insulin secretion can be described in patients with insulinoma: the autonomous secretion type, the inadequate suppression type, and the late-burst secretion type.
  • [MeSH-major] Insulin / secretion. Insulinoma / secretion. Pancreatic Neoplasms / secretion

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  • (PMID = 18259806.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 51110-01-1 / Somatostatin
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42. Kenney B, Tormey CA, Qin L, Sosa JA, Jain D, Neto A: Adult nesidioblastosis. Clinicopathologic correlation between pre-operative selective arterial calcium stimulation studies and post-operative pathologic findings. JOP; 2008;9(4):504-11
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  • CONTEXT: Adult nesidioblastosis, a rare form of abnormal islet cell proliferation arising from the pancreatic ductal epithelium, is usually associated with severe hyperinsulinemic hypoglycemia.
  • CASE REPORT: We present the case of a previously healthy 45-year-old woman with new-onset severe hypoglycemia 4 and seizures.
  • The differential diagnosis at presentation included factitious hypoglycemia and insulinoma.
  • Extensive imaging and laboratory examination, including repeated CT and MRI scans, toxicology assays, and insulin-based chemical studies, were either inconclusive or negative.
  • Subsequent testing involved stimulation of the pancreas through cannulation of the pancreatic vascular supply by interventional radiology.
  • This testing revealed marked insulin release to low-level calcium challenge across multiple pancreatic segments.
  • Gross and histologic examination of the resected tissue revealed no evidence of a pancreatic mass.
  • Diffuse islet cell hyperplasia was noted in a pattern consistent with nesidioblastosis.
  • [MeSH-major] Calcium Gluconate. Nesidioblastosis / diagnosis. Pancreas / pathology
  • [MeSH-minor] Catheterization. Diagnosis, Differential. Female. Hepatic Artery. Hepatic Veins. Humans. Hypoglycemia / diagnosis. Hypoglycemia / etiology. Insulin / blood. Mesenteric Arteries. Middle Aged. Pancreatectomy. Seizures / etiology. Splenic Artery. Treatment Outcome

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  • (PMID = 18648143.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Insulin; SQE6VB453K / Calcium Gluconate
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43. Barbé-Tuana FM, Klein D, Ichii H, Berman DM, Coffey L, Kenyon NS, Ricordi C, Pastori RL: CD40-CD40 ligand interaction activates proinflammatory pathways in pancreatic islets. Diabetes; 2006 Sep;55(9):2437-45
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  • [Title] CD40-CD40 ligand interaction activates proinflammatory pathways in pancreatic islets.
  • Pancreatic islet transplantation is becoming an alternative to insulin therapy in patients suffering from brittle type 1 diabetes.
  • A major obstacle to the procedure is the early graft loss caused by nonspecific inflammation at the site of implantation.
  • We recently discovered that CD40, a member of tumor necrosis factor (TNF) receptor family, is expressed in pancreatic beta-cells.
  • CD40 expression in nonhematopoietic cells is generally associated with inflammation.
  • Islet beta-cells responded to CD40L interaction by secreting interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, and macrophage inflammatory protein (MIP)-1beta, the latter a chemokine first reported to be produced by islets.
  • MIP-1beta expression in beta-cells was verified by double-immunofluorescence staining.
  • CD40-CD40L interaction activates extracellular signal-regulated kinase 1/2 and nuclear factor-kappaB pathways in insulinoma NIT-1 cells, and inhibitors of either pathway suppress cytokine/chemokine production in islets.
  • Our results in vitro indicate that the CD40 receptor expressed by beta-cells could be activated in vivo, inducing proinflammatory responses contributing to early islet graft loss after transplantation.

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  • (PMID = 16936191.001).
  • [ISSN] 0012-1797
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5U42RR016603; United States / NIDDK NIH HHS / DK / DK55347
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Chemokine CCL2; 0 / Chemokine CCL4; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Macrophage Inflammatory Proteins; 0 / NF-kappa B; 126547-89-5 / Intercellular Adhesion Molecule-1; 147205-72-9 / CD40 Ligand; EC 2.7.11.1 / raf Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases
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44. Virgolini I, Traub-Weidinger T, Decristoforo C: Nuclear medicine in the detection and management of pancreatic islet-cell tumours. Best Pract Res Clin Endocrinol Metab; 2005 Jun;19(2):213-27
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  • [Title] Nuclear medicine in the detection and management of pancreatic islet-cell tumours.
  • Over the last decade somatostatin receptor scintigraphy using various derivatives of long-acting somatostatin analogues has gained its place in the management of pancreatic islet-cell tumours.
  • Scintigraphy is based on the high-affinity binding of such somatostatin analogues to receptors over-expressed by these tumour types.
  • Following the introduction of (111)In-DTPA-D-Phe(1)-octreotide, clinical studies with radiolabelled DOTA-Tyr(3)-octreotide and DOTA-Tyr(3)-octreotate derivatives have shown considerable improvement of imaging results with increased tumour uptake.
  • One of the newer developments, (68)Ga-labelled DOTA-Tyr(3)-octreotide, has shown promising results in patients with pancreatic islet-cell tumours, based on the high-affinity binding to the somatostatin receptor subtype 2 in combination with positron emission tomography (PET) technology.
  • Other peptides--such as ligands for the gastrin/CCK2 receptors or vasoactive intestinal peptide (VIP)--have also been studied for imaging pancreatic cell tumours.
  • Whereas small-sized gastrinoma, somatostatinoma, glucagonoma, carcinoid and VIPoma are frequently detected by somatostatin receptor scintigraphy, insulinoma may escape detection due to reduced receptor expression.
  • When labelled with (90)Y or (177)Lu, some somatostatin analogues have been applied to patients in advanced stages of the disease.
  • [MeSH-major] Adenoma, Islet Cell / radionuclide imaging. Adenoma, Islet Cell / radiotherapy. Islets of Langerhans / radionuclide imaging. Pancreatic Neoplasms / radionuclide imaging. Pancreatic Neoplasms / radiotherapy

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  • (PMID = 15763696.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 51110-01-1 / Somatostatin
  • [Number-of-references] 56
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45. Kann PH, Meyer S, Zielke A, Langer P, Ivan D: [The new role for endoscopic ultrasound in endocrinology: imaging of the adrenals and the endocrine pancreas]. Dtsch Med Wochenschr; 2006 Mar 17;131(11):567-72
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  • [Title] [The new role for endoscopic ultrasound in endocrinology: imaging of the adrenals and the endocrine pancreas].
  • [Transliterated title] Die neue Rolle der Endosonographie in der Endokrinologie: Bildgebung der Nebennieren und des endokrinen Pankreas.
  • Endoscopic ultrasound imaging of the adrenals and the endocrine pancreas enriches the diagnostic repertoire and improves the clinical opportunities of endocrinology.
  • Its resolution enables detection of tumors as small as 2-3 mm.
  • Endoscopic ultrasound imaging is especially relevant in the diagnosis of insulinomas and primary hyperaldosteronism, because it has direct consequences in planning a diagnostic and therapeutic strategy.
  • [MeSH-major] Adrenal Gland Diseases / ultrasonography. Adrenal Glands / ultrasonography. Endosonography / methods. Pancreas / ultrasonography. Pancreatic Diseases / ultrasonography

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  • (PMID = 16538563.001).
  • [ISSN] 0012-0472
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 23
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46. Cvjetićanin T, Stojanović I, Timotijević G, Stosić-Grujicić S, Miljković D: T cells cooperate with palmitic acid in induction of beta cell apoptosis. BMC Immunol; 2009;10:29
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  • [Title] T cells cooperate with palmitic acid in induction of beta cell apoptosis.
  • BACKGROUND: Diabetes is characterized by progressive failure of insulin producing beta cells.
  • It is well known that both saturated fatty acids and various products of immune cells can contribute to the reduction of beta cell viability and functionality during diabetes pathogenesis.
  • However, their joint action on beta cells has not been investigated, so far.
  • Therefore, we explored the possibility that leukocytes and saturated fatty acids cooperate in beta cell destruction.
  • RESULTS: Rat pancreatic islets or insulinoma cells (RIN) were co-cultivated with concanavalin A (ConA)-stimulated rat lymph node cells (LNC), or they were treated with cell-free supernatants (Sn) obtained from ConA-stimulated spleen cells or from activated CD3+ cells, in the absence or presence of palmitic acid (PA).
  • ConA-stimulated LNC or Sn and PA cooperated in inducing caspase-3-dependent RIN cell apoptosis.
  • The observed effect of PA and Sn on RIN cell viability was mediated by p38 mitogen-activated protein kinase (MAPK)-signaling and was achieved through auto-destructive nitric oxide (NO) production.
  • The cooperative effect of Sn was mimicked with the combination of interleukin-1beta, interleukin-2, interleukin-6, interleukin-17, interferon-gamma and tumor necrosis factor-alpha.
  • CONCLUSION: These results imply that stimulated T cells produce cytokines that cooperate with saturated free fatty acids in beta cell destruction during diabetes pathogenesis.
  • [MeSH-major] Apoptosis / immunology. Cell Communication. Insulin-Secreting Cells / immunology. Insulinoma / immunology. Palmitic Acid / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / metabolism
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Cell Line, Tumor. Coculture Techniques. Cytokines / immunology. Cytokines / metabolism. Lymphocyte Activation. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Inbred CBA. Rats. Signal Transduction. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19463182.001).
  • [ISSN] 1471-2172
  • [Journal-full-title] BMC immunology
  • [ISO-abbreviation] BMC Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 2V16EO95H1 / Palmitic Acid; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ PMC2693514
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47. Shen W, Liu K, Tian C, Yang L, Li X, Ren J, Packer L, Head E, Sharman E, Liu J: Protective effects of R-alpha-lipoic acid and acetyl-L-carnitine in MIN6 and isolated rat islet cells chronically exposed to oleic acid. J Cell Biochem; 2008 Jul 1;104(4):1232-43
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  • [Title] Protective effects of R-alpha-lipoic acid and acetyl-L-carnitine in MIN6 and isolated rat islet cells chronically exposed to oleic acid.
  • Mitochondrial dysfunction due to oxidative stress and concomitant impaired beta-cell function may play a key role in type 2 diabetes.
  • In the present study, the oxidative mechanism of mitochondrial dysfunction in pancreatic beta-cells exposed to sublethal levels of oleic acid (OA) and the protective effects of mitochondrial nutrients [R-alpha-lipoic acid (LA) and acetyl-L-carnitine (ALC)] were investigated.
  • Chronic exposure (72 h) of insulinoma MIN6 cells to OA (0.2-0.8 mM) increased intracellular oxidant formation, decreased mitochondrial membrane potential (MMP), enhanced uncoupling protein-2 (UCP-2) mRNA and protein expression, and consequently, decreased glucose-induced ATP production and suppressed glucose-stimulated insulin secretion.
  • Pretreatment with LA and/or ALC reduced oxidant formation, increased MMP, regulated UCP-2 mRNA and protein expression, increased glucose-induced ATP production, and restored glucose-stimulated insulin secretion.
  • The key findings on ATP production and insulin secretion were verified with isolated rat islets.
  • These results suggest that mitochondrial dysfunction is involved in OA-induced pancreatic beta-cell dysfunction and that pretreatment with mitochondrial protective nutrients could be an effective strategy to prevent beta-cell dysfunction.
  • [MeSH-minor] Animals. Cell Line, Tumor. Insulinoma / pathology. Rats

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  • [Copyright] 2008 Wiley-Liss, Inc.
  • (PMID = 18260126.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protective Agents; 2UMI9U37CP / Oleic Acid; 6DH1W9VH8Q / Acetylcarnitine; 73Y7P0K73Y / Thioctic Acid
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48. Hardy OT, Hohmeier HE, Becker TC, Manduchi E, Doliba NM, Gupta RK, White P, Stoeckert CJ Jr, Matschinsky FM, Newgard CB, Kaestner KH: Functional genomics of the beta-cell: short-chain 3-hydroxyacyl-coenzyme A dehydrogenase regulates insulin secretion independent of K+ currents. Mol Endocrinol; 2007 Mar;21(3):765-73
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  • [Title] Functional genomics of the beta-cell: short-chain 3-hydroxyacyl-coenzyme A dehydrogenase regulates insulin secretion independent of K+ currents.
  • In this study, we describe a rational and efficient approach to identifying novel regulators of insulin secretion by the pancreatic beta-cell.
  • Computational analysis of expression profiles of several mouse and cellular models of impaired insulin secretion identified 373 candidate genes involved in regulation of insulin secretion.
  • Using RNA interference, we assessed the requirements of 10 of these candidates and identified four genes (40%) as being essential for normal insulin secretion.
  • Among the genes identified was Hadhsc, which encodes short-chain 3-hydroxyacyl-coenzyme A dehydrogenase (SCHAD), an enzyme of mitochondrial beta-oxidation of fatty acids whose mutation results in congenital hyperinsulinism.
  • RNA interference-mediated gene suppression of Hadhsc in insulinoma cells and primary rodent islets revealed enhanced basal but normal glucose-stimulated insulin secretion.
  • This increase in basal insulin secretion was not attenuated by the opening of the KATP channel with diazoxide, suggesting that SCHAD regulates insulin secretion through a KATP channel-independent mechanism.
  • [MeSH-major] Butyryl-CoA Dehydrogenase / physiology. Genomics / methods. Insulin / secretion. Insulin-Secreting Cells. Potassium Channels / physiology
  • [MeSH-minor] Animals. Cells, Cultured. Gene Expression Profiling. Mice. Mice, Transgenic. Models, Biological. RNA Interference. Rats

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  • (PMID = 17185391.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK19525; United States / NIDDK NIH HHS / DK / DK22122; United States / NIDDK NIH HHS / DK / DK55342; United States / NIDDK NIH HHS / DK / DK56947; United States / NHGRI NIH HHS / HG / HG2296; United States / NIDDK NIH HHS / DK / P30-DK19525; United States / NIDDK NIH HHS / DK / T32 DK63688
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 0 / Potassium Channels; EC 1.3.8.1 / Butyryl-CoA Dehydrogenase
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49. Kim YK, Park JH, Park SH, Lim B, Baek WK, Suh SI, Lim JG, Ryu GR, Song DK: Protective role of glucagon-like peptide-1 against glucosamine-induced cytotoxicity in pancreatic beta cells. Cell Physiol Biochem; 2010;25(2-3):211-20
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  • [Title] Protective role of glucagon-like peptide-1 against glucosamine-induced cytotoxicity in pancreatic beta cells.
  • High doses of glucosamine have been known to induce apoptosis of pancreatic beta cells.
  • We aimed to explore the potential mechanisms for glucosamine toxicity in the rat insulinoma cell line INS-1 and in rat native beta cells.
  • Glucosamine exhibited dose-dependent inhibition of cell survival and an increase in the cell population at the sub-G1 phase.
  • Taken together, these data demonstrate that glucosamine may inhibit beta-cell survival by diminishing cellular glucose uptake independent of glycosylation.
  • [MeSH-major] Glucagon-Like Peptide 1 / physiology. Glucosamine / toxicity. Insulin-Secreting Cells / drug effects
  • [MeSH-minor] AMP-Activated Protein Kinases / metabolism. Animals. Apoptosis. Cell Line, Tumor. G1 Phase. Glucose / metabolism. Phosphorylation. Rats. Ribosomal Protein S6 / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / metabolism

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20110682.001).
  • [ISSN] 1421-9778
  • [Journal-full-title] Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
  • [ISO-abbreviation] Cell. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Ribosomal Protein S6; 89750-14-1 / Glucagon-Like Peptide 1; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; IY9XDZ35W2 / Glucose; N08U5BOQ1K / Glucosamine
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50. Goel A, Chiu H, Felton J, Palmer JP, Brooks-Worrell B: T-cell responses to islet antigens improves detection of autoimmune diabetes and identifies patients with more severe beta-cell lesions in phenotypic type 2 diabetes. Diabetes; 2007 Aug;56(8):2110-5
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  • [Title] T-cell responses to islet antigens improves detection of autoimmune diabetes and identifies patients with more severe beta-cell lesions in phenotypic type 2 diabetes.
  • Latent autoimmune diabetes in adults or type 1.5 diabetes is considered to be a T-cell-mediated autoimmune disease.
  • To determine whether measuring T-cell reactivity to islet proteins compared with measuring Abs improves detection of autoimmune diabetes and how beta-cell function correlates with T-cell reactivity compared with Ab positivity, we assessed the T-cell proliferative responses and Ab responses (islet cell autoantibodies, insulin autoantibodies, insulinoma-associated protein-2 autoantibodies, and GAD Abs) to islet proteins of 36 phenotypic type 2 diabetic patients.
  • To be considered Ab(+) or T-cell(+), patients were required to be positive for a minimum of two consecutive time points. beta-Cell function was measured with fasting and glucagon-stimulated C-peptide.
  • Independent of T-cell reactivity, Ab(+) and Ab(-) patients had comparable fasting and glucagon-stimulated C-peptide.
  • Independent of Ab status, T-cell(+) patients demonstrated significantly lower glucagon-stimulated (P < 0.003) C-peptide compared with T-cell(-) patients.
  • These data suggest that measuring T-cell responses to multiple islet proteins in phenotypic type 2 diabetic patients improves identification of patients with autoimmune diabetes and delineates those who have a more severe beta-cell lesion compared with Ab assessment alone.
  • [MeSH-minor] Adult. Aged. Autoantibodies / immunology. C-Peptide / blood. Cell Proliferation. Fasting. Female. Glucagon / pharmacology. Glucose / pharmacology. Humans. Male. Middle Aged

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  • (PMID = 17473222.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01-RR00037; United States / NIDDK NIH HHS / DK / P01-DK053004; United States / NIDDK NIH HHS / DK / P30-DK17047
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Autoantibodies; 0 / C-Peptide; 9007-92-5 / Glucagon; IY9XDZ35W2 / Glucose
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51. Viola KV, Sosa JA: Current advances in the diagnosis and treatment of pancreatic endocrine tumors. Curr Opin Oncol; 2005 Jan;17(1):24-7
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  • [Title] Current advances in the diagnosis and treatment of pancreatic endocrine tumors.
  • PURPOSE OF REVIEW: A comprehensive literature review of more than 200 original manuscripts published in the last 18 months was conducted to summarize landmark studies performed on the molecular biology, diagnosis, imaging, and treatment of endocrine tumors of the pancreas.
  • Identification of a novel insulin splice variant with increased translation efficiency moved forward the understanding of the molecular biology of insulinomas.
  • Results of a 29-year prospective study from the National Institutes of Health clarified the epidemiology of multiple endocrine neoplasia-1 syndrome.
  • Chromogranin A was identified as a promising marker for pancreatic endocrine tumors.
  • New imaging, including F-dopa positron emission tomography and laparoscopic ultrasound, and the effective combination of existing modalities localized and staged tumors with greater accuracy.
  • Nonoperative treatment strategies show promise; discovery of the antiangiogenic properties of octreotide and the overexpression of tyrosine kinase receptors such as c-kit, epidermal growth factor receptor, and platelet-derived growth factor receptor on malignant endocrine pancreatic tumors may lead to promising pharmacologic treatment.
  • SUMMARY: There have been exciting recent advancements in research surrounding endocrine pancreas that hopefully will pave the way for potential improvement in clinical outcomes for patients with these tumors.
  • [MeSH-major] Gastrinoma / diagnosis. Gastrinoma / drug therapy. Insulinoma / diagnosis. Insulinoma / drug therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Biomarkers, Tumor / blood. Chromogranin A. Chromogranins / blood. Humans. Incidence. Multiple Endocrine Neoplasia Type 1 / epidemiology. Multiple Endocrine Neoplasia Type 1 / pathology

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  • (PMID = 15608508.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Chromogranins
  • [Number-of-references] 14
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52. Dlasková A, Spacek T, Santorová J, Plecitá-Hlavatá L, Berková Z, Saudek F, Lessard M, Bewersdorf J, Jezek P: 4Pi microscopy reveals an impaired three-dimensional mitochondrial network of pancreatic islet beta-cells, an experimental model of type-2 diabetes. Biochim Biophys Acta; 2010 Jun-Jul;1797(6-7):1327-41
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  • [Title] 4Pi microscopy reveals an impaired three-dimensional mitochondrial network of pancreatic islet beta-cells, an experimental model of type-2 diabetes.
  • Insulin production in pancreatic beta-cells is critically linked to mitochondrial oxidative phosphorylation.
  • Increased ATP production triggered by blood glucose represents the beta-cells' glucose sensor.
  • Type-2 diabetes mellitus results from insulin resistance in peripheral tissues and impaired insulin secretion.
  • Pathology of diabetic beta-cells might be reflected by the altered morphology of mitochondrial network.
  • Its characterization is however hampered by the complexity and density of the three-dimensional (3D) mitochondrial tubular networks in these cell types.
  • However, mitochondrial network morphology in fixed cells can also be studied by 4Pi microscopy, a laser scanning microscopy technique which provides an approximately 7-fold improved axial resolution (approximately 100 nm) over conventional confocal microscopy.
  • Here we present a quantitative study of these networks in insulinoma INS-1E cells and primary beta-cells in Langerhans islets.
  • The former were a stably-transfected cell line while the latter were transfected with lentivirus, both expressing mitochondrial matrix targeted redox-sensitive GFP.
  • We demonstrate that beta-cells within the Langerhans islets from diabetic Goto Kakizaki rats exhibited a more disintegrated mitochondrial network compared to those from control Wistar rats and model insulinoma INS-1E cells.
  • Standardization of these patterns may lead to development of morphological diagnostics for Langerhans islets, for the assessment of beta-cell condition, before their transplantations.
  • [MeSH-major] Diabetes Mellitus, Type 2 / pathology. Insulin-Secreting Cells / pathology. Microscopy, Confocal / methods. Mitochondria / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Green Fluorescent Proteins / genetics. Imaging, Three-Dimensional. In Vitro Techniques. Insulinoma / pathology. Pancreatic Neoplasms / pathology. Rats. Rats, Wistar. Recombinant Fusion Proteins / genetics. Transfection

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  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20144584.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Recombinant Fusion Proteins; 147336-22-9 / Green Fluorescent Proteins
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53. Tsuboi T, Ravier MA, Parton LE, Rutter GA: Sustained exposure to high glucose concentrations modifies glucose signaling and the mechanics of secretory vesicle fusion in primary rat pancreatic beta-cells. Diabetes; 2006 Apr;55(4):1057-65
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  • [Title] Sustained exposure to high glucose concentrations modifies glucose signaling and the mechanics of secretory vesicle fusion in primary rat pancreatic beta-cells.
  • The mechanism(s) by which chronic hyperglycemia impairs glucose-stimulated insulin secretion is poorly defined.
  • Here, we compare the "nanomechanics" of single exocytotic events in primary rat pancreatic beta-cells cultured for 48 h at optimal (10 mmol/l) or elevated (30 mmol/l) glucose concentrations.
  • Cargo release was imaged by total internal reflection fluorescence microscopy of lumen-targeted probes (neuropeptide Y [NPY]-pH-insensitive yellow fluorescent protein [NPY-Venus] or NPY-monomeric red fluorescent protein), while the fate of the vesicle membrane was reported simultaneously with phosphatase-on-the-granule-of-insulinoma-enhanced green fluorescent protein.
  • While essentially complete release of NPY-Venus was observed in 24 +/- 1% of glucose-stimulated exocytotic events in cells maintained at 10 mmol/l glucose, this value was reduced reversibly to 5 +/- 2% of events by culture at 30 mmol/l glucose, in line with decreases in Glut2 and glucokinase gene expression, and attenuated glucose-stimulated increases in NADPH and intracellular [Ca2+].
  • Since vesicle release in response to cell depolarization with KCl was not affected by culture at 30 mmol/l glucose, we conclude that hyperglycemia causes the abnormal termination of individual insulin release events principally by inhibiting glucose signaling.
  • [MeSH-major] Glucose / pharmacology. Insulin / secretion. Islets of Langerhans / physiology
  • [MeSH-minor] Animals. Calcium / metabolism. Cell Line. Cells, Cultured. DNA Primers. Exocytosis. Genes, Reporter. Hydrogen-Ion Concentration. Microscopy, Confocal. Neuropeptide Y / pharmacology. Proinsulin / analysis. Protein Precursors / analysis. Rats. Reverse Transcriptase Polymerase Chain Reaction. Synaptotagmins / genetics

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  • (PMID = 16567529.001).
  • [ISSN] 0012-1797
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Insulin; 0 / Neuropeptide Y; 0 / Protein Precursors; 134193-27-4 / Synaptotagmins; 61116-24-3 / preproinsulin; 9035-68-1 / Proinsulin; IY9XDZ35W2 / Glucose; SY7Q814VUP / Calcium
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54. Erdogan A, Kose F, Akkaya H, Bascil Tutuncu N, Ozyilkan O: Rapidly progressing malignant insulinoma presented with multiple liver metastases: a case report. J Gastrointest Cancer; 2010 Dec;41(4):272-4
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  • [Title] Rapidly progressing malignant insulinoma presented with multiple liver metastases: a case report.
  • Her blood glucose level from fingertip was 33 mg/dl, and insulin level was 55 (normal range, 4-17 IU).
  • Abdominal ultrasonography revealed pancreatic mass with diffuse liver metastases.
  • Biopsy of liver metastases showed differentiated neuroendocrine carcinoma.
  • However, the disease showed progression, and death occurred 8 months later.
  • CONCLUSION: In conclusion, this case may suggest that biologic behavior may differ from histological behavior in insulinoma and platin-based systemic chemotherapy may provide some benefit in patients those who had diazoxide- and octreotide-resistant tumors.
  • [MeSH-major] Insulinoma / secondary. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology

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  • [ErratumIn] J Gastrointest Cancer. 2010 Dec;41(4):288. Askin, Erdogan [corrected to Erdogan, Askin]; Fatih, Kose [corrected to Kose, Fatih]; Hampar, Akkaya [corrected to Akkaya, Hampar]; Tutuncu, Neslihan Bascil [corrected to Bascil Tutuncu, Neslihan]; Ozgur, Ozyilkan [corrected to Ozyilkan, Ozgur]
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  • (PMID = 20419482.001).
  • [ISSN] 1941-6636
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vasodilator Agents; O5CB12L4FN / Diazoxide; RWM8CCW8GP / Octreotide
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55. Dai XQ, Kolic J, Marchi P, Sipione S, Macdonald PE: SUMOylation regulates Kv2.1 and modulates pancreatic beta-cell excitability. J Cell Sci; 2009 Mar 15;122(Pt 6):775-9
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  • [Title] SUMOylation regulates Kv2.1 and modulates pancreatic beta-cell excitability.
  • The voltage-dependent K(+) (Kv) channel Kv2.1 regulates pancreatic beta-cell excitability and insulin secretion.
  • We found that YFP-tagged SUMO1 (SUMO1-YFP) can be immunoprecipitated with Kv2.1 when these two proteins are coexpressed in HEK 293 cells.
  • Insulin-secreting cells express SUMO variants 1 and 3, and expression of the SUMO1-YFP in human beta-cells or insulinoma cells inhibited native Kv currents (by 49% and 33%, respectively).
  • Inhibition of the channel resulted from an acceleration of channel inactivation and an inhibition of recovery from inactivation, resulting in the widening of beta-cell action potentials and a decreased firing frequency.
  • Thus, protein SUMOylation can exert a strong inhibitory action on the voltage-dependent K(+) channel Kv2.1 and can regulate cellular excitability in native beta-cells.
  • [MeSH-major] Insulin-Secreting Cells / physiology. Shab Potassium Channels / metabolism. Small Ubiquitin-Related Modifier Proteins / metabolism


76. Pannequin J, Delaunay N, Buchert M, Surrel F, Bourgaux JF, Ryan J, Boireau S, Coelho J, Pélegrin A, Singh P, Shulkes A, Yim M, Baldwin GS, Pignodel C, Lambeau G, Jay P, Joubert D, Hollande F: Beta-catenin/Tcf-4 inhibition after progastrin targeting reduces growth and drives differentiation of intestinal tumors. Gastroenterology; 2007 Nov;133(5):1554-68
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  • [Title] Beta-catenin/Tcf-4 inhibition after progastrin targeting reduces growth and drives differentiation of intestinal tumors.
  • BACKGROUND & AIMS: Aberrant activation of the beta-catenin/Tcf-4 transcriptional complex represents an initiating event for colorectal carcinogenesis, shifting the balance from differentiation toward proliferation in colonic crypts.
  • Here, we assessed whether endogenous progastrin, encoded by a target gene of this complex, was in turn able to regulate beta-catenin/Tcf-4 activity in adenomatous polyposis coli (APC)-mutated cells, and we analyzed the impact of topical progastrin depletion on intestinal tumor growth in vivo.
  • METHODS: Stable or transient RNA silencing of the GAST gene was induced in human tumor cells and in mice carrying a heterozygous Apc mutation (APCDelta14), which overexpress progastrin but not amidated or glycine-extended gastrin.
  • RESULTS: Depletion of endogenous progastrin production strongly decreased intestinal tumor growth in vivo through a marked inhibition of constitutive beta-catenin/Tcf-4 activity in tumor cells.
  • This effect was mediated by the de novo expression of the inhibitor of beta-catenin and Tcf-4 (ICAT), resulting from a down-regulation of integrin-linked kinase in progastrin-depleted cells.
  • Accordingly, ICAT down-regulation was correlated with progastrin overexpression and Tcf-4 target gene activation in human colorectal tumors, and ICAT repression was detected in the colon epithelium of tumor-prone, progastrin-overexpressing mice.
  • In APCDelta14 mice, small interfering RNA-mediated progastrin depletion not only reduced intestinal tumor size and numbers, but also increased goblet cell lineage differentiation and cell apoptosis in the remaining adenomas.
  • CONCLUSIONS: Thus, depletion of endogenous progastrin inhibits the tumorigenicity of APC-mutated colorectal cancer cells in vivo by promoting ICAT expression, thereby counteracting Tcf-4 activity.

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  • (PMID = 17920061.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM065926-05; United States / NIGMS NIH HHS / GM / R01 GM065926; United States / NIGMS NIH HHS / GM / R01 GM065926-05
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Ctnnbip1 protein, mouse; 0 / Gastrins; 0 / Protein Precursors; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf7l2 protein, mouse; 0 / Transcription Factor 7-Like 2 Protein; 0 / Transcription Factors; 0 / beta Catenin; 53988-98-0 / big gastrin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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77. Zhou JQ, Li WP, Xiang Z, Schutt M: [Effects of various HIV protease inhibitors on function of rat insulinoma cells]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2006 May;35(3):251-4
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  • [Title] [Effects of various HIV protease inhibitors on function of rat insulinoma cells].
  • OBJECTIVE: To investigate the effects of various HIV protease inhibitors on the function of pancreatic beta-cells.
  • METHODS: Rat insulinoma INS-1 cells were incubated with different concentrations of ritonavir or amprenavir for 48 h and stimulated with 20 mmol/L D-glucose for 30 min.
  • The rate of insulin release was measured in the supernatant by ELISA, normalized to cellular DNA contents.
  • Cells were counted with trypan blue and MTT test were determined to evaluate the effect of protease inhibitors on cell viability.
  • RESULT: Ritonavir treatment significantly decreased baseline insulin release and glucose-stimulated insulin release in a dose-dependent manner (r=-0.861, -0.839, both P<0.01).
  • For 10 micromol/L of ritonavir, the decrease rate of baseline insulin secretion and glucose-stimulated insulin secretion was 46% and 47%, respectively.
  • Amprenavir had no effect on the rate of insulin release.
  • CONCLUSION: Various HIV protease inhibitors present different effect on the insulin release of pancreatic beta-cells.
  • [MeSH-major] Carbamates / pharmacology. HIV Protease Inhibitors / pharmacology. Insulin / secretion. Insulinoma / metabolism. Ritonavir / pharmacology. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Islets of Langerhans / metabolism. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Rats

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  • (PMID = 16764025.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Carbamates; 0 / HIV Protease Inhibitors; 0 / Insulin; 0 / Sulfonamides; 5S0W860XNR / amprenavir; O3J8G9O825 / Ritonavir
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78. Adsay NV: Cystic neoplasia of the pancreas: pathology and biology. J Gastrointest Surg; 2008 Mar;12(3):401-4
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  • [Title] Cystic neoplasia of the pancreas: pathology and biology.
  • In contrast with solid tumors, most of which are invasive ductal adenocarcinoma with dismal prognosis, cystic lesions of the pancreas are often either benign or low-grade indolent neoplasia.
  • While many are innocuous adenomas--in particular, those that are small and less complex, and in the case of IPMN, those that are branch-duct type are more commonly benign, some harbor or progress into in situ or invasive carcinomas.
  • For this reason, pancreatic cysts with mucinous differentiation ought to be evaluated carefully, preferably by experts familiar with subtle evidences of malignancy in these tumors.
  • The presence of ovarian-type stroma has now almost become a requirement for the diagnosis of MCN, and when defined as such, MCN is seen almost exclusively in women of perimenopausal age group as thick-walled multilocular cystic mass in the tail of the pancreas in contrast with IPMN which afflicts an elder population, both genders in almost equal numbers, and occur predominantly in the head of the organ.
  • While mucinous lesions have well-established pre-malignant properties, most of the entities that fall into the nonmucinous true cyst category such as serous tumors, lymphoepithelial cysts, congenital cysts, and squamoid cyst of ducts have virtually no malignant potential.
  • In contrast, the rare cystic tumors that occur as a result of degenerative/necrotic changes in otherwise solid neoplasia such as the rare cystic ductal adenocarcinomas, cystic endocrine neoplasia, and most importantly, solid-pseudopapillary tumor (SPT) in which cystic change is so common that it used to be incorporated into its name ("solid-cystic," "papillary-cystic") are malignant neoplasia, albeit variable degrees of aggressiveness.
  • SPT holds a distinctive place among pancreatic neoplasia because of its highly peculiar characteristics, undetermined cell lineage, occurrence almost exclusively in young females, association with beta-catenin pathway, and also by being a very low-grade curable malignancy.
  • In conclusion, cystic lesions in the pancreas constitute a biologically and pathologically diverse category most (but not all) of which are either benign or treatable diseases; however, a substantial subset, especially mucinous ones, has malignant potential that requires careful analysis.
  • [MeSH-major] Adenoma / pathology. Carcinoma in Situ / pathology. Neoplasms, Cystic, Mucinous, and Serous / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma, Mucinous / mortality. Adenocarcinoma, Mucinous / pathology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / mortality. Carcinoma, Papillary / pathology. Cystadenoma / pathology. Cystadenoma, Serous / pathology. Dilatation, Pathologic. Humans. Necrosis

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  • (PMID = 17957438.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 19
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79. Hekerman P, Zeidler J, Korfmacher S, Bamberg-Lemper S, Knobelspies H, Zabeau L, Tavernier J, Becker W: Leptin induces inflammation-related genes in RINm5F insulinoma cells. BMC Mol Biol; 2007;8:41
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  • [Title] Leptin induces inflammation-related genes in RINm5F insulinoma cells.
  • BACKGROUND: Leptin acts not only on hypothalamic centers to control food intake but has additional functions in peripheral tissues, e.g. inhibition of insulin secretion from pancreatic islets.
  • In this study, we characterise the regulation of inflammation-related genes by leptin in insulinoma cells and compare the effect of transcriptional regulation by leptin with that of other cytokines.
  • RESULTS: We have used RINm5F insulinoma cells as a model system for a peripheral target cell of leptin.
  • Six transcripts encoding inflammation-related proteins were found to be upregulated by activation of LEPRb, namely lipocalin-2, pancreatitis-associated protein, preprotachykinin-1, fibrinogen-beta, tissue-type plasminogen activator (tPA) and manganese-dependent superoxide dismutase (MnSOD).
  • Four of these transcripts (fibrinogen-beta, lipocalin-2, tPA, MnSOD) were also induced by the proinflammatory cytokine interleukin-1beta (IL-1beta).
  • Finally, leptin treatment increased caspase 3-like proteolytic activity in RINm5F cells.
  • CONCLUSION: The present data show that leptin induces a cytokine-like transcriptional response in RINm5F cells, consistent with the proposed function of leptin as a modulator of immune and inflammatory responses.
  • [MeSH-major] Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Inflammation / genetics. Insulinoma. Leptin / metabolism
  • [MeSH-minor] Animals. Carrier Proteins / genetics. Carrier Proteins / metabolism. Caspases / metabolism. Cricetinae. Genes, Reporter. Interferon-gamma / metabolism. Interleukin-1beta / metabolism. Lipocalins. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis. Point Mutation. Promoter Regions, Genetic. Protein Precursors / genetics. Protein Precursors / metabolism. Rats. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Receptors, Leptin. STAT1 Transcription Factor / genetics. STAT1 Transcription Factor / metabolism. STAT3 Transcription Factor / genetics. STAT3 Transcription Factor / metabolism. Signal Transduction / physiology. Tachykinins / genetics. Tachykinins / metabolism. Tyrosine / metabolism

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  • (PMID = 17521427.001).
  • [ISSN] 1471-2199
  • [Journal-full-title] BMC molecular biology
  • [ISO-abbreviation] BMC Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Interleukin-1beta; 0 / Lcn2 protein, rat; 0 / Leptin; 0 / Lipocalins; 0 / Protein Precursors; 0 / Receptors, Cell Surface; 0 / Receptors, Leptin; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / Tachykinins; 0 / preprotachykinin; 42HK56048U / Tyrosine; 82115-62-6 / Interferon-gamma; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC1890559
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80. Cortina C, Palomo-Ponce S, Iglesias M, Fernández-Masip JL, Vivancos A, Whissell G, Humà M, Peiró N, Gallego L, Jonkheer S, Davy A, Lloreta J, Sancho E, Batlle E: EphB-ephrin-B interactions suppress colorectal cancer progression by compartmentalizing tumor cells. Nat Genet; 2007 Nov;39(11):1376-83
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  • [Title] EphB-ephrin-B interactions suppress colorectal cancer progression by compartmentalizing tumor cells.
  • The genes encoding tyrosine kinase receptors EphB2 and EphB3 are beta-catenin and Tcf4 target genes in colorectal cancer (CRC) and in normal intestinal cells.
  • In the intestinal epithelium, EphB signaling controls the positioning of cell types along the crypt-villus axis.
  • In CRC, EphB activity suppresses tumor progression beyond the earliest stages.
  • Here we show that EphB receptors compartmentalize the expansion of CRC cells through a mechanism dependent on E-cadherin-mediated adhesion.
  • We demonstrate that EphB-mediated compartmentalization restricts the spreading of EphB-expressing tumor cells into ephrin-B1-positive territories in vitro and in vivo.
  • Our results indicate that CRC cells must silence EphB expression to avoid repulsive interactions imposed by normal ephrin-B1-expressing intestinal cells at the onset of tumorigenesis.
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adenoma / prevention & control. Animals. Cell Line, Tumor. Disease Progression. Female. Genes, APC / physiology. Humans. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Intestinal Neoplasms / metabolism. Intestinal Neoplasms / pathology. Intestinal Neoplasms / prevention & control. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. RNA, Messenger / antagonists & inhibitors. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Eph Family / antagonists & inhibitors. Receptors, Eph Family / genetics. Receptors, Eph Family / metabolism. Signal Transduction. Subcellular Fractions. TCF Transcription Factors / metabolism. Transcription Factor 7-Like 2 Protein. beta Catenin / metabolism


81. Karawagh AM, Abdullah LS, Gasim AM, Abdelaziz MM: Noninsulinoma pancreatogenous hypoglycemia syndrome in a Saudi male. Saudi Med J; 2008 Nov;29(11):1654-7
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  • [Title] Noninsulinoma pancreatogenous hypoglycemia syndrome in a Saudi male.
  • Nesidioblastosis is focal or diffuse islet hyperplasia leading to hyperinsulinism with subsequent hypoglycemia in the absence of insulinoma, usually described in neonates and infancy.
  • [MeSH-major] Hypoglycemia / etiology. Pancreatic Diseases / complications
  • [MeSH-minor] Aged. Humans. Insulinoma. Male. Saudi Arabia. Syndrome

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  • (PMID = 18998019.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Saudi Arabia
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82. Gao C, Fu X, Pan Y, Li Q: Surgical treatment of pancreatic neuroendocrine tumors: report of 112 cases. Dig Surg; 2010 Aug;27(3):197-204
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  • [Title] Surgical treatment of pancreatic neuroendocrine tumors: report of 112 cases.
  • OBJECTIVES: To review the clinical data of a group of patients with pancreatic neuroendocrine tumors (pNETs) and to investigate the role of surgery in the treatment for pNETs by analyzing clinical manifestations and postoperative course of this rare disease.
  • Patients' data related to demographics and characteristics, diagnostic studies, surgical and tumor characteristics and survival were retrospectively reviewed.
  • RESULTS: Forty-six patients (41.1%) had a well-differentiated neuroendocrine tumor (WDT), 44 (48.2%) a well-differentiated neuroendocrine carcinoma (WD-Ca) and 12 (10.7%) a poorly differentiated neuroendocrine carcinoma (PD-Ca).
  • Nonfunctional tumors were seen in 65 (58.0%) patients, whereas functional tumors were found in 47 (42.0%) patients, including 26 insulinomas, 17 gastrinomas, 2 VIPomas, 1 glucagonoma, and 1 ACTHoma.
  • The common postoperative complications were pancreatic fistula (15.2%), wound infection (13.4%) and delayed gastric emptying (6.3%).
  • Twenty-six (55.3%) of the 47 functional tumors were malignant, whereas 40 (61.5%) of the 65 nonfunctional tumors were malignant.
  • Survival was significantly related to the type of neuroendocrine tumor (p = 0.001).
  • The 5-year survival rate differed significantly between patients with tumor node metastasis (TNM) stage I and II disease and those with stage III and IV tumors (p = 0.011).
  • Patients with stage III had better prognosis than those with stage IV tumors (p = 0.007).
  • Malignant cases should be treated with aggressive radical surgery to achieve complete tumor resection and potential for long-term survival.
  • [MeSH-major] Neuroendocrine Tumors / surgery. Pancreatic Neoplasms / surgery

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  • (PMID = 20571266.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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83. Gamero AM, Young MR, Mentor-Marcel R, Bobe G, Scarzello AJ, Wise J, Colburn NH: STAT2 contributes to promotion of colorectal and skin carcinogenesis. Cancer Prev Res (Phila); 2010 Apr;3(4):495-504
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  • Signal transducer and activator of transcription 2 (STAT2) is an essential transcription factor in the type I IFN (IFN-alpha/beta) signal transduction pathway and known for its role in mediating antiviral immunity and cell growth inhibition.
  • Contrary to our hypothesis, deletion of STAT2 inhibited azoxymethane/dextran sodium sulfate-induced colorectal carcinogenesis as measured by prolonged survival, lower adenoma incidence, smaller polyps, and less chronic inflammation.
  • Deletion of STAT2 decreased azoxymethane/dextran sodium sulfate-induced expression and release of proinflammatory mediators, such as interleukin-6 and CCL2, and decreased interleukin-6 release from skin carcinoma cells, which then decreased STAT3 activation.

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  • [Copyright] (c) 2010 AACR.
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  • (PMID = 20233899.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA162545; United States / NCI NIH HHS / CA / K22 CA095326; United States / NCI NIH HHS / CA / CA095326-02; United States / NCI NIH HHS / CA / R01 CA140499; United States / NCI NIH HHS / CA / K22 CA095326-02; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / K22CA095326; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / STAT2 Transcription Factor
  • [Other-IDs] NLM/ NIHMS181318; NLM/ PMC2851485
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84. Le Berre JP, Bey Boeglin M, Duverger V, Garcia C, Bordier L, Dupuy O, Mayaudon H, Bauduceau B: [Seizure and Bourneville tuberous sclerosis: think about insulinoma]. Rev Med Interne; 2009 Feb;30(2):179-80
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  • [Title] [Seizure and Bourneville tuberous sclerosis: think about insulinoma].
  • [Transliterated title] Crise comitiale et sclérose tubéreuse de Bourneville: penser à l'insulinome.
  • We report a case of a Bourneville tuberous sclerosis in a 41-year-old-man with hypoglycemia leading to seizures, resulting from an insulinoma.


85. Boesgaard TW, Nielsen TT, Josefsen K, Hansen T, Jørgensen T, Pedersen O, Nørremølle A, Nielsen JE, Hasholt L: Huntington's disease does not appear to increase the risk of diabetes mellitus. J Neuroendocrinol; 2009 Sep;21(9):770-6
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  • [Title] Huntington's disease does not appear to increase the risk of diabetes mellitus.
  • Huntington's disease (HD) is an autosomal, dominantly inherited, neurodegenerative disorder characterised by neurological, cognitive and psychiatric symptoms.
  • In transgenic mice, the severity of the diabetic phenotype appears to correlate with the length of a polyglutamine expansion in the protein huntingtin.
  • In the present study, we investigated the association between diabetes mellitus and HD by performing an oral glucose-tolerance test (OGTT) to evaluate the glucose-tolerance status and OGTT-related insulin release in 14 HD patients.
  • Furthermore, we expressed N-terminal huntingtin fragments with different polyglutamine lengths in an insulinoma-cell line (INS-1E) to investigate how mutant huntingtin influences glucose-stimulated insulin release in vitro.
  • However, the glucose-stimulated induction of insulin release was significantly reduced in the insulinoma-cell line expressing highly expanded huntingtin compared to cells expressing huntingtin with modestly elongated polyglutamine stretches.
  • These data indicate that insulin release from beta-cells expressing mutant huntingtin appears to be polyglutamine length-dependent, and that polyglutamine lengths within the range normally found in adult onset HD do not influence insulin release.
  • [MeSH-major] Diabetes Mellitus / etiology. Huntington Disease / complications
  • [MeSH-minor] Adult. Aged. Animals. Blood Glucose / analysis. Case-Control Studies. Cells, Cultured. Female. Humans. Insulin / blood. Insulin / metabolism. Insulin-Secreting Cells / metabolism. Male. Mice. Middle Aged. Mutant Proteins / genetics. Mutant Proteins / metabolism. Mutant Proteins / physiology. Nerve Tissue Proteins / chemistry. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / metabolism. Nerve Tissue Proteins / physiology. Nuclear Proteins / chemistry. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Nuclear Proteins / physiology. Risk Factors. Transduction, Genetic

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  • (PMID = 19602103.001).
  • [ISSN] 1365-2826
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Huntington protein, mouse; 0 / Insulin; 0 / Mutant Proteins; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins
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86. Yoshida A, Sen C, Asa SL, Rosenblum MK: Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation. Am J Surg Pathol; 2008 Nov;32(11):1736-41
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  • [Title] Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation.
  • The patient was treated with thyroid radioablation and hormone replacement and followed for 7 years, during which time the tumor grew to 4.6 cm.
  • At transsphenoidal surgery, a tumor consisting of a pituitary adenoma and adamantinomatous craniopharyngiomalike components was resected.
  • Both components were closely intermingled, but there was no evidence of an intermediate morphologic phenotype.
  • Immunohistochemically, the adenoma was not only positive for beta-thyroid stimulating hormone, alpha subunit, and pituitary transcription factor 1, but also stained for beta-follicle stimulating hormone, steroidogenic factor-1, adrenocorticotropic hormone, and pituitary-restricted transcription factor (Tpit), exhibiting an unusual plurihormonal profile.
  • This lesion may represent an unusual composite tumor attributable to divergent differentiation of a common precursor.
  • Alternatively, it may be viewed as a pituitary adenoma showing metaplastic change analogous to the development of squamous cell nests of the pars tuberalis from adenohypophyseal endocrine cells.
  • [MeSH-major] Adenoma / pathology. Craniopharyngioma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary Neoplasms / pathology

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  • (PMID = 18769335.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-71-5 / Thyrotropin
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87. Fernández-Cruz L, Blanco L, Cosa R, Rendón H: Is laparoscopic resection adequate in patients with neuroendocrine pancreatic tumors? World J Surg; 2008 May;32(5):904-17
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  • [Title] Is laparoscopic resection adequate in patients with neuroendocrine pancreatic tumors?
  • Since the first reports with laparoscopic resection of islet cell tumors in 1996, the experience worldwide is still limited, with only short-term outcomes available.
  • Some have suggested that a malignant tumor is a contraindication to laparoscopic resection.
  • Aim The aim of this study was to evaluate the feasibility, safety, and long-term outcome of the laparoscopic approach in patients with functioning, nonfunctioning, or overt malignant pancreatic neuroendocrine tumor (PNT).
  • Patients and methods A total of 49 consecutive patients (43 women, 6 men; mean age 58 years, range 22-83 years) underwent laparoscopic pancreatic surgery (LPS) from April 1998 to June 2007.
  • Other than 9 PNTs localized in the head of the pancreas, all tumors were located in the left pancreas.
  • There were 33 patients with functioning tumors: 4 with gastrinomas (mean size 1.2 cm), 1 with a glucagonoma (4 cm), 3 with vipomas (3.2 cm), 2 with carcinoids (5.2 cm), 20 with sporadic insulinomas (1.4 cm), 2 with insulinoma/multiple endocrine neoplasia type 1 (MEN-1) (4.4 cm), and 1 with a malignant insulinoma (13 cm).
  • Sixteen patients had a nonfunctioning tumor (mean size 5 cm).
  • Evaluation criteria included operative and postoperative factors, pathologic data including R0 or R1 resection (the pancreatic transection margin and all transection margins on the specimen were inked).
  • Long-term outcomes were analyzed by tumor recurrence and patient survival.
  • The group of patients with malignant tumors undergoing Lap SxDP had a longer operating time and greater blood loss compared with the other distal pancreatectomy (Lap DP) techniques.
  • These complications were mainly pancreatic fistula: 8.7% after Lap DP and 38% after Lap En.
  • Conclusions This series demonstrates that LPS is feasible and safe in benign-appearing and malignant neuroendocrine pancreatic tumors (NEPTs).
  • The benefits of minimally invasive surgery were manifest in the short hospital stay and acceptable pancreas-related complications in high-risk patients.
  • LPS can achieve negative tangential margins in a high percentage of patients with malignant tumors.
  • [MeSH-major] Carcinoma, Islet Cell / surgery. Laparoscopy. Neuroendocrine Tumors / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery

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  • (PMID = 18264824.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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88. Service GJ, Thompson GB, Service FJ, Andrews JC, Collazo-Clavell ML, Lloyd RV: Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl J Med; 2005 Jul 21;353(3):249-54
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  • Except for equivocal evidence in one patient, there was no radiologic evidence of insulinoma.
  • Nesidioblastosis was identified in resected specimens from each patient, and multiple insulinomas were identified in one.
  • We speculate that hyperfunction of pancreatic islets did not lead to obesity but that beta-cell trophic factors may have increased as a result of gastric bypass.
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Humans. Hyperplasia. Insulinoma / complications. Insulinoma / diagnosis. Islets of Langerhans / pathology. Islets of Langerhans / physiopathology. Male. Middle Aged. Obesity / pathology. Obesity / surgery. Obesity, Morbid / pathology. Obesity, Morbid / physiopathology. Obesity, Morbid / surgery. Pancreatic Ducts / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Postprandial Period

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  • [CommentIn] N Engl J Med. 2005 Jul 21;353(3):300-2 [16034017.001]
  • [CommentIn] N Engl J Med. 2005 Nov 17;353(20):2192-4; author reply 2192-4 [16299937.001]
  • [CommentIn] N Engl J Med. 2005 Nov 17;353(20):2192-4; author reply 2192-4 [16291992.001]
  • [CommentIn] N Engl J Med. 2005 Dec 29;353(26):2822-3 [16382076.001]
  • (PMID = 16034010.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Grant] United States / PHS HHS / / 32385
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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89. Fabbri HC, Mello MP, Soardi FC, Esquiaveto-Aun AM, Oliveira DM, Denardi FC, Moura-Neto A, Garmes HM, Baptista MT, Matos PS, Lemos-Marini SH, D'Souza-Li LF, Guerra-Júnior G: Long-term follow-up of an 8-year-old boy with insulinoma as the first manifestation of a familial form of multiple endocrine neoplasia type 1. Arq Bras Endocrinol Metabol; 2010 Nov;54(8):754-60
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  • [Title] Long-term follow-up of an 8-year-old boy with insulinoma as the first manifestation of a familial form of multiple endocrine neoplasia type 1.
  • Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant hereditary cancer syndrome characterized mostly by parathyroid, enteropancreatic, and anterior pituitary tumors.
  • His diagnosis was pancreatic insulinoma.
  • At a first evaluation, the father presented only gastric ulceration but subsequently developed hyperparathyroidism and lung carcinoid tumor.
  • Molecular study showed a G to A substitution in intron 4, at nine nucleotides upstream of the splicing acceptor site, causing a splicing mutation.
  • [MeSH-major] Insulinoma / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Pancreatic Neoplasms / genetics. Proto-Oncogene Proteins / genetics


90. Sansom OJ, Reed KR, van de Wetering M, Muncan V, Winton DJ, Clevers H, Clarke AR: Cyclin D1 is not an immediate target of beta-catenin following Apc loss in the intestine. J Biol Chem; 2005 Aug 5;280(31):28463-7
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  • [Title] Cyclin D1 is not an immediate target of beta-catenin following Apc loss in the intestine.
  • Cyclin D1 is postulated to be a target of the canonical Wnt pathway and critical for intestinal adenoma development.
  • Cyclin D1 levels do, however, increase in a delayed manner in a small subset of cells, suggesting such up-regulation occurs as a secondary event.
  • In these circumstances, all adenomas (but not smaller lesions) showed cyclin D1 up-regulation.
  • Finally in a smaller study, we analyzed whether cyclin D1 deficiency affected adenoma formation 20 days following induced loss of Apc.
  • Unlike AhCre(+) Apc(fl/fl) mice (which all developed adenomas), doubly mutant AhCre(+) Apc(fl/fl) cyclin D1(-/-) mice only developed small lesions.
  • Taken together, this argues that cyclin D1 up-regulation in intestinal neoplasia is important for tumor progression rather than initiation.
  • [MeSH-minor] Adenoma. Animals. Cell Line, Tumor. Colorectal Neoplasms. Gene Deletion. Gene Expression Regulation, Neoplastic. Integrases / metabolism. Intestinal Neoplasms. Mice. Mice, Inbred C57BL. Phenotype. beta Catenin


91. Tittiger M, Ma X, Xu L, Ponder KP: Neonatal intravenous injection of a gammaretroviral vector has a low incidence of tumor induction in mice. Hum Gene Ther; 2008 Nov;19(11):1317-23
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  • [Title] Neonatal intravenous injection of a gammaretroviral vector has a low incidence of tumor induction in mice.
  • Neonatal intravenous injection of gammaretroviral vectors (gamma-RVs) with an intact long terminal repeat (LTR) and an internal liver promoter can result in long-term expression in liver cells and correction of mucopolysaccharidosis.
  • Some expression also occurs in blood cells and brain, which likely derives from the LTR, and may contribute to clinical efficacy.
  • The goal of this project was to determine whether neonatal gene therapy with an LTR-intact gamma-RV would induce tumors in mice.
  • Fifty-one normal newborn C57BL/6 mice were injected intravenously at 10(10) transducing units/kg with a gamma-RV expressing canine beta-glucuronidase (GUSB) cDNA.
  • This resulted in transduction of 23 +/- 9% of hepatocytes as determined by histochemical staining, and 0.24 +/- 0.20 copy of gamma-RV DNA per cell in liver as determined by real-time polymerase chain reaction.
  • One gamma-RV-treated mouse (2%) developed a small (diameter, 2 mm) liver adenoma, which was similar to the frequency of liver adenomas (2%) or hepatocellular carcinoma (2%) in untreated mice.
  • Although 22% of gamma-RV-treated mice developed hematopoietic tumors, none contained high gamma-RV DNA copy numbers, and the frequency was similar to that in the control group (22%).
  • [MeSH-major] Adenoma / pathology. Carcinoma, Hepatocellular / pathology. Gammaretrovirus / genetics. Genetic Vectors. Hematologic Neoplasms / pathology. Liver Neoplasms, Experimental / pathology

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  • (PMID = 19866493.001).
  • [ISSN] 1557-7422
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R56 DK066448; United States / NIDDK NIH HHS / DK / R01 DK066448-06A2; United States / NIDDK NIH HHS / DK / R01 DK066448; United States / NIDDK NIH HHS / DK / R56 DK066448-06; United States / NIDDK NIH HHS / DK / R01 DK054061-05; United States / NIDDK NIH HHS / DK / DK20579; United States / NIDDK NIH HHS / DK / R01 DK066448-01; United States / NIDDK NIH HHS / DK / P60 DK020579-307480; United States / NIDDK NIH HHS / DK / DK66448; United States / NIDDK NIH HHS / DK / P60 DK020579; United States / NIDDK NIH HHS / DK / R56 DK066448-06A1; United States / NIDDK NIH HHS / DK / P30 DK52574; United States / NIDDK NIH HHS / DK / P30 DK052574; United States / NIDDK NIH HHS / DK / R01 DK054061; United States / NIDDK NIH HHS / DK / P30 DK052574-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.1.31 / Glucuronidase
  • [Other-IDs] NLM/ NIHMS101923; NLM/ PMC2891155
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92. Batlle E, Bacani J, Begthel H, Jonkheer S, Gregorieff A, van de Born M, Malats N, Sancho E, Boon E, Pawson T, Gallinger S, Pals S, Clevers H: EphB receptor activity suppresses colorectal cancer progression. Nature; 2005 Jun 23;435(7045):1126-30
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  • Most sporadic colorectal cancers are initiated by activating Wnt pathway mutations, characterized by the stabilization of beta-catenin and constitutive transcription by the beta-catenin/T cell factor-4 (Tcf-4) complex.
  • Here we show that, although Wnt signalling remains constitutively active, most human colorectal cancers lose expression of EphB at the adenoma-carcinoma transition.
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Animals. Cell Line, Tumor. Disease Progression. Down-Regulation. Gene Expression Regulation, Neoplastic. Genes, APC. Genes, Dominant / genetics. Humans. Intercellular Signaling Peptides and Proteins / metabolism. Mice. Mice, Transgenic. Mutation / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Signal Transduction. Wnt Proteins


93. Huang L, Yan M, Kirschke CP: Over-expression of ZnT7 increases insulin synthesis and secretion in pancreatic beta-cells by promoting insulin gene transcription. Exp Cell Res; 2010 Oct 1;316(16):2630-43
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  • [Title] Over-expression of ZnT7 increases insulin synthesis and secretion in pancreatic beta-cells by promoting insulin gene transcription.
  • The mechanism by which zinc regulates insulin synthesis and secretion in pancreatic beta-cells is still unclear.
  • In this study, we demonstrated that zinc transporter 7 (ZnT7, Slc30a7) was co-expressed with insulin in the islet of Langerhans in the mouse pancreas.
  • In RIN5mF cells (rat insulinoma cells), ZnT7 was found mainly residing in the perinuclear region of the cell, which is consistent with its Golgi apparatus localization.
  • Over-expression of ZnT7 in RIN5mF cells increased the total cellular insulin content leading to a high basal insulin secretion.
  • Furthermore, glucose-induced insulin secretion was not altered in RIN5mF cells over-expressing ZnT7.
  • Quantitative RT-PCR and (35)S metabolic labeling analysis demonstrated that over-expression of ZnT7 in RIN5mF cells led to an increase of insulin mRNA expression and subsequent insulin protein synthesis in the cell.
  • Mtf1, a metal-responsive transcription factor, was shown to specifically bind to the MRE in the Ins genes and activated the insulin gene transcription.
  • Together, the data strongly suggest that ZnT7 plays an important role in regulating insulin expression by modulating Mtf1 transcriptional activity.
  • [MeSH-major] Cation Transport Proteins / metabolism. Glucose / pharmacology. Insulin / genetics. Insulin / secretion. Insulin-Secreting Cells / metabolism. Transcription, Genetic / drug effects
  • [MeSH-minor] Animals. Blotting, Western. Cells, Cultured. Electrophoretic Mobility Shift Assay. Fluorescent Antibody Technique. Immunoprecipitation. Insulinoma / drug therapy. Insulinoma / metabolism. Insulinoma / pathology. Islets of Langerhans / cytology. Islets of Langerhans / metabolism. Male. Mice. Mice, Inbred C57BL. RNA, Messenger / genetics. Rats. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Published by Elsevier Inc.
  • (PMID = 20599947.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cation Transport Proteins; 0 / Insulin; 0 / RNA, Messenger; 0 / ZnT7 protein, mouse; IY9XDZ35W2 / Glucose
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94. Higa M, Shimabukuro M, Shimajiri Y, Takasu N, Shinjyo T, Inaba T: Protein kinase B/Akt signalling is required for palmitate-induced beta-cell lipotoxicity. Diabetes Obes Metab; 2006 Mar;8(2):228-33
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  • [Title] Protein kinase B/Akt signalling is required for palmitate-induced beta-cell lipotoxicity.
  • AIM: This study was conducted to clarify cell death and survival signals in pancreatic beta-cell lipotoxicity.
  • METHODS: Rat insulinoma INS-1 cells, with or without expression of dominant-negative mutant of Akt (K179M), were cultured with palmitate (C16:0) or oleate (C18:1) and cell numbers were determined by 0.2% eosin dye exclusion assay.
  • RESULTS: Twenty-four hours treatment with palmitate increased the INS-1 cell number at 0.1-0.2 mM but decreased the cell number at 0.5-1 mM.
  • Oleate did not affect cell number at 0.1-1.0 mM.
  • The K179M form of Akt/PKB abolished palmitate-induced cell proliferation at the low dose and death at the high dose.
  • CONCLUSION: Results suggest that Akt/PKB signalling is involved in palmitate-induced cell death and survival of pancreatic beta cell.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Insulin-Secreting Cells / metabolism. Palmitic Acid / pharmacology. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Animals. Cell Death / drug effects. Cell Proliferation. Cell Survival. Cells, Cultured. Dose-Response Relationship, Drug. Electrophoretic Mobility Shift Assay. Insulinoma / metabolism. NF-kappa B / metabolism. Oleic Acid / pharmacology. Oleic Acid / toxicity. Rats. Triglycerides / metabolism

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  • (PMID = 16448528.001).
  • [ISSN] 1462-8902
  • [Journal-full-title] Diabetes, obesity & metabolism
  • [ISO-abbreviation] Diabetes Obes Metab
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / Triglycerides; 2UMI9U37CP / Oleic Acid; 2V16EO95H1 / Palmitic Acid; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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95. Song GM, Huan Y, Sun SJ, Chen YT, Liu Q, Shen ZF: Biological activity of EXf, a peptide analogue of exendin-4. Eur J Pharmacol; 2010 Feb 25;628(1-3):261-7
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  • After a single subcutaneous injection, EXf significantly decreased plasma glucose concentration and glucose excursion following the administration of an oral glucose challenge both in non-diabetic (ICR), monosodium l-glutamate induced insulin resistance (MSG-IR) and diabetic KK-ay mice.
  • Meanwhile, EXf resulted in an increase of first-phase insulin secretion in normal mice and KK-ay mice following the glucose challenge.
  • EXf activated the cAMP response element (CRE) of the rat insulin I gene promoter (RIP1) GFP-construct in a dose-dependent manner in the cultured mouse insulinoma cell line, termed NIT-1, and this agonist activity was blocked by the glucagon-like peptide 1 (GLP-1) receptor antagonist exendin(9-39).
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Blood Glucose / metabolism. Cell Line. Cyclic AMP / genetics. Fasting. Female. Insulin / genetics. Insulin / secretion. Intestine, Small / drug effects. Intestine, Small / physiology. Male. Mice. Molecular Sequence Data. Postprandial Period. Pregnancy. Promoter Regions, Genetic / genetics. Rats. Response Elements / genetics. Transcription, Genetic / drug effects

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  • (PMID = 19919832.001).
  • [ISSN] 1879-0712
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Peptides; 0 / Venoms; 9P1872D4OL / exenatide; E0399OZS9N / Cyclic AMP
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96. Suri A, Walters JJ, Rohrs HW, Gross ML, Unanue ER: First signature of islet beta-cell-derived naturally processed peptides selected by diabetogenic class II MHC molecules. J Immunol; 2008 Mar 15;180(6):3849-56
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  • [Title] First signature of islet beta-cell-derived naturally processed peptides selected by diabetogenic class II MHC molecules.
  • The diversity of Ags targeted by T cells in autoimmune diabetes is unknown.
  • In this study, we identify and characterize a limited number of naturally processed peptides from pancreatic islet beta-cells selected by diabetogenic I-A(g7) molecules of NOD mice.
  • We used insulinomas transfected with the CIITA transactivator, which resulted in their expression of class II histocompatibility molecules and activation of diabetogenic CD4 T cells.
  • Peptides bound to I-A(g7) were isolated and examined by mass spectrometry: some peptides derived from proteins present in secretory granules of endocrine cells, and a number were shared with cells of neuronal lineage.
  • All proteins to which peptides were identified were expressed in beta cells from normal islets.
  • The draining pancreatic lymph nodes of prediabetic NOD mice contained CD4 T cells that recognized three different natural peptides.
  • Furthermore, four different peptides elicited CD4 T cells, substantiating the presence of such self-reactive T cells.
  • The overall strategy of identifying natural peptides from islet beta-cells opens up new avenues to evaluate the repertoire of self-reactive T cells and its role in onset of diabetes.
  • [MeSH-major] Diabetes Mellitus, Type 1 / immunology. Histocompatibility Antigens Class II / metabolism. Insulin-Secreting Cells / immunology. Insulin-Secreting Cells / metabolism. Peptides / metabolism. Protein Processing, Post-Translational / immunology
  • [MeSH-minor] Amino Acid Sequence. Animals. Antigen Presentation / genetics. Antigen Presentation / immunology. Antigen-Presenting Cells / immunology. Antigen-Presenting Cells / metabolism. Autoimmune Diseases / immunology. Autoimmune Diseases / metabolism. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Humans. Insulinoma / immunology. Insulinoma / secretion. Mice. Mice, Inbred NOD. Molecular Sequence Data. Protein Binding / immunology. T-Lymphocytes / immunology. T-Lymphocytes / metabolism

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  • (PMID = 18322192.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class II; 0 / I-A g7 antigen; 0 / Peptides
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97. Hesselson D, Anderson RM, Beinat M, Stainier DY: Distinct populations of quiescent and proliferative pancreatic beta-cells identified by HOTcre mediated labeling. Proc Natl Acad Sci U S A; 2009 Sep 1;106(35):14896-901
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct populations of quiescent and proliferative pancreatic beta-cells identified by HOTcre mediated labeling.
  • Pancreatic beta-cells are critical regulators of glucose homeostasis, and they vary dramatically in their glucose stimulated metabolic response and levels of insulin secretion.
  • It is unclear whether these parameters are influenced by the developmental origin of individual beta-cells.
  • Using HOTcre, a Cre-based genetic switch that uses heat-induction to precisely control the temporal expression of transgenes, we labeled two populations of beta-cells within the developing zebrafish pancreas.
  • These populations originate in distinct pancreatic buds and exhibit gene expression profiles suggesting distinct functions during development.
  • We find that the dorsal bud derived beta-cells are quiescent and exhibit a marked decrease in insulin expression postembryonically.
  • In contrast, ventral bud derived beta-cells proliferate actively, and maintain high levels of insulin expression compared with dorsal bud derived beta-cells.
  • Therapeutic strategies to regulate beta-cell proliferation and function are required to cure pathological states that result from excessive beta-cell proliferation (e.g., insulinoma) or insufficient beta-cell mass (e.g., diabetes mellitus).
  • Our data reveal the existence of distinct populations of beta-cells in vivo and should help develop better strategies to regulate beta-cell differentiation and proliferation.


98. de Herder WW, Kwekkeboom DJ, Valkema R, Feelders RA, van Aken MO, Lamberts SW, van der Lely AJ, Krenning EP: Neuroendocrine tumors and somatostatin: imaging techniques. J Endocrinol Invest; 2005;28(11 Suppl International):132-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroendocrine tumors and somatostatin: imaging techniques.
  • Tumors and metastases bearing the somatostatin receptor subtypes 2 (SSTR2) or SSTR5 can be visualized in vivo after injection of radiolabeled octapeptide somatostatin analogs like 111In-pentetreotide.
  • The sensitivity of 111In-pentetreotide scintigraphy for the detection of carcinoid tumors is 86-95%.
  • The sensitivity of 111In-pentetreotide scintigraphy for the detection of gastrinomas, vasoactive intestinal polypeptide-secreting tumors, and glucagonomas as well as clinically non-functioning lesions is 75-100%.
  • However, for insulinoma this is 50-60%.
  • Most GH- and TSH-secreting pituitary adenomas can be visualized using 111In-pentetreotide.
  • 111In-pentetreotide scintigraphy has been successful for the localization of extra-pituitary ACTH-secreting tumors and their metastases, and especially for occult tumors.
  • [MeSH-major] Neuroendocrine Tumors / radionuclide imaging. Somatostatin
  • [MeSH-minor] Carcinoid Tumor / radionuclide imaging. Gastrointestinal Neoplasms / radionuclide imaging. Humans. Indium Radioisotopes. Paraganglioma / radionuclide imaging. Pheochromocytoma / radionuclide imaging. Pituitary Neoplasms / radionuclide imaging. Receptors, Somatostatin / analysis

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  • (PMID = 16625862.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Indium Radioisotopes; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; G083B71P98 / pentetreotide
  • [Number-of-references] 49
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99. Giles RH, Lolkema MP, Snijckers CM, Belderbos M, van der Groep P, Mans DA, van Beest M, van Noort M, Goldschmeding R, van Diest PJ, Clevers H, Voest EE: Interplay between VHL/HIF1alpha and Wnt/beta-catenin pathways during colorectal tumorigenesis. Oncogene; 2006 May 18;25(21):3065-70
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  • [Title] Interplay between VHL/HIF1alpha and Wnt/beta-catenin pathways during colorectal tumorigenesis.
  • Activation of the Wnt signaling pathway initiates the transformation of colorectal epithelial cells, although the transition to metastatic cancer requires angiogenesis.
  • We have investigated the expression of the von Hippel-Lindau (VHL) tumor suppressor in the intestines from humans and mice.
  • [MeSH-major] Adenocarcinoma / etiology. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / etiology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Nerve Tissue Proteins / physiology. TCF Transcription Factors / physiology. Von Hippel-Lindau Tumor Suppressor Protein / physiology. Wnt Proteins / physiology. beta Catenin / physiology
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli / pathology. Animals. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Line. Colon / cytology. Colon / metabolism. Colon / pathology. Colonic Polyps / genetics. Colonic Polyps / metabolism. Colonic Polyps / pathology. Disease Progression. Epithelial Cells / metabolism. Erythropoietin / genetics. Gene Expression Regulation, Neoplastic. Genes, Reporter. Humans. Intestinal Mucosa / cytology. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Kidney. L Cells (Cell Line). Mice. Mice, Knockout. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Promoter Regions, Genetic. Recombinant Fusion Proteins / biosynthesis. Recombinant Fusion Proteins / genetics. Signal Transduction / physiology. Transcription Factor 7-Like 2 Protein. Wnt3 Protein

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
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  • (PMID = 16407833.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / CTNNB1 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf4 protein, mouse; 0 / Tcf7l2 protein, mouse; 0 / Transcription Factor 7-Like 2 Protein; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / beta Catenin; 11096-26-7 / Erythropoietin; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Vhlh protein, mouse; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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100. Mabrut JY, Fernandez-Cruz L, Azagra JS, Bassi C, Delvaux G, Weerts J, Fabre JM, Boulez J, Baulieux J, Peix JL, Gigot JF, Hepatobiliary and Pancreatic Section (HBPS) of the Royal Belgian Society of Surgery, Belgian Group for Endoscopic Surgery (BGES), Club Coelio: Laparoscopic pancreatic resection: results of a multicenter European study of 127 patients. Surgery; 2005 Jun;137(6):597-605
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic pancreatic resection: results of a multicenter European study of 127 patients.
  • BACKGROUND: The reported experience with laparoscopic pancreatic resections (LPR) remains limited to case reports or small series of patients.
  • Detailed questionnaires were used, focusing on patients, tumors, operative data, and late outcome.
  • RESULTS: During the study period, 127 patients with presumed pancreatic neoplasms were enrolled in this series.
  • Final diagnoses included benign pancreatic diseases in 111 patients (87%; insulinoma: 22, neuroendocrine neoplasm: 20, mucinous cystadenoma: 26, serous cystadenoma: 21, chronic pancreatitis: 11, others: 11), and 16 patients (13%) had malignant pancreatic diseases (insulinoma: 3, neuroendocrine neoplasm: 5, ductal adenocarcinoma: 4, cystadenocarcinoma: 2, renal metastases: 2).
  • Five patients with presumed benign pancreatic disease had malignancy at final pathology.
  • The median tumor size was 30 mm (range, 5-120 mm); 89% of tumors were located in the left pancreas.
  • The rate of overall postoperative pancreatic-related complications was 31%, including a 17% rate of clinical pancreatic fistula.
  • During a median follow-up of 15 months (range, 3-47 months), 23% of the patients with pancreatic malignancies had tumor recurrence.
  • CONCLUSIONS: LPR is feasible and safe in selected patients with presumed benign and distal pancreatic tumors.
  • The management of the pancreatic stump remains a challenge.
  • The role of LPR for pancreatic malignancies remains controversial.
  • [MeSH-major] Laparoscopy. Pancreatectomy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Follow-Up Studies. Humans. Length of Stay. Neoplasm Recurrence, Local. Reoperation. Retrospective Studies. Treatment Outcome

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  • (PMID = 15962401.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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