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6. 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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7. 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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  • (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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8. 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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9. 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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10. 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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11. 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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12. 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


13. van der Weyden L, Arends MJ, Dovey OM, Harrison HL, Lefebvre G, Conte N, Gergely FV, Bradley A, Adams DJ: Loss of Rassf1a cooperates with Apc(Min) to accelerate intestinal tumourigenesis. Oncogene; 2008 Jul 24;27(32):4503-8
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  • Promoter methylation of the RAS-association domain family 1, isoform A gene (RASSF1A) is one of the most frequent events found in human tumours.
  • Further, loss of RASSF1A has also been reported to occur in premalignant adenomas of the bowel.
  • RASSF1A has been implicated in an array of pivotal cellular processes, including regulation of the cell cycle, apoptosis, microtubule stability and most recently in the beta-catenin signalling pathway.
  • By interbreeding isoform specific Rassf1a knockout mice with Apc(+/Min) mice, we showed that loss of Rassf1a results in a significant increase in adenomas of the small intestine and accelerated intestinal tumourigenesis leading to the earlier death of adenocarcinoma-bearing mice and decreased overall survival.
  • Comparative genomic hybridization of adenomas from Rassf1a(-/-); Apc(+/Min) mice revealed no evidence of aneuploidy or gross chromosomal instability (no difference to adenomas from Rassf1a(+/+); Apc(+/Min) mice).
  • Immunohistochemical analysis of adenomas revealed increased nuclear beta-catenin accumulation in adenomas from Rassf1a(-/-); Apc(+/Min) mice, compared to those from Rassf1a(+/+); Apc(+/Min) mice, but no differences in proliferation marker (Ki67) staining patterns.
  • Collectively these data demonstrate cooperation between inactivation of Rassf1a and Apc resulting in accelerated intestinal tumourigenesis, with adenomas showing increased nuclear accumulation of beta-catenin, supporting a mechanistic link via loss of the known interaction of Rassf1 with beta-TrCP that usually mediates degradation of beta-catenin.
  • [MeSH-major] Genes, APC. Intestinal Neoplasms / etiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Adenoma / etiology. Adenoma / genetics. Aneuploidy. Animals. Cell Nucleus / metabolism. Chromosomal Instability. Humans. Ki-67 Antigen / analysis. Mice. Mice, Inbred C57BL. Signal Transduction. beta Catenin / metabolism

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  • (PMID = 18391979.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 079643; United Kingdom / Cancer Research UK / / A8449; United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Mki67 protein, mouse; 0 / RASSF1 protein, mouse; 0 / Tumor Suppressor Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ EMS52273; NLM/ PMC3706934
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4. 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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15. 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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16. Kim Y, Sills RC, Houle CD: Overview of the molecular biology of hepatocellular neoplasms and hepatoblastomas of the mouse liver. Toxicol Pathol; 2005;33(1):175-80
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  • In the majority of the hepatoblastomas examined by immunohistochemical methods, both nuclear and cytoplasmic localization of P-catenin protein were detected, whereas in hepatocellular adenomas and carcinomas and normal liver only membrane staining was observed.
  • Genomic DNA was isolated from paraffin sections of each liver tumor.
  • Hepatocellular adenomas and carcinomas from treated mice had mutations in exon 2 of the B-catenin gene which ranged from 32-43%, while 10% P-catenin mutations were detected in spontaneous neoplasms.
  • Cyclin D1 may provide an advantage during tumor progression of hepatocellular neoplasms and hepatoblastomas.
  • The review will also focus on other genes which are important in mouse and human liver tumors.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Carcinoma, Hepatocellular / genetics. Liver Neoplasms / genetics. Liver Neoplasms, Experimental / genetics. Molecular Biology
  • [MeSH-minor] Animals. Cytoskeletal Proteins / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Mice. Mice, Inbred Strains. Mutation. Trans-Activators / metabolism. Wnt Proteins. beta Catenin

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  • (PMID = 15805069.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Trans-Activators; 0 / Wnt Proteins; 0 / beta Catenin
  • [Number-of-references] 73
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17. Shen HC, Adem A, Ylaya K, Wilson A, He M, Lorang D, Hewitt SM, Pechhold K, Harlan DM, Lubensky IA, Schmidt LS, Linehan WM, Libutti SK: Deciphering von Hippel-Lindau (VHL/Vhl)-associated pancreatic manifestations by inactivating Vhl in specific pancreatic cell populations. PLoS One; 2009;4(4):e4897
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  • [Title] Deciphering von Hippel-Lindau (VHL/Vhl)-associated pancreatic manifestations by inactivating Vhl in specific pancreatic cell populations.
  • The von Hippel-Lindau (VHL) syndrome is a pleomorphic familial disease characterized by the development of highly vascularized tumors, such as hemangioblastomas of the central nervous system, pheochromocytomas, renal cell carcinomas, cysts and neuroendocrine tumors of the pancreas.
  • Up to 75% of VHL patients are affected by VHL-associated pancreatic lesions; however, very few reports in the published literature have described the cellular origins and biological roles of VHL in the pancreas.
  • Since homozygous loss of Vhl in mice resulted in embryonic lethality, this study aimed to characterize the functional significance of VHL in the pancreas by conditionally inactivating Vhl utilizing the Cre/LoxP system.
  • Specifically, Vhl was inactivated in different pancreatic cell populations distinguished by their roles during embryonic organ development and their endocrine lineage commitment.
  • With Cre recombinase expression directed by a glucagon promoter in alpha-cells or an insulin promoter in beta-cells, we showed that deletion of Vhl is dispensable for normal functions of the endocrine pancreas.
  • In addition, deficiency of VHL protein (pVHL) in terminally differentiated alpha-cells or beta-cells is insufficient to induce pancreatic neuroendocrine tumorigenesis.
  • Most significantly, we presented the first mouse model of VHL-associated pancreatic disease in mice lacking pVHL utilizing Pdx1-Cre transgenic mice to inactivate Vhl in pancreatic progenitor cells.
  • The highly vascularized microcystic adenomas and hyperplastic islets that developed in Pdx1-Cre;Vhl f/f homozygous mice exhibited clinical features similar to VHL patients.
  • Establishment of three different, cell-specific Vhl knockouts in the pancreas have allowed us to provide evidence suggesting that VHL is functionally important for postnatal ductal and exocrine pancreas, and that VHL-associated pancreatic lesions are likely to originate from progenitor cells, not mature endocrine cells.
  • The novel model systems reported here will provide the basis for further functional and genetic studies to define molecular mechanisms involved in VHL-associated pancreatic diseases.

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  • (PMID = 19340311.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / PHS HHS / / HHSN 261200800001E; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Other-IDs] NLM/ PMC2660574
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18. Diehl D, Oesterle D, Elmlinger MW, Hoeflich A, Wolf E, Lahm H: IGF-II transgenic mice display increased aberrant colon crypt multiplicity and tumor volume after 1,2-dimethylhydrazine treatment. J Carcinog; 2006;5:24
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  • [Title] IGF-II transgenic mice display increased aberrant colon crypt multiplicity and tumor volume after 1,2-dimethylhydrazine treatment.
  • In colorectal cancer insulin-like growth factor II (IGF-II) is frequently overexpressed.
  • Aberrant crypt foci (ACF) served as markers of early lesions in the colonic mucosa, whereas adenomas and carcinomas characterized the endpoints of tumor development.
  • Nevertheless, adenomas and adenocarcinomas of the colon, present after 34 weeks in both genetic groups, were not found at different frequency.
  • Tumor volumes, however, were significantly higher in IGF-II transgenic mice and correlated with serum IGF-II levels.
  • Immunohistochemical staining for markers of proliferation and apoptosis revealed increased cell proliferation rates in tumors of IGF-II transgenic mice without significant affection of apoptosis.
  • Increased proliferation was accompanied by elevated localization of beta-catenin in the cytosol and cell nuclei and reduced appearance at the inner plasma membrane.
  • In conclusion, we provide evidence that IGF-II, via activation of the beta-catenin signaling cascade, promotes growth of ACF and tumors without affecting tumor numbers.

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  • (PMID = 17118177.001).
  • [ISSN] 1477-3163
  • [Journal-full-title] Journal of carcinogenesis
  • [ISO-abbreviation] J Carcinog
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1660565
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19. 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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20. 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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21. 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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22. 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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23. 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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24. Hanson PL, Aylwin SJ, Monson JP, Burrin JM: FSH secretion predominates in vivo and in vitro in patients with non-functioning pituitary adenomas. Eur J Endocrinol; 2005 Mar;152(3):363-70
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  • [Title] FSH secretion predominates in vivo and in vitro in patients with non-functioning pituitary adenomas.
  • OBJECTIVE: Non-functioning pituitary adenomas (NFPAs) are characterised by the lack of symptoms of hormone hypersecretory syndromes but in vitro studies have demonstrated that tumour cells may stain for gonadotrophins and/or their alpha- or beta-subunits.
  • In this study, we aimed to examine the pattern of secretion of LH and FSH from a series of pituitary adenomas cultured in vitro and where data were available to relate the results to pre-operative serum gonadotrophin levels.
  • Peritumorous 'normal' pituitary cell cultures from 20 additional pituitary tumour patients were used for comparison with the NFPA group.
  • Peritumorous 'normal' pituitary cells released LH and FSH in a reversed ratio (median LH:FSH ratio = 3.6:1, P < 0.01 compared with NFPAs).
  • By demonstrating that NFPAs cultured in vitro reflect the in vivo situation of preferential secretion of FSH, it may be possible in future to perform functional studies using this system to elucidate the cellular and molecular mechanisms involved in the development of an imbalance in gonadotroph cells preferentially overproducing FSH in NFPAs.

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  • (PMID = 15757852.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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25. Masi G, Lavezzo E, Iacobone M, Favia G, Palù G, Barzon L: Investigation of BRAF and CTNNB1 activating mutations in adrenocortical tumors. J Endocrinol Invest; 2009 Jul;32(7):597-600
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  • [Title] Investigation of BRAF and CTNNB1 activating mutations in adrenocortical tumors.
  • BACKGROUND: Activating mutations of the BRAF oncogene play a central role in the development of various cancer types, but their role in human adrenocortical tumors is unknown.
  • At variance, activating mutations of another oncogene, CTNNB1, which encodes beta-catenin, have been shown to be common events in both benign and malignant adrenocortical tumors.
  • AIM: To investigate the prevalence of BRAF and CTNNB1 activating mutations in sporadic adrenocortical tumors.
  • MATERIALS AND METHODS: Tissue samples from 15 adrenocortical carcinomas and 41 adrenocortical adenomas were investigated for the presence of BRAF and CTNNB1 activating mutations by PCR amplification and direct sequencing.
  • RESULTS: An advanced invasive non-functioning adrenocortical carcinoma carried a somatic heterozygous BRAF V600E mutation, while 4 functioning and 4 non-functioning adenomas and 3 functioning carcinomas carried different CTNNB1 activating mutations.
  • [MeSH-major] Adrenal Cortex Neoplasms. Cell Transformation, Neoplastic / genetics. Mutation. Proto-Oncogene Proteins B-raf / genetics. beta Catenin / genetics

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  • (PMID = 19498322.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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26. 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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27. Doviner V, Maly B, Kaplan V, Gingis-Velitski S, Ilan N, Vlodavsky I, Sherman Y: Spatial and temporal heparanase expression in colon mucosa throughout the adenoma-carcinoma sequence. Mod Pathol; 2006 Jun;19(6):878-88
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  • [Title] Spatial and temporal heparanase expression in colon mucosa throughout the adenoma-carcinoma sequence.
  • Heparanase is a mammalian endo-beta-D-glucuronidase that cleaves heparan sulfate side chains at a limited number of sites.
  • Such enzymatic activity is thought to participate in degradation and remodeling of the extracellular matrix and to facilitate cell invasion associated with tumor metastasis, angiogenesis and inflammation.
  • Traditionally, heparanase activity was well correlated with the metastatic potential of a large number of tumor-derived cell types.
  • More recently, heparanase upregulation has been documented in an increasing number of primary human tumors, correlating with poor postoperative survival and increased tumor vascularity.
  • Here, we employed anti-heparanase 733 polyclonal antibody that preferentially recognizes the 50 kDa active heparanase subunit over the 65 kDa proenzyme, as well as anti-heparanase 92.4 monoclonal antibody that recognizes both the latent and the active enzyme, to follow heparanase expression, processing and localization throughout the adenoma-carcinoma transition of the colon epithelium.
  • Normal (nondysplastic) mucosa of the large bowel near epithelial neoplasms, as well as areas of mild dysplasia in adenomas, exhibited a strong reactivity with antibody 733 that became even stronger in foci of moderate dysplasia.
  • Interestingly, although reactivity with antibody 733 was markedly reduced in severe dysplasia and in colorectal carcinoma, response to antibody 92.4 exhibited the opposite trend and staining intensities increased in parallel with tumor stage, the highest being in carcinoma cells.
  • Involvement of latent heparanase (detected by 92.4, but not by 733 antibody) in tumor progression was suggested by activation of the Akt/PKB signal transduction pathway upon heparanase overexpression or exogenous addition to HT29 human colon carcinoma cells.
  • These results suggest that heparanase expression is induced during colon carcinogenesis, and that its processing, conformation and localization are tightly regulated during the course of colon adenoma-carcinoma progression.
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Cell Line, Tumor / enzymology. Cell Line, Tumor / pathology. Disease Progression. Female. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques. Mice. Mice, SCID. Neoplasm Transplantation. Transfection

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  • (PMID = 16607375.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106456
  • [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 / Biomarkers, Tumor; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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28. 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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29. 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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30. 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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51. 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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52. 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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53. 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


54. Zamora V, Cabanne A, Salanova R, Bestani C, Domenichini E, Marmissolle F, Giacomi N, O'Connor J, Méndez G, Roca E, Buenos Aires and La Plata Argentina Argentum Working Group: Immunohistochemical expression of somatostatin receptors in digestive endocrine tumours. Dig Liver Dis; 2010 Mar;42(3):220-5
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  • [Title] Immunohistochemical expression of somatostatin receptors in digestive endocrine tumours.
  • INTRODUCTION: Somatostatin receptors are expressed in a large number of human tumours.
  • The somatostatin receptors types 1-5 expression in a series including 100 gastro-entero-pancreatic endocrine tumours were analysed.
  • METHODS: From a prospectively built database of patients with gastro-entero-pancreatic endocrine tumours referred from three institutions, 100 cases with clinical and pathological data were selected.
  • RESULTS: Of the 100 cases, 67 were gastrointestinal tumours, 25 pancreatic and 8 liver metastasis of unknown origin.
  • Thirty-one of them were functioning tumours: 2 insulinomas, 5 gastrinomas, 1 glucagonoma and 23 carcinoids.
  • Somatostatin receptors expression was observed in 94 tumours.
  • The six negative cases were all non-functioning tumours.
  • Somatostatin receptors expression was less frequent in pancreatic than in gastrointestinal tumours.
  • CONCLUSIONS: Immunohistochemistry revealed that somatostatin receptors were highly expressed in both primary and metastatic gastro-entero-pancreatic endocrine tumours with heterogeneous staining distribution.
  • It proved to be a reliable technique even in small tumour samples.

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  • [Copyright] 2009 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
  • [CommentIn] Dig Liver Dis. 2010 Mar;42(3):173-4 [20117969.001]
  • (PMID = 19819769.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Somatostatin
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55. Song MY, Jeong GS, Kwon KB, Ka SO, Jang HY, Park JW, Kim YC, Park BH: Sulfuretin protects against cytokine-induced beta-cell damage and prevents streptozotocin-induced diabetes. Exp Mol Med; 2010 Sep 30;42(9):628-38
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  • [Title] Sulfuretin protects against cytokine-induced beta-cell damage and prevents streptozotocin-induced diabetes.
  • NF-kappaB activation has been implicated as a key signaling mechanism for pancreatic beta-cell damage.
  • Therefore, we isolated sulfuretin from Rhus verniciflua and evaluated if sulfuretin could inhibit cytokine- or streptozotocin-induced beta-cell damage.
  • Rat insulinoma RINm5F cells and isolated rat islets were treated with IL-1 beta and IFN-gamma to induce cytotoxicity.
  • Incubation of cells and islets with sulfuretin resulted in a significant reduction of cytokine-induced NF-gamma B activation and its downstream events, iNOS expression, and nitric oxide production.
  • The cytotoxic effects of cytokines were completely abolished when cells or islets were pretreated with sulfuretin.
  • The protective effect of sulfuretin was further demonstrated by normal insulin secretion of cytokine-treated islets in response to glucose.
  • Collectively, these results indicate that sulfuretin may have therapeutic value in preventing beta-cell damage.
  • [MeSH-major] Benzofurans / pharmacology. Cytokines / adverse effects. Diabetes Mellitus, Experimental / prevention & control. Insulin-Secreting Cells / drug effects. NF-kappa B / metabolism
  • [MeSH-minor] Animals. Cell Line. Flavonoids / pharmacology. Flavonoids / therapeutic use. Hypoglycemic Agents / pharmacology. Hypoglycemic Agents / therapeutic use. Male. Mice. Mice, Inbred ICR. Rats. Rats, Sprague-Dawley. Rhus / chemistry

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  • (PMID = 20661005.001).
  • [ISSN] 2092-6413
  • [Journal-full-title] Experimental & molecular medicine
  • [ISO-abbreviation] Exp. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Benzofurans; 0 / Cytokines; 0 / Flavonoids; 0 / Hypoglycemic Agents; 0 / NF-kappa B; M6410VY6MI / sulfuretin
  • [Other-IDs] NLM/ PMC2947020
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56. Philbrook C, Fritz E, Weiher H: Expressional and functional studies of Wolframin, the gene function deficient in Wolfram syndrome, in mice and patient cells. Exp Gerontol; 2005 Aug-Sep;40(8-9):671-8
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  • [Title] Expressional and functional studies of Wolframin, the gene function deficient in Wolfram syndrome, in mice and patient cells.
  • Wolfram Syndrome is an autosomal recessive degenerative disorder of the neuroendocrine system.
  • This protein was preliminarily localised in the endoplasmatic reticulum (ER) in cells of mice and rats.
  • Mice lacking the WFS1 gene display degeneration of pancreatic beta-cells following induction of ER stress.
  • Expression was detected in both pancreatic beta-cells and the limbic system of mice.
  • Using the rat insulinoma cell line RIN 5AH and fractionated mouse brain tissue, we confirmed wolframin localisation to the endoplasmic reticulum.
  • However, cell proliferation was indistinguishable from non-mutated cells.
  • In contrast to data obtained on murine pancreatic islets, we found no increased apoptosis following induction of ER stress but rather by staurosporine treatment in the absence of WFS1 function.
  • This indicates a new role of WFS1 deficiency in programmed cell death.
  • [MeSH-major] Endoplasmic Reticulum / metabolism. Insulin-Secreting Cells / metabolism. Membrane Proteins / genetics. Wolfram Syndrome / genetics
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western / methods. Brain / metabolism. Cell Line. Cells, Cultured. Extracellular Matrix Proteins / metabolism. Fibroblasts / metabolism. Fluorescent Antibody Technique / methods. Gene Expression Profiling. Humans. Mice. Oligonucleotide Array Sequence Analysis. Phosphoric Diester Hydrolases / metabolism. Pyrophosphatases / metabolism. Rats


57. Gianani R, Eisenbarth GS: The stages of type 1A diabetes: 2005. Immunol Rev; 2005 Apr;204:232-49
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  • Type 1A diabetes is a chronic autoimmune disease usually preceded by a long prodrome during which autoantibodies to islet autoantigens are present.
  • These antibodies are directed to a variety of antigens, but the best characterized are glutamic acid decarboxylase-65, insulinoma-associated antigen-2, and insulin.
  • We hypothesize that the natural history of type 1A diabetes can be represented by several stages, starting from genetic susceptibility and ending in complete beta-cell destruction and overt diabetes.
  • In both humans and animal models, the major determinants of the disease are genes within the major histocompatibility complex.
  • The next best-characterized susceptibility locus is the insulin gene, the variable nucleotide tandem repeat locus.
  • This gene affects the expression of insulin in the thymus and thus may play a role in the modulation of tolerance to this molecule.
  • In this review, we provide evidence that insulin has a fundamental role in anti-islet autoimmunity.
  • [MeSH-minor] Animals. Autoantibodies / immunology. Autoantigens / immunology. Humans. Insulin / metabolism. Insulin / secretion. Islets of Langerhans / immunology. Islets of Langerhans / metabolism. Islets of Langerhans / pathology

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  • (PMID = 15790362.001).
  • [ISSN] 0105-2896
  • [Journal-full-title] Immunological reviews
  • [ISO-abbreviation] Immunol. Rev.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI15416; United States / NIAID NIH HHS / AI / AI39213; United States / NIAID NIH HHS / AI / AI50864; United States / NIDDK NIH HHS / DK / DK32083; United States / NIDDK NIH HHS / DK / DK32493; United States / NIDDK NIH HHS / DK / DK55969; United States / NIDDK NIH HHS / DK / DK62718; United States / NCRR NIH HHS / RR / M01 RR00051; United States / NCRR NIH HHS / RR / M01 RR00069
  • [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] Denmark
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Autoantigens; 0 / Insulin
  • [Number-of-references] 158
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58. Nakagawa A, Ueno K, Ito M, Okamoto S, Uehara K, Ito H, Mishina S, Kinoshita E, Nojima T, Takahashi H, Ikawa H, Takashima S, Nishizawa M, Nakano S, Kigoshi T, Nakabayashi H, Uchida K: Insulin responses to selective arterial calcium infusion under hyperinsulinemic euglycemic glucose clamps: case studies in adult nesidioblastosis and childhood insulinoma. Endocr J; 2007 Feb;54(1):27-33
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  • [Title] Insulin responses to selective arterial calcium infusion under hyperinsulinemic euglycemic glucose clamps: case studies in adult nesidioblastosis and childhood insulinoma.
  • Selective arterial calcium stimulation and hepatic venous sampling (ASVS) for insulin secretion is used as a diagnostic procedure in patients with insulinomas or adult nesidioblastosis.
  • A 9-year-old girl with an insulinoma that showed atypical hypovascularity on imaging examinations had ASVS tests under a glucose clamp for safety.
  • Hyperinsulinemic (approximately 100 microU/ml) euglycemic (approximately 90 mg/dl) clamps were achieved by an artificial endocrine pancreas.
  • The insulin analogue lispro was utilized for clamps and endogenous insulin was measured with an assay that does not cross-react with the analogue.
  • Diagnostically significant responses (more than twofold) of insulin secretion were observed under hyperinsulinemic clamps in both cases.
  • [MeSH-major] Calcium / administration & dosage. Glucose Clamp Technique / methods. Hyperinsulinism / chemically induced. Insulin / secretion. Insulinoma / blood. Nesidioblastosis / blood. Pancreatic Neoplasms / blood

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  • (PMID = 17053293.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; SY7Q814VUP / Calcium
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59. Tomita T, Masuzaki H, Noguchi M, Iwakura H, Fujikura J, Tanaka T, Ebihara K, Kawamura J, Komoto I, Kawaguchi Y, Fujimoto K, Doi R, Shimada Y, Hosoda K, Imamura M, Nakao K: GPR40 gene expression in human pancreas and insulinoma. Biochem Biophys Res Commun; 2005 Dec 30;338(4):1788-90
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  • [Title] GPR40 gene expression in human pancreas and insulinoma.
  • To assess gene expression of a membrane-bound G-protein-coupled fatty acid receptor, GPR40, in the human pancreas and islet cell tumors obtained at surgery were analyzed.
  • The mRNA level of the GPR40 gene in isolated pancreatic islets was approximately 20-fold higher than that in the pancreas, and the level was comparable to or rather higher than that of the sulfonylurea receptor 1 gene, which is known to be expressed abundantly in human pancreatic beta cells.
  • A large amount of GPR40 mRNA was detected in tissue extracts from two cases of insulinoma, whereas the expression was undetectable in glucagonoma or gastrinoma.
  • The present study demonstrates that GPR40 mRNA is expressed predominantly in pancreatic islets in humans and that GPR40 mRNA is expressed solely in human insulinoma among islet cell tumors.
  • These results indicate that GPR40 is probably expressed in pancreatic beta cells in the human pancreas.
  • [MeSH-major] Insulinoma / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Receptors, G-Protein-Coupled / biosynthesis

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  • (PMID = 16289108.001).
  • [ISSN] 0006-291X
  • [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 / FFAR1 protein, human; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled
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60. Yamaguchi C, Wanibuchi H, Kakehashi A, Tanaka R, Fukushima S: Chemopreventive effects of a serratane-type triterpenoid, 3alpha-methoxyserrat-14-en-21beta-ol (PJ-1), against rat lung carcinogenesis. Food Chem Toxicol; 2008 Jun;46(6):1882-8
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  • [Title] Chemopreventive effects of a serratane-type triterpenoid, 3alpha-methoxyserrat-14-en-21beta-ol (PJ-1), against rat lung carcinogenesis.
  • Cancer-chemopreventive effects of a serratane-type triterpenoid from the bark of Picea jezoensis, 3alpha-methoxyserrat-14-en-21beta-ol (PJ-1), were here examined in a revised rat multi-organ carcinogenesis (DMBDD) model.
  • At the termination at week 30, significant decrease of adenomas (P<0.01) and total tumors (P<0.01) and a trend for reduction of adenocarcinoma multiplicity in the lung were observed, but without any modulating influence in other major organs.
  • The cell proliferation indices in the lungs tended to be decreased in the PJ-1 administered groups, with apparent induction of CYP2B1/2 mRNA expression to recover the values observed in non-initiated controls.
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Cytochrome P-450 Enzyme System / biosynthesis. Immunohistochemistry. Indicators and Reagents. Isoenzymes / biosynthesis. Lung / pathology. Male. Proliferating Cell Nuclear Antigen / metabolism. RNA / biosynthesis. RNA / isolation & purification. RNA, Messenger / biosynthesis. Rats. Rats, Inbred F344. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18343553.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 3-alpha-methoxyserrat-14-en-21-beta-yl formate; 0 / Anticarcinogenic Agents; 0 / Carcinogens; 0 / Indicators and Reagents; 0 / Isoenzymes; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Messenger; 0 / Triterpenes; 63231-63-0 / RNA; 9035-51-2 / Cytochrome P-450 Enzyme System
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61. Vitale G, Caraglia M, van Koetsveld PM, Maroni P, Marra M, Colao A, Lamberts SW, Cavagnini F, Hofland LJ: Potential role of type I interferons in the treatment of pituitary adenomas. Rev Endocr Metab Disord; 2009 Jun;10(2):125-33
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  • [Title] Potential role of type I interferons in the treatment of pituitary adenomas.
  • Treatment with type I IFNs of patients affected by chronic viral hepatitis, multiple sclerosis and tumors influences the secretion of pituitary hormones.
  • This article reviews the current knowledge about the effects of IFN-alpha and IFN-beta on hypothalamic-pituitary function and describes the potential role of type I IFNs in the treatment of pituitary adenomas.
  • [MeSH-minor] Humans. Hypothalamo-Hypophyseal System / drug effects. Pituitary-Adrenal System / drug effects. Receptor, Interferon alpha-beta / metabolism

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  • (PMID = 18604644.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon Type I; 156986-95-7 / Receptor, Interferon alpha-beta
  • [Number-of-references] 72
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62. Chen X, Halberg RB, Burch RP, Dove WF: Intestinal adenomagenesis involves core molecular signatures of the epithelial-mesenchymal transition. J Mol Histol; 2008 Jun;39(3):283-94
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  • Microarray data demonstrated elevation of vimentin, a mesenchymal marker, in intestinal adenomas from Apc Min/+ (Min) mice.
  • Elevated vimentin RNA expression and protein production were detected within neoplastic cells in murine intestinal adenomas.
  • Similarly, vimentin protein was detected in both adenomas and invasive adenocarcinomas of the human colon, but not in the normal colonic epithelium or in hyperplastic polyps.
  • Canonical E-cadherin suppressors, such as Snail, were not elevated in the same tumor.
  • Elevated vimentin expression in the adenoma was not correlated with persistent Ras signaling, but was strongly correlated with reduced proliferation indices, active Wnt signaling, and TGF-beta signaling, as demonstrated by its dependence on Smad3.
  • These unexpected observations are interpreted as reflecting the involvement of a core of the EMT system during the tissue remodeling of early tumorigenesis.

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  • (PMID = 18327651.001).
  • [ISSN] 1567-2379
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA084227-05; United States / NCI NIH HHS / CA / U01 CA084227; United States / NCI NIH HHS / CA / R37 CA063677; United States / NCI NIH HHS / CA / R37 CA063677-14; United States / NCI NIH HHS / CA / R37-CA63677; United States / NCI NIH HHS / CA / U01-CA-84227; United States / NCI NIH HHS / CA / U01 CA084227-05; United States / NCI NIH HHS / CA / CA063677-14
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cadherins; 0 / Fibronectins; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; 0 / Vimentin; 0 / Wnt Proteins; 0 / snail family transcription factors; EC 3.6.5.2 / ras Proteins; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS59539; NLM/ PMC2544376
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63. Størling J, Allaman-Pillet N, Karlsen AE, Billestrup N, Bonny C, Mandrup-Poulsen T: Antitumorigenic effect of proteasome inhibitors on insulinoma cells. Endocrinology; 2005 Apr;146(4):1718-26
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  • [Title] Antitumorigenic effect of proteasome inhibitors on insulinoma cells.
  • Malignant insulinoma is a critical cancer form with a poor prognosis.
  • Induction of cell death in tumor cells by proteasome inhibitors is emerging as a potential strategy in cancer therapy.
  • Here we investigated whether inhibition of the proteasome has an antitumorigenic potential in insulinoma cells.
  • Exposure of mouse betaTC3 insulinoma cells to the proteasome inhibitor N-Acetyl-Leu-Leu-Nle-CHO (ALLN) reduced cell viability, activated caspase-3, induced apoptosis, and suppressed insulin release.
  • Treatment with ALLN also resulted in phosphorylation of c-jun N-terminal kinase (JNK) and an increase in in vitro phosphorylation of c-jun.
  • In insulinoma cells with impaired JNK signaling, ALLN-induced apoptosis was significantly suppressed.
  • Another proteasome inhibitor, lactacystin, also stimulated JNK activation, caused activation of caspase-3, suppressed cell viability, and induced apoptosis in betaTC3 and rat INS-1E cells.
  • Both ALLN and lactacystin caused a marked decrease in the cellular amount of the JNK scaffold protein JNK-interacting protein 1/islet-brain-1.
  • In primary pancreatic rat islet cells, proteasome inhibition reduced insulin secretion but had no impact on cell viability and even partially protected against the toxic effect of proinflammatory cytokines.
  • Our findings demonstrate that proteasome inhibitors possess antitumorigenic and antiinsulinogenic effects on insulinoma cells.
  • [MeSH-major] Acetylcysteine / analogs & derivatives. Antineoplastic Agents / pharmacology. Cysteine Proteinase Inhibitors / pharmacology. Insulinoma / drug therapy. Pancreatic Neoplasms / drug therapy. Proteasome Inhibitors
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / antagonists & inhibitors. Animals. Apoptosis / drug effects. Binding Sites. Cell Line, Tumor. JNK Mitogen-Activated Protein Kinases / metabolism. Leupeptins / pharmacology. Mice. Rats. Signal Transduction / drug effects. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15618349.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / Cysteine Proteinase Inhibitors; 0 / Leupeptins; 0 / Mapk8ip protein, mouse; 0 / Proteasome Inhibitors; 0 / Tumor Suppressor Protein p53; 110044-82-1 / acetylleucyl-leucyl-norleucinal; 133343-34-7 / lactacystin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; WYQ7N0BPYC / Acetylcysteine
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64. Tadjine M, Lampron A, Ouadi L, Bourdeau I: Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas. Clin Endocrinol (Oxf); 2008 Feb;68(2):264-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas.
  • OBJECTIVE: Molecular alterations remain largely unknown in most sporadic adrenocortical tumours and hyperplasias.
  • In our previous work, we demonstrated the differential expression of several Wnt/beta-catenin signalling-related genes implicated in ACTH-independent macronodular adrenal hyperplasias (AIMAH).
  • To better understand the role of Wnt/beta-catenin signalling in adrenocortical tumours, we performed mutational analysis of the beta-catenin gene.
  • METHODS: We studied 53 human adrenocortical samples (33 adenomas, 4 carcinomas, 13 AIMAH, 3 ACTH-dependent adrenal hyperplasias) and the human adrenocortical cancer cell line NCI-H295R.
  • All samples were screened for somatic mutations in exons 3 and 5 of the beta-catenin gene.
  • Eleven and six samples were analysed for beta-catenin protein expression by Western blotting and immunohistochemistry, respectively.
  • Genetic alterations were found in 5 (15%) out of 33 adenomas: three cortisol-secreting adenomas, one aldosterone-secreting adenoma and one nonfunctional adenoma.
  • The remaining three tumours contained deletions of 6, 55 and 271 bp.
  • H295R cells carry an activating S45P mutation.
  • Western blot analysis of samples with 55- and 271-bp deletions showed an additional shorter and more intense band representing an accumulation of the mutated form of beta-catenin protein.
  • In addition, cytoplasmic and/or nuclear accumulation of beta-catenin was observed in mutated adenomas by immunohistochemistry.
  • CONCLUSIONS: Activating mutations of exon 3 of the beta-catenin gene are frequent in adrenocortical adenomas, and further characterization of the Wnt/beta-catenin signalling pathway should lead to a better understanding of adrenal tumourigenesis.
  • [MeSH-major] Adrenocortical Adenoma / genetics. Adrenocortical Adenoma / metabolism. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 17854394.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin
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65. Xue HD, Liu W, Sun H, Merges R, Wang X, Zhang XN, Wang Y, Zhao WM, Chen JH, Jin ZY: Spectrum of functioning islet cell tumor on multislice computed tomography: experience on 70 patients. Chin Med Sci J; 2008 Mar;23(1):1-9
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  • [Title] Spectrum of functioning islet cell tumor on multislice computed tomography: experience on 70 patients.
  • OBJECTIVE: To review experience in preoperative detection of islet cell tumors using multislice computed tomography (MSCT) and summarize various imaging features of functioning islet cell tumors on enhanced MSCT.
  • METHODS: Seventy patients with clinical or pathological diagnosis of functioning pancreatic islet cell tumor between October 2003 and February 2007 were included in this retrospective study.
  • Surgery and pathology reports were used to confirm the diagnosis, localization, and size of tumors.
  • RESULTS: Totally, 73 functioning islet cell tumors including 65 benign insulinomas, 2 benign glucagonomas, 3 malignant insulinomas, and 3 malignant glucagonomas were pathologically diagnosed.
  • Tumors in only two cases were not found by MSCT.
  • In 67 benign lesions, 32 showed typical enhancement style, 21 showed prolonged enhancement in portal venous phase, 4 showed delayed enhancement, 4 had iso-dense enhancement with normal pancreatic parenchyma, 2 had no enhancement at all in arterial phase and portal venous phase, and 4 had inhomogeneous enhancement with necrosis or cyst-formation.
  • Patchy or spotty calcifications were found in 3 of the 67 tumors.
  • In 6 malignant islet cell tumors, vessel invasion (2/6) and bowel invasion (1/6) were seen.
  • CONCLUSIONS: Pancreatic islet cell tumor may display a wide spectrum of presentations in MSCT.
  • Tumors with unusual appearances often present as diagnostic challenges.
  • Non-contrast and post-contrast multiphase scans are recommended for the localization of functioning islet cell tumors.

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  • (PMID = 18437902.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
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66. Pilz JB, Portmann D, Bayerl C, Wildi SM: Insulinoma. Clin Gastroenterol Hepatol; 2008 Dec;6(12):e43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Insulinoma.
  • [MeSH-major] Insulinoma / diagnosis. Insulinoma / pathology

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  • (PMID = 19081524.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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67. Liu F, Qiu J, Zhang CM, Ji CB, Guo XR: [Resistin inhibits rat insulinoma cell RINm5F proliferation]. Zhongguo Dang Dai Er Ke Za Zhi; 2010 Jan;12(1):43-6
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  • [Title] [Resistin inhibits rat insulinoma cell RINm5F proliferation].
  • This study aimed to investigate the effect of resistin on insulinoma cell proliferation.
  • METHODS: pcDNA3.1-resistin was transfected into rat insulinoma cells RINm5F.
  • Cell proliferation was assessed by the MTT assay.
  • RESULTS: The over-expressed resistin inhibited the RINm5F cell proliferation (p<0.05).
  • CONCLUSIONS: Resistin impairs the rat insulinoma cell RINm5F proliferation.
  • [MeSH-major] Insulinoma / pathology. Pancreatic Neoplasms / pathology. Resistin / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. Rats. Suppressor of Cytokine Signaling Proteins / genetics. Transfection

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  • (PMID = 20113634.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Resistin; 0 / Retn protein, rat; 0 / Socs3 protein, rat; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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68. Sabates-Bellver J, Van der Flier LG, de Palo M, Cattaneo E, Maake C, Rehrauer H, Laczko E, Kurowski MA, Bujnicki JM, Menigatti M, Luz J, Ranalli TV, Gomes V, Pastorelli A, Faggiani R, Anti M, Jiricny J, Clevers H, Marra G: Transcriptome profile of human colorectal adenomas. Mol Cancer Res; 2007 Dec;5(12):1263-75
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  • [Title] Transcriptome profile of human colorectal adenomas.
  • Colorectal cancers are believed to arise predominantly from adenomas.
  • To characterize the molecular processes underlying the transformation of normal colonic epithelium, we compared the transcriptomes of 32 prospectively collected adenomas with those of normal mucosa from the same individuals.
  • Important differences emerged not only between the expression profiles of normal and adenomatous tissues but also between those of small and large adenomas.
  • In normal mucosa, KIAA1199 expression was confined to cells in the lower portion of intestinal crypts, where Wnt signaling is physiologically active, but it was markedly increased in all adenomas, where it was expressed in most of the epithelial cells, and in colon cancer cell lines, it was markedly reduced by inactivation of the beta-catenin/T-cell factor(s) transcription complex, the pivotal mediator of Wnt signaling.
  • Our transcriptomic profiles of normal colonic mucosa and colorectal adenomas shed new light on the early stages of colorectal tumorigenesis and identified KIAA1199 as a novel target of the Wnt signaling pathway and a putative marker of colorectal adenomatous transformation.
  • [MeSH-major] Adenoma / genetics. Biomarkers, Tumor / genetics. Colorectal Neoplasms / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / genetics. Female. Genetic Markers. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Phylogeny. RNA, Messenger / metabolism. Transcription, Genetic

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  • (PMID = 18171984.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / RNA, Messenger
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69. Toniato A, Foletto M: Laparoscopic versus open approach for solitary insulinoma. Surg Endosc; 2008 Jan;22(1):258
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  • [Title] Laparoscopic versus open approach for solitary insulinoma.
  • [MeSH-major] Insulinoma / surgery. Laparoscopy / methods. Laparotomy / methods
  • [MeSH-minor] Humans. Pancreatectomy / methods. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery. Sensitivity and Specificity. Treatment Outcome

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  • [CommentOn] Surg Endosc. 2007 Jan;21(1):103-8 [17008952.001]
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  • (PMID = 17943382.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Comment; Comparative Study; Letter
  • [Publication-country] Germany
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70. O'Sullivan SS, Redmond J: Insulinoma presenting as refractory late-onset epilepsy. Epilepsia; 2005 Oct;46(10):1690-1
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  • [Title] Insulinoma presenting as refractory late-onset epilepsy.
  • [MeSH-major] Epilepsy / diagnosis. Insulinoma / diagnosis. Pancreatic Neoplasms / diagnosis


71. Heni M, Schott S, Horger M, Dudziak K, Thamer C, Häring HU, Fritsche A, Müssig K: [A rare cause of hypoglycaemia in a patient with type 2 diabetes]. Dtsch Med Wochenschr; 2009;134 Suppl Falldatenbank:F2
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  • BACKGROUND: Insulinomas are rare neuroendocrine tumours with an incidence of four cases per million a year.
  • Only few cases of insulinoma in patients with preexisting diabetes mellitus have been reported.
  • 72-hour fast revealed hypoglycaemia in the presence of inadequately high C-peptide and insulin levels.
  • Magnetic resonance imaging and selective arterial calcium stimulation test confirmed a mass in the body of the pancreas.
  • The tumor was removed surgically.
  • Pathological examination demonstrated a benign insulinoma.
  • CONCLUSION: Clinicians should be alert to insulinoma as a, though rare, differential diagnosis of hypoglycaemia in diabetes, in particular in patients with recurrent, otherwise unexplained hypoglycaemia.
  • [MeSH-major] Diabetes Mellitus, Type 2 / complications. Hypoglycemia / etiology. Insulin / secretion. Insulinoma / complications. Pancreatic Neoplasms / complications


72. Tomita H, Yamada Y, Oyama T, Hata K, Hirose Y, Hara A, Kunisada T, Sugiyama Y, Adachi Y, Linhart H, Mori H: Development of gastric tumors in Apc(Min/+) mice by the activation of the beta-catenin/Tcf signaling pathway. Cancer Res; 2007 May 1;67(9):4079-87
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  • [Title] Development of gastric tumors in Apc(Min/+) mice by the activation of the beta-catenin/Tcf signaling pathway.
  • To examine the role of the Apc/beta-catenin signaling pathway in the development of gastric cancers, we investigated the gastric mucosa of the Apc(Min/+) mouse, which is a murine model for familial adenomatous polyposis, carrying a germ-line mutation at codon 850 of Apc.
  • We found that aged Apc(Min/+) mice spontaneously develop multiple tumors in the stomach, which are accompanied by loss of heterozygosity of Apc.
  • Such tumors consisted of adenomatous glands with strong nuclear accumulation of beta-catenin.
  • Even a single adenomatous gland already showed nuclear accumulation of beta-catenin, suggesting that Apc/beta-catenin pathway is an initiating event in gastric tumorigenesis in Apc(Min/+) mice.
  • Myc and cyclin D1 expressions, which are transcriptional targets of beta-catenin/Tcf, increased in the adenomatous lesions.
  • Furthermore, beta-catenin/Tcf reporter transgenic mice with Apc(Min) allele showed higher levels of the transcriptional activity of beta-catenin/Tcf in the gastric tumors.
  • We also treated Apc(Min/+) and wild-type mice with N-methyl-N-nitrosourea (MNU), an alkylating agent that induces adenomas and adenocarcinomas in the stomach.
  • Consequently, MNU-treated Apc(Min/+) mice significantly enhanced the tumor development in comparison with Apc(Min/+) mice or MNU-treated wild-type mice.
  • Several gastric tumors in MNU-treated Apc(Min/+) mice showed invasion into the submucosal layer.
  • These results indicate that the Apc/beta-catenin pathway may play an important role in at least subset of gastric carcinomas.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Stomach Neoplasms / genetics. Stomach Neoplasms / metabolism. T Cell Transcription Factor 1 / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Animals. Cell Nucleus / metabolism. Female. Gene Expression. Genes, APC. Loss of Heterozygosity. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Invasiveness. Signal Transduction. Transcription, Genetic


73. Haas S, Merkelbach-Bruse S, Justenhoven C, Brauch H, Fischer HP: Expression of xenobiotic and steroid hormone metabolizing enzymes in hepatocellular tumors of the non-cirrhotic liver. Pathol Res Pract; 2009;205(10):716-25
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  • [Title] Expression of xenobiotic and steroid hormone metabolizing enzymes in hepatocellular tumors of the non-cirrhotic liver.
  • Hepatocellular adenomas (HCA) and some hepatocellular carcinomas (HCC) arise in the non-cirrhotic liver.
  • Although the liver is involved in the metabolism of a huge number of exogenous and endogenous substances, little is known about the role of metabolic enzymes in the development of liver tumors in the absence of cirrhosis.
  • Therefore, reduced expression of GST alpha and CYP3A4 may indicate specific metabolic defects in the tumor tissue characterizing subgroups of HCA and HCC.
  • [MeSH-major] Adenoma, Liver Cell / enzymology. Carcinoma, Hepatocellular / enzymology. Cytochrome P-450 Enzyme System / biosynthesis. Glutathione Transferase / biosynthesis. Liver Neoplasms / enzymology
  • [MeSH-minor] Adolescent. Biomarkers, Tumor / analysis. Female. Gonadal Steroid Hormones / metabolism. Humans. Immunohistochemistry. Male. Mutation. Polymerase Chain Reaction. Xenobiotics / metabolism. beta Catenin / genetics

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  • (PMID = 19596526.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Gonadal Steroid Hormones; 0 / Xenobiotics; 0 / beta Catenin; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 2.5.1.18 / Glutathione Transferase
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74. Sachdeva MM, Claiborn KC, Khoo C, Yang J, Groff DN, Mirmira RG, Stoffers DA: Pdx1 (MODY4) regulates pancreatic beta cell susceptibility to ER stress. Proc Natl Acad Sci U S A; 2009 Nov 10;106(45):19090-5
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  • [Title] Pdx1 (MODY4) regulates pancreatic beta cell susceptibility to ER stress.
  • Type 2 diabetes mellitus (T2DM) results from pancreatic beta cell failure in the setting of insulin resistance.
  • Heterozygous mutations in the gene encoding the beta cell transcription factor pancreatic duodenal homeobox 1 (Pdx1) are associated with both T2DM and maturity onset diabetes of the young (MODY4), and low levels of Pdx1 accompany beta cell dysfunction in experimental models of glucotoxicity and diabetes.
  • Here, we find that Pdx1 is required for compensatory beta cell mass expansion in response to diet-induced insulin resistance through its roles in promoting beta cell survival and compensatory hypertrophy.
  • Pdx1-deficient beta cells show evidence of endoplasmic reticulum (ER) stress both in the complex metabolic milieu of high-fat feeding as well as in the setting of acutely reduced Pdx1 expression in the Min6 mouse insulinoma cell line.
  • Further, Pdx1 deficiency enhances beta cell susceptibility to ER stress-associated apoptosis.
  • These findings suggest that Pdx1 deficiency leads to a failure of beta cell compensation for insulin resistance at least in part by impairing critical functions of the ER.

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  • (PMID = 19855005.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK49210; United States / NIDDK NIH HHS / DK / R01 DK068157; United States / NIDDK NIH HHS / DK / R01 DK060581; United States / NIDDK NIH HHS / DK / P30 DK050306; United States / NIGMS NIH HHS / GM / T32 GM008216; United States / NIGMS NIH HHS / GM / T32-GM08216; United States / NIDDK NIH HHS / DK / P01 DK049210; United States / NIDDK NIH HHS / DK / P30-DK050306; United States / NIDDK NIH HHS / DK / DK 19525; United States / NIDDK NIH HHS / DK / P30 DK019525; United States / NIDDK NIH HHS / DK / R01 DK60581
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein
  • [Other-IDs] NLM/ PMC2776433
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75. Tamarina NA, Kuznetsov A, Philipson LH: Reversible translocation of EYFP-tagged STIM1 is coupled to calcium influx in insulin secreting beta-cells. Cell Calcium; 2008 Dec;44(6):533-44
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  • [Title] Reversible translocation of EYFP-tagged STIM1 is coupled to calcium influx in insulin secreting beta-cells.
  • Calcium (Ca(2+)) signaling regulates insulin secretion in pancreatic beta-cells.
  • Here we studied the translocation of EYFP-STIM1 in response to ER calcium depletion in mouse insulinoma MIN6 cells by fluorescent microscopy.
  • While in resting cells EYFP-STIM1 is co-localized with an ER marker, in thapsigargin (Tg)-stimulated cells it occupied highly defined areas of the peri-PM space in punctae adjacent to, but not entirely coincident with the ER.
  • Use of the SOCE blocker in MIN6 cells, 2-aminoethoxy diphenylborate (2-APB), prevented store depletion-dependent translocation of EYFP-STIM1 to the PM in a concentration-dependent (3.75-100muM) and reversible manner.
  • We conclude from this data that in these cells EYFP-STIM1 is delivered to a peri-PM location from the ER upon store depletion and this trafficking is reversibly blocked by 2-APB.
  • [MeSH-major] Bacterial Proteins / metabolism. Calcium Signaling. Insulin-Secreting Cells / metabolism. Luminescent Proteins / metabolism. Membrane Glycoproteins / metabolism. Recombinant Fusion Proteins / metabolism
  • [MeSH-minor] Animals. Boron Compounds / pharmacology. Calcium / pharmacology. Calcium Channels. Cell Membrane / drug effects. Cell Membrane / metabolism. Endoplasmic Reticulum / drug effects. Endoplasmic Reticulum / metabolism. Mice. Protein Transport / drug effects

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  • (PMID = 18452988.001).
  • [ISSN] 1532-1991
  • [Journal-full-title] Cell calcium
  • [ISO-abbreviation] Cell Calcium
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-20595; United States / NIDDK NIH HHS / DK / DK-48494; United States / NIDDK NIH HHS / DK / DK-63493
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Boron Compounds; 0 / Calcium Channels; 0 / Luminescent Proteins; 0 / Membrane Glycoproteins; 0 / Recombinant Fusion Proteins; 0 / Stim1 protein, mouse; 0 / yellow fluorescent protein, Bacteria; 83075-94-9 / diphenylborate; SY7Q814VUP / Calcium
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76. Takahashi M, Shibutani M, Woo GH, Inoue K, Fujimoto H, Igarashi K, Kanno J, Hirose M, Nishikawa A: Cellular distributions of molecules with altered expression specific to the tumor promotion process from the early stage in a rat two-stage hepatocarcinogenesis model. Carcinogenesis; 2008 Nov;29(11):2218-26
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  • [Title] Cellular distributions of molecules with altered expression specific to the tumor promotion process from the early stage in a rat two-stage hepatocarcinogenesis model.
  • A global gene expression profiling specific to the early process of tumor promotion by fenbendazole (FB) or phenobarbital (PB) in a rat two-stage hepatocarcinogenesis model revealed 33 genes to show altered expression in common with both chemicals.
  • The immunohistochemical distribution of transferrin receptor (Tfrc), nuclear receptor subfamily 0, group B, member 2 (Nr0b2) and minichromosome maintenance deficient 6 (MCM6), included in the altered expression profile, were therefore examined in FB- and PB-induced proliferative lesions at both early and late stages of tumor promotion.
  • In addition, immunoexpression of transforming growth factor beta receptor (TGFbetaR) I, TGFbetaRII, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and phosphorylated phosphatase and tensin homolog deleted on chromosome 10 (pPTEN) was also examined.
  • In the late stage, selective expression of TGFbetaRI, but not TGFbetaRII, was also observed in many adenomas and carcinomas consistently expressing GST-P.
  • Like the GST-P-positive foci, adenomas and carcinomas consistently lacked PTEN and pPTEN.
  • In conclusion, loss of PTEN and dysregulation of transforming growth factor beta signaling can be considered to be involved in rat hepatocarcinogenesis from early stages.
  • Selective expression of Tfrc in proliferative lesions suggests an involvement of changes in iron homeostasis during the process of tumor promotion/progression driven by FB or PB.
  • [MeSH-major] Cell Transformation, Neoplastic. Liver Neoplasms, Experimental / metabolism

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  • (PMID = 18586688.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers
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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. 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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79. 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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80. Tzelepi V, Grivas P, Kefalopoulou Z, Kalofonos H, Varakis JN, Melachrinou M, Sotiropoulou-Bonikou G: Estrogen signaling in colorectal carcinoma microenvironment: expression of ERbeta1, AIB-1, and TIF-2 is upregulated in cancer-associated myofibroblasts and correlates with disease progression. Virchows Arch; 2009 Apr;454(4):389-99
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  • [Title] Estrogen signaling in colorectal carcinoma microenvironment: expression of ERbeta1, AIB-1, and TIF-2 is upregulated in cancer-associated myofibroblasts and correlates with disease progression.
  • Epidemiological and molecular data suggest the involvement of estrogen signaling in colorectal tissue, mediated mainly through estrogen receptor beta (ERbeta).
  • Estrogens may mediate their effects in epithelial cells indirectly by acting on stromal cells.
  • Expression of ERalpha, ERbeta1, and the ER coregulators, amplified in breast cancer-1 (AIB-1) and transcriptional intermediary factor 2 (TIF-2), was evaluated in myofibroblasts of 107 colorectal carcinomas, 77 paired samples of normal mucosa, and 29 adenomas by immunohistochemistry.
  • Double immunostaining with a-SMA was used to identify the myofibroblasts of normal tissue, adenomas, and cancer microenvironment.
  • ERalpha was not expressed in stromal cells.
  • Nuclear expression of ERbeta1, AIB-1, and TIF-2 in myofibroblasts gradually increased from normal mucosa, through adenomas, to carcinomas.
  • Cytoplasmic ERbeta1 and TIF-2 expression was enhanced in carcinomas compared to normal mucosa and adenomas.
  • [MeSH-major] Carcinoma / metabolism. Colorectal Neoplasms / metabolism. Estrogen Receptor beta / biosynthesis. Estrogens / metabolism. Histone Acetyltransferases / biosynthesis. Nuclear Receptor Coactivator 2 / biosynthesis. Trans-Activators / biosynthesis
  • [MeSH-minor] Adenoma / metabolism. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic / metabolism. Disease Progression. Female. Fibroblasts / metabolism. Gene Expression. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Myocytes, Smooth Muscle / metabolism. Neoplasm Staging. Nuclear Receptor Coactivator 3. Signal Transduction / physiology. Up-Regulation

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  • (PMID = 19277704.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogen Receptor beta; 0 / Estrogens; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Trans-Activators; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / NCOA3 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 3
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81. 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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82. 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.


83. 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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84. 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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85. 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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86. 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


87. Shibata H, Takano H, Ito M, Shioya H, Hirota M, Matsumoto H, Kakudo Y, Ishioka C, Akiyama T, Kanegae Y, Saito I, Noda T: Alpha-catenin is essential in intestinal adenoma formation. Proc Natl Acad Sci U S A; 2007 Nov 13;104(46):18199-204
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  • [Title] Alpha-catenin is essential in intestinal adenoma formation.
  • Although the molecular mechanism of tumor initiation is complex, several modifier genes have been identified using mouse models, including the ApcMin mouse.
  • Among the familial adenomatous polyposis mouse lines carrying a truncation mutation at codon 580 in Apc (Apc580D), one line (line19-Apc(580D/+)) showed a remarkably reduced incidence of intestinal adenomas (<5% compared with other lines).
  • In all adenomas generated in line19-Apc(580D/+), somatic recombination between the Apc and Ctnna1 loci retained the wild-type Ctnna1 allele.
  • These data strongly indicate that simultaneous inactivation of alpha-catenin and Apc during tumor initiation suppresses adenoma formation in line19-Apc(580D/+), suggesting that alpha-catenin plays an essential role in the initiation of intestinal adenomas.
  • Although accumulating evidence obtained from human colon tumors with invasive or metastatic potential has established a tumor-suppressive role for alpha-catenin in late-stage tumorigenesis, the role of alpha-catenin in the initiation of intestinal tumorigenesis is not well documented, especially compared with that of beta-catenin.
  • A mouse model used in this study focused on the early stage of tumor initiation and clearly indicated an essential role for alpha-catenin.
  • Thus, alpha-catenin has dual roles in intestinal tumorigenesis, a supporting role in tumor initiation, and a suppressive role in tumor progression.
  • [MeSH-major] Adenoma / pathology. Intestinal Neoplasms / pathology. alpha Catenin / physiology


88. Caldwell GM, Jones CE, Taniere P, Warrack R, Soon Y, Matthews GM, Morton DG: The Wnt antagonist sFRP1 is downregulated in premalignant large bowel adenomas. Br J Cancer; 2006 Mar 27;94(6):922-7
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  • [Title] The Wnt antagonist sFRP1 is downregulated in premalignant large bowel adenomas.
  • Our previous studies have implicated the Wnt antagonist, sFRP1, as a tumour suppressor gene in advanced colorectal cancer.
  • In this study, we set out to investigate the relationship between sFRP1 expression and large bowel adenomas, a precursor of colorectal cancer.
  • The induction of beta-catenin/TCF mediated transcription is both a frequent early event in colorectal neoplasia, and a key downstream effect of wnt growth factor signalling.
  • Lithium treatment of a small bowel mucosal cell line (FHs 74 int) induced sFRP1 within 8 h, indicating that this gene is positively regulated by beta-catenin, contrasting with the suppression of sFRP1 expression, we saw previously in advanced colorectal cancers.
  • We therefore investigated a series of 12 adenomas and matched large bowel mucosa samples.
  • Real-time RT-PCR analysis showed a reduction in sFRP1 expression in all 12 dysplastic lesions (median 485-fold, IQR 120- to 1500-fold), indicating factors other than beta-catenin influence sFRP1 levels.
  • In a second series of 11 adenomas, we identified methylation of the sFRP1 promotor region in all 11 samples, and this was increased compared with the surrounding normal mucosa in seven cases.
  • Immunohistochemical analysis using a polyclonal antibody supported these findings, with sFRP1 expression reduced in many of the adenoma samples examined. sFRP1 staining in normal mucosa adjacent to the dysplastic tissue was also reduced compared with the normal controls, suggesting that sFRP1 expression may be suppressed in a field of mucosa rather than in individual cells.
  • This study identifies sFRP1 inactivation at the premalignant stage of colorectal cancer development, indicating that these pathways may be useful targets for chemoprevention strategies in this common solid tumour.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Intercellular Signaling Peptides and Proteins / biosynthesis. Membrane Proteins / biosynthesis
  • [MeSH-minor] Cell Transformation, Neoplastic. Chemoprevention. DNA Methylation. Down-Regulation. Humans. Immunohistochemistry. Intestinal Mucosa. Intestine, Large / physiology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tumor Cells, Cultured. Wnt Proteins / physiology

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  • (PMID = 16523202.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / SFRP1 protein, human; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC2361362
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89. 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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90. 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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91. 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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92. 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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93. 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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  • [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.


94. 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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  • [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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95. 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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  • [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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96. Happel B, Niederle B, Puespoek A, Ba-Ssalamah A, Schima W: [Benign neuroendocrine and other rare benign tumors of the pancreas]. Radiologe; 2008 Aug;48(8):752-63
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  • [Title] [Benign neuroendocrine and other rare benign tumors of the pancreas].
  • [Transliterated title] Benigne neuroendokrine und andere seltene benigne Tumoren des Pankreas.
  • Neuroendocrine tumors (NET) of the pancreas are rare neoplasms, which arise from cells of the islets of Langerhans.
  • The most common NET are the insulinoma, gastrinoma and hormone inactive NET.
  • [MeSH-major] Image Enhancement / methods. Magnetic Resonance Imaging / methods. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis. Tomography, X-Ray Computed / methods. Ultrasonography / methods

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  • [ISSN] 0033-832X
  • [Journal-full-title] Der Radiologe
  • [ISO-abbreviation] Radiologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 41
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97. Boyault S, Rickman DS, de Reyniès A, Balabaud C, Rebouissou S, Jeannot E, Hérault A, Saric J, Belghiti J, Franco D, Bioulac-Sage P, Laurent-Puig P, Zucman-Rossi J: Transcriptome classification of HCC is related to gene alterations and to new therapeutic targets. Hepatology; 2007 Jan;45(1):42-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hepatocellular carcinomas (HCCs) are a heterogeneous group of tumors that differ in risk factors and genetic alterations.
  • Global transcriptome analyses were performed on 57 HCCs and 3 hepatocellular adenomas and validated by quantitative RT-PCR using 63 additional HCCs.
  • We determined loss of heterozygosity, gene mutations, promoter methylation of CDH1 and CDKN2A, and HBV DNA copy number for each tumor.
  • G1 tumors were associated with low copy number of HBV and overexpression of genes expressed in fetal liver and controlled by parental imprinting.
  • G3 tumors were typified by mutation of TP53 and overexpression of genes controlling the cell cycle.
  • G4 was a heterogeneous subgroup of tumors including TCF1-mutated hepatocellular adenomas and carcinomas.
  • G5 and G6 were strongly related to beta-catenin mutations that lead to Wnt pathway activation; in particular, G6 tumors were characterized by satellite nodules, higher activation of the Wnt pathway, and E-cadherin underexpression.
  • CONCLUSION: These results have furthered our understanding of the genetic diversity of human HCC and have provided specific identifiers for classifying tumors.
  • In addition, our classification has potential therapeutic implications because 50% of the tumors were related to WNT or AKT pathway activation, which potentially could be targeted by specific inhibiting therapies.
  • [MeSH-major] Carcinoma, Hepatocellular / classification. Carcinoma, Hepatocellular / genetics. Genes, Neoplasm. Liver Neoplasms / classification. Liver Neoplasms / genetics. Transcription, Genetic
  • [MeSH-minor] Adenoma / classification. Adenoma / drug therapy. Adenoma / genetics. Adenoma / metabolism. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. DNA, Neoplasm / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Multigene Family. Mutation / genetics. Nuclear Pore Complex Proteins / genetics. Nuclear Pore Complex Proteins / metabolism. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / genetics. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Wnt Proteins / genetics. Wnt Proteins / metabolism


98. Goh BK, Ooi LL, Cheow PC, Tan YM, Ong HS, Chung YF, Chow PK, Wong WK, Soo KC: Accurate preoperative localization of insulinomas avoids the need for blind resection and reoperation: analysis of a single institution experience with 17 surgically treated tumors over 19 years. J Gastrointest Surg; 2009 Jun;13(6):1071-7
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  • [Title] Accurate preoperative localization of insulinomas avoids the need for blind resection and reoperation: analysis of a single institution experience with 17 surgically treated tumors over 19 years.
  • INTRODUCTION: Presently, the need for and choice of preoperative localization tests for insulinomas remain controversial.
  • MATERIALS AND METHODS: From 1990 to 2008, 17 patients with a clinical and biochemical diagnosis of an insulinoma who underwent surgery were retrospectively reviewed.
  • The diagnosis of all insulinomas were confirmed pathologically.
  • RESULTS: All tumors were localized preoperatively and an average of 2.2 preoperative localization studies including 1.4 noninvasive studies and 0.8 invasive studies were utilized per patient.
  • Invasive localization modalities were more sensitive (92%) than noninvasive modalities in localizing insulinomas (71%).
  • Fifteen of 17 tumors (88%) were localized intraoperatively via inspection/palpation and/or intraoperative ultrasonography.
  • Both insulinomas which were not localized intraoperatively were localized correctly to the distal pancreas via preoperative transhepatic portal venous sampling.
  • CONCLUSION: Accurate preoperative localization of insulinomas is useful as it eliminates the need for blind distal pancreatectomy and avoids reoperation.
  • Complete surgical resection is the treatment of choice, and whenever possible, a pancreas-sparing approach such as enucleation should be adopted.
  • [MeSH-major] Insulinoma / surgery. Pancreatic Neoplasms / surgery

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  • (PMID = 19291334.001).
  • [ISSN] 1873-4626
  • [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
  • [Publication-country] United States
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99. Alliouachene S, Tuttle RL, Boumard S, Lapointe T, Berissi S, Germain S, Jaubert F, Tosh D, Birnbaum MJ, Pende M: Constitutively active Akt1 expression in mouse pancreas requires S6 kinase 1 for insulinoma formation. J Clin Invest; 2008 Nov;118(11):3629-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Constitutively active Akt1 expression in mouse pancreas requires S6 kinase 1 for insulinoma formation.
  • Factors that promote pancreatic beta cell growth and function are potential therapeutic targets for diabetes mellitus.
  • In mice, genetic experiments suggest that signaling cascades initiated by insulin and IGFs positively regulate beta cell mass and insulin secretion.
  • Akt and S6 kinase (S6K) family members are activated as part of these signaling cascades, but how the interplay between these proteins controls beta cell growth and function has not been determined.
  • Here, we found that although transgenic mice overexpressing the constitutively active form of Akt1 under the rat insulin promoter (RIP-MyrAkt1 mice) had enlarged beta cells and high plasma insulin levels, leading to improved glucose tolerance, a substantial proportion of the mice developed insulinomas later in life, which caused decreased viability.
  • This oncogenic transformation tightly correlated with nuclear exclusion of the tumor suppressor PTEN.
  • The resulting mice displayed reduced insulinemia and glycemia compared with RIP-MyrAkt1 mice due to a combined effect of improved insulin secretion and insulin sensitivity.
  • Importantly, although the increase in beta cell size in RIP-MyrAkt1 mice was not affected by S6K1 deficiency, the hyperplastic transformation required S6K1.
  • Our results therefore identify S6K1 as a critical element for MyrAkt1-induced tumor formation and suggest that it may represent a useful target for anticancer therapy downstream of mTOR.
  • [MeSH-major] Insulinoma / metabolism. Pancreas / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Ribosomal Protein S6 Kinases / metabolism
  • [MeSH-minor] Animals. Cell Size. Crosses, Genetic. Disease Models, Animal. Insulin / blood. Insulin / genetics. Insulin / metabolism. Insulin-Secreting Cells / metabolism. Mice. Mice, Inbred C57BL. Mice, Transgenic. Promoter Regions, Genetic. Rats


100. Yang YM, Liu TH, Chen YJ, Jiang WJ, Qian JM, Lu X, Gao J, Wu SF, Sang XT, Chen J: Chromosome 1q loss of heterozygosity frequently occurs in sporadic insulinomas and is associated with tumor malignancy. Int J Cancer; 2005 Nov 1;117(2):234-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosome 1q loss of heterozygosity frequently occurs in sporadic insulinomas and is associated with tumor malignancy.
  • The pathogenesis of sporadic insulinomas is not clear, and there are no reliable genetic determinants that are useful to distinguish malignant and benign forms of this tumor.
  • It was reported that 1q LOH might contribute to pathogenesis in gastrinomas and was correlated with tumor progression.
  • However, little data are available on 1q LOH in sporadic insulinomas.
  • In our study, we determine whether 1q LOH occurs in sporadic insulinomas and is associated with tumor malignancy by performing 1q allelotyping with 17 markers in 40 tumors and pair normal DNA.
  • Thirty-five (88%) insulinomas had 1q LOH.
  • Of the 35 insulinomas with 1q LOH, 14 (40%) had 1q21.3-23.2 LOH over a 7.5 cM region (SRO-1), whereas LOH in 21 tumors (60%) occurred at 1q31.3 over an 11.4 cM area (SRO-2).
  • Of 24 tumors without MEN1 LOH, 20 had either SRO-1 or SRO-2 LOH (83%), whereas in 16 tumors with MEN1 LOH, 9 were shown to have LOH at either SRO-1 or SRO-2 (56%) (p = 0.065).
  • This result suggests that LOH at 2 SRO might be MEN1 gene independent and may contribute to the pathogenesis in a subset of insulinomas without MEN1 gene LOH.
  • The presence of 1q21.3-23.2 LOH is significantly associated with malignancy of insulinomas (p = 0.014).
  • The high frequency of LOH at 1q 21.3-23.2 and 1q31.3 suggests these 2 areas may harbor putative tumor suppressor genes that may play an important role in the tumorigenesis of a subset of insulinomas.
  • LOH at 1q21.3-23.2, which was associated with tumor malignancy, could be one of the genetic markers for identifying malignancy in sporadic insulinomas.
  • [MeSH-major] Chromosomes, Human, Pair 1. Insulinoma / genetics. Loss of Heterozygosity. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosome Mapping. DNA, Neoplasm / genetics. Female. Humans. Insulin / blood. Male. Microsatellite Repeats. Middle Aged

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 15900598.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Insulin
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