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1. Poggi G, Villani L, Bernardo G: Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma. Rare Tumors; 2009;1(1):e6

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  • [Title] Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma.
  • Glucagonomas are pancreatic islet cell tumors arising from the alpha cells which belong to neuroendocrine tumors.
  • We report the case of a 52- year old man with a pancreatic glucagonoma with synchronous multiple liver metastases treated by surgery, transarterial chemoembolization, percutaneous radiofrequency thermal ablation and long-acting octreotide.
  • Our report confirms that a multimodal approach is very effective in patients with unresectable liver metastases from pancreatic endocrine tumors providing long-lasting palliation and probably prolonging survival.

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  • (PMID = 21139900.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2994425
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2. Okauchi Y, Nammo T, Iwahashi H, Kizu T, Hayashi I, Okita K, Yamagata K, Uno S, Katsube F, Matsuhisa M, Kato K, Aozasa K, Kim T, Osuga K, Nakamori S, Tamaki Y, Funahashi T, Miyagawa J, Shimomura I: Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS). Intern Med; 2009;48(12):1025-30
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  • [Title] Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS).
  • To identify the location of pancreatic endocrine tumors, arterial stimulation and venous sampling (ASVS) is known to be useful for insulinoma and gastrinoma, but its usefulness for glucagonoma has not been verified to date.
  • Here we report a case of glucagonoma that was diagnosed by ASVS with calcium loading, in which an approximately 6-fold increase of glucagon was observed in the splenic artery territory.
  • MEN1 gene analysis verified the presence of a mutation and the glucagonoma was confirmed after operation.
  • In conclusion, ASVS could be useful for the diagnosis of glucagonoma.
  • [MeSH-major] Glucagon / blood. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 19525592.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9007-92-5 / Glucagon; SY7Q814VUP / Calcium
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3. Docherty HM, Hay CW, Ferguson LA, Barrow J, Durward E, Docherty K: Relative contribution of PDX-1, MafA and E47/beta2 to the regulation of the human insulin promoter. Biochem J; 2005 Aug 1;389(Pt 3):813-20
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  • Of these, the homoeodomain protein PDX-1 (pancreatic duodenal homeobox factor-1), the basic leucine zipper protein MafA and the basic helix-loop-helix heterodimer E47/BETA2 (beta-cell E box transactivator 2; referred to here as beta2) bind to important regulatory sites.
  • Mutagenesis of the PDX-1, MafA and E47/beta2 binding sites reduced promoter activity by 60, 74 and 94% respectively, in INS-1 beta-cells.
  • In the islet glucagonoma cell line alphaTC1.6, overexpression of PDX-1 and MafA separately increased promoter activity approx.
  • In HeLa cells, PDX-1 stimulated the basal promoter by approx.
  • PDX-1 was shown further to activate the endogenous insulin 1 gene in alphaTC1.6 cells, whereas MafA activated the insulin 2 gene.

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  • (PMID = 15862113.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / HMGB Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / MAFA protein, human; 0 / Maf Transcription Factors, Large; 0 / NEUROD1 protein, human; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Tcf7l1 protein, rat; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein
  • [Other-IDs] NLM/ PMC1180732
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4. Yoshida M, Hayashi K, Ohara H, Miyabe K, Okumura F, Naitoh I, Tanaka H, Ando T, Nakazawa T, Takahashi S, Joh T: A case of pancreatic glucagonoma with erythema. Nihon Shokakibyo Gakkai Zasshi; 2010 Jun;107(6):930-6
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  • [Title] A case of pancreatic glucagonoma with erythema.
  • Full-body computed tomography (CT) scanning revealed a tumor mass in the tail of the pancreas; CT and magnetic resonance imaging (MRI) scans confirmed the presence of a spherical mass.
  • In contrast CT scans, although the contrast was gradually increased, no strong contrast differences were observed between the tumor and the surrounding tissue.
  • Blood test results revealed that the patient had a high glucagon level.
  • We diagnosed glucagonoma syndrome on the basis of the above results and resected the tail of the pancreas.
  • Pathological analysis revealed that the tumor cells had proliferated in ribbon-like, cord-like structures.
  • Immunostaining results were positive for glucagon, which confirmed our diagnosis.
  • [MeSH-major] Erythema / etiology. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20530930.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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5. de Mestier L, Hammel P, Hentic O, Dove P, Lévy P, Ruszniewski P: [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency]. Gastroenterol Clin Biol; 2010 Jan;34(1):106-10
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  • [Title] [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency].
  • [Transliterated title] Efficacité spectaculaire d'une chimiothérapie par 5-fluoro-uracile et dacarbazine chez un malade atteint de glucagonome métastatique avec insuffisance cardiaque.
  • Malignant glucagonoma is an exceptional pancreatic endocrine tumour, with frequent dermatologic symptoms, diabetes and degradation of the general health status.
  • We report here an observation of a patient who was treated for a glucagonoma with multiple liver metastases, migratory necrolytic erythema, dilated cardiomypathy and diabetes that dramatically improved after a dacarbazin-based chemotherapy, allowing subsequent surgical resection of the primary.
  • The patient was still alive and asymptomatic without progressive disease nearly two years after surgery.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cardiomyopathy, Dilated / complications. Glucagonoma / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Adult. Dacarbazine / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright 2009. Published by Elsevier Masson SAS.
  • (PMID = 19875259.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; U3P01618RT / Fluorouracil
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6. Lobo I, Carvalho A, Amaral C, Machado S, Carvalho R: Glucagonoma syndrome and necrolytic migratory erythema. Int J Dermatol; 2010 Jan;49(1):24-9
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  • [Title] Glucagonoma syndrome and necrolytic migratory erythema.
  • The glucagonoma syndrome is a rare disorder, characterized by necrolytic migratory erythema, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia in association with a glucagon-secreting alpha-cell tumor of the pancreas.
  • The clinical investigation revealed a pancreatic glucagonoma with resolution of the cutaneous and systemic features after surgical removal.
  • The dermatologic and endocrine approach to this syndrome is discussed here.
  • Early recognition and treatment may prevent metastatic disease and ensure its cure with resolution of the cutaneous and catabolic manifestations.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Skin / pathology
  • [MeSH-minor] Aged. Biopsy. Glucagon / blood. Humans. Male. Necrosis. Pancreatectomy. Tomography, X-Ray Computed

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  • (PMID = 20465606.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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7. Marko PB, Miljković J, Zemljic TG: Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors. Acta Dermatovenerol Alp Pannonica Adriat; 2005 Dec;14(4):161-4, 166
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  • [Title] Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors.
  • The computed tomographic scan of the abdomen revealed multiple hepatic tumors.
  • Histopathological examination of ultrasound-guided needle biopsy from a hepatic lesion demonstrated a neuroendocrine tumor.
  • Somatostatin-receptor scintigraphy with radio-labelled octreotide confirmed the likelihood of the neuroendocrine nature of the hepatic tumors and excluded the presence of other such lesions throughout the rest of the body, including the pancreas.
  • The serum glucagon level was markedly increased.
  • The diagnosis of necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors was made and therapy with the long-acting somatostatin analogue octreotide was started.
  • Having reached the final stage of the disease, which was further complicated by congestive heart failure, the patient died one year later.
  • As no autopsy was performed, we were unable to establish whether the hepatic tumors represented a metastatic process of previously undetected pancreatic glucagonoma or if they were extra-pancreatic glucagon-secreting tumors.
  • The correct diagnosis of necrolytic migratory erythema is important, since it might be the clue for early detection of glucagonoma or of extra-pancreatic glucagon-secreting tumors.
  • [MeSH-major] Dermatitis / etiology. Erythema / etiology. Liver Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Paraneoplastic Syndromes / diagnosis
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Glucagon / blood. Humans. Male. Middle Aged. Octreotide / therapeutic use

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  • (PMID = 16435046.001).
  • [ISSN] 1318-4458
  • [Journal-full-title] Acta dermatovenerologica Alpina, Pannonica, et Adriatica
  • [ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Slovenia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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8. Simonenko VB, Dulin PA, Beliaev LB, Makanin MA, Dem'ianenko AV, Zykova AA, Zhuravleva SI, Kolesnikova VN: [A case of pancreatic glucagonoma]. Klin Med (Mosk); 2007;85(8):67-70
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  • [Title] [A case of pancreatic glucagonoma].
  • Neuroendocrine tumor consisting of pancreatic alpha-cells -- glucagonoma -- is a very rare finding (one case per two million people a year).
  • This functionally active, usually malignant tumor has typical clinical manifestations.
  • Glucagonoma syndrome is a disease that has an original clinical picture that includes necrolytic migrating erythema with secondary bullous dermatitis, glucose tolerance disorder or diabetes mellitus, weight loss, anemia, hypoaminoacidemia, venous thrombosis, and alimentary and mental disturbances.
  • By the time diagnosis is made, 60 to 70% of glucagonomas already give metastases, and even small glucagonomas should be considered tumors with unknown malignant potential or malignant tumors.
  • Glucagonomas grow slowly, and patients live long (the survival median is approximately 15 years).
  • [MeSH-major] Glucagonoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17926496.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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9. Technau K, Renkl A, Norgauer J, Ziemer M: Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma. Eur J Dermatol; 2005 Mar-Apr;15(2):110-2
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  • [Title] Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma.
  • Necrolytic migratory erythema is a cutaneous paraneoplastic manifestation, which is usually associated with a glucagon-secreting pancreatic tumor.
  • However, it also may occur in other circumstances in which serum glucagon is elevated, as in hepatic cirrhosis.
  • Rarely, necrolytic migratory erythema is reported in association with a jejunal and rectal adenocarcinoma or villous atrophy of the small intestine without any evidence for increased serum glucagon levels.
  • In this context we report the case of an 85-year-old male with myelodysplastic syndrome who developed typical necrolytic migratory erythema without glucagonoma syndrome or evidence for other pancreatic or liver disease.
  • We suggest that, in addition to the diseases listed, myelodysplastic syndrome might be able to cause necrolytic migratory erythema.
  • [MeSH-major] Erythema / complications. Glucagonoma / complications. Myelodysplastic Syndromes / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / complications


10. Cruz-Bautista I, Lerman I, Perez-Enriquez B, Padilla LS, Torres CL, Lopez A, Cabrera T, Mehta RP, Gómez-Pérez FJ, Rull JA, Orozco-Topete R: Diagnostic challenge of glucagonoma: case report and literature review. Endocr Pract; 2006 Jul-Aug;12(4):422-6
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  • [Title] Diagnostic challenge of glucagonoma: case report and literature review.
  • OBJECTIVE: To report the diagnostic difficulties encountered in a case of glucagonoma.
  • METHODS: We provide a literature review and present the clinical findings, pertinent laboratory data, and results of related studies in a patient with a glucagonoma.
  • The patient was hospitalized, and because of the dermatologic findings suggestive of necrolytic migratory erythema, the presence of a glucagonoma was suspected.
  • Glucagon levels were found to be elevated, and imaging studies confirmed the presence of an enlarged mass in the pancreatic tail, without evidence of extension to surrounding structures.
  • After surgical removal of the tumor, the skin and oral mucosal lesions disappeared spontaneously.
  • The histologic appearance and immunohistochemical staining results confirmed the diagnosis of a glucagonoma.
  • Subsequently, all related symptoms resolved, and the glucagon levels normalized.
  • CONCLUSION: The diagnosis of glucagonoma is often delayed.
  • Clinicians should be aware of the unusual initial manifestations of this tumor and the potential for less than a full spectrum of the characteristic features of the glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / diagnosis
  • [MeSH-minor] Erythema / etiology. Humans. Hyperpigmentation / etiology. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / ultrasonography. Pancreatic Neoplasms / ultrastructure. Regional Blood Flow. Tomography, X-Ray Computed. Wound Healing

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  • (PMID = 16901799.001).
  • [ISSN] 1530-891X
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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11. Oberkirchner U, Linder KE, Zadrozny L, Olivry T: Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide. Vet Dermatol; 2010 Oct;21(5):510-6
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  • [Title] Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide.
  • Necrolytic migratory erythema (NME; also known as superficial necrolytic dermatitis) is a syndrome most often associated with certain chronic liver diseases or pancreatic glucagonomas.
  • In humans with glucagonoma-associated NME, skin lesions usually respond to octreotide, a somatostatin analogue that inhibits glucagon release.
  • In this report an 11-year-old golden retriever dog with pancreatic glucagonoma and metastasis to the regional lymph nodes, spleen and liver was diagnosed with NME.
  • The dog was later euthanized because of progressive metastatic disease.
  • In conclusion, subcutaneous octreotide injections were beneficial in this dog with glucagonoma-associated NME.
  • This somatostatin analogue could be a valuable option to treat canine patients with non-resectable or relapsing pancreatic glucagonoma-associated NME.
  • [MeSH-major] Dog Diseases / drug therapy. Glucagonoma / veterinary. Necrolytic Migratory Erythema / veterinary. Octreotide / therapeutic use. Pancreatic Neoplasms / veterinary
  • [MeSH-minor] Animals. Anorexia / chemically induced. Anorexia / veterinary. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Dogs. Dose-Response Relationship, Drug. Lymph Nodes / pathology. Male. Paraneoplastic Syndromes / pathology. Paraneoplastic Syndromes / veterinary

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  • [Copyright] © 2010 The Authors. Journal compilation © 2010 ESVD and ACVD.
  • (PMID = 20500495.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
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12. Peros G, Sakorafas GH, Konstantoudakis G, Giannopoulos GA, Petropoulou K, Parasi A: Duodeno-pancreatic neuroendocrine tumours. Eur J Cancer Care (Engl); 2010 May;19(3):393-402
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Duodeno-pancreatic neuroendocrine tumours.
  • Duodeno-pancreatic neuroendocrine tumours (DP-ETs) are increasingly diagnosed today due to the widespread use of modern imaging methods.
  • Duodeno-pancreatic endocrine tumours should be treated by radical surgical resection, which offers a high chance for cure when the disease is localized.
  • A high index of suspicion is required in these patients for the presence of a multiple endocrine neoplasia type syndrome.
  • Histological/immunohistochemical diagnosis was somatostatin-producing tumour in the first patient, oncocytic endocrine tumour positive for neurone-specific enolase and focally for chromogranin in the second patient, glucagonoma and pancreatic polypeptide-producing endocrine pancreatic tumour in the third patient, and gastrin, somatostatin, calcitonin, insulin and adrenocorticotropic hormone (ACTH)-producing tumour in the fourth.
  • The second patient died 6.5 years following surgery due to disseminated disease.
  • [MeSH-major] Duodenal Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Biopsy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Proteins / metabolism. Treatment Outcome

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  • (PMID = 19708940.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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13. Kovács RK, Korom I, Dobozy A, Farkas G, Ormos J, Kemény L: Necrolytic migratory erythema. J Cutan Pathol; 2006 Mar;33(3):242-5
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  • The classical symptoms are associated with alpha-cell pancreatic islet cell tumor or 'glucagonoma'.
  • Generally, extracutaneous hallmarks of this disease include weight loss, diabetes, anaemia and diarrhoea.
  • OBSERVATION: We report a case of a 39-year-old woman with a 3-year history of recalcitrant psoriasiform eruption, who had no other associated symptoms on routine examination.
  • Abdominal computer tomography was performed, which revealed a tumor in the tail of the pancreas.
  • After distal resection of the pancreas her skin symptoms resolved in a few days time.
  • Histology was consistent with glucagonoma.
  • CONCLUSIONS: It is infrequent to have only necrolytic migratory erythema, hyperglucagonaemia and islet-cell tumor but no other extracutaneous symptoms in glucagonoma syndrome.
  • Skin symptoms are important, often they are the clue to the diagnosis of glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Glucagonoma / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Female. Humans. Necrosis. Paraneoplastic Syndromes. Treatment Outcome

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  • (PMID = 16466513.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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14. Kindmark H, Sundin A, Granberg D, Dunder K, Skogseid B, Janson ET, Welin S, Oberg K, Eriksson B: Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years. Med Oncol; 2007;24(3):330-7
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  • [Title] Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years.
  • BACKGROUND: Glucagon-secreting endocrine pancreatic tumor is a rare disease, hence controlled studies on clinical management are lacking.
  • In an attempt to assess the efficacy of diagnostic and therapeutic measures in patients with glucagonoma, a retrospective study was performed using the archives of a tertiary care center.
  • PATIENTS AND METHODS: Records from 340 patients with endocrine pancreatic tumors were reassessed and 23 patients with malignant endocrine pancreatic tumor and elevated plasma glucagon levels were identified.
  • RESULTS: About 7% of patients with histologically verified tumors fullfilled our criteria for glucagonoma.
  • Only 22% of these patients had developed diabetes prior to the diagnosis of glucagonoma.
  • Seventy eight percent had metastatic disease to the liver at diagnosis.
  • During the study period, 11 patients died at a median of 80 months from diagnosis whereas 11 patients are still alive after a median follow up of 52 months.
  • CONCLUSIONS: Glucagonomas represent 7% of our comprehensive referral material of endocrine pancreatic tumors.
  • Necrolytic migratory erythema was a common finding (52%) and diabetes less frequent at presentation than previously reported.
  • Tumors were positive on somatostatin receptor scintigraphy and objective responses were seen to chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Erythema / complications. Glucagonoma / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Glucagon / blood. Humans. Interferons. Liver Neoplasms / secondary. Male. Middle Aged. Receptors, Somatostatin / metabolism. Retrospective Studies. Sex Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 17873310.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Somatostatin; 9007-92-5 / Glucagon; 9008-11-1 / Interferons
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15. Mendoza-Guil F, Hernández-Jurado I, Burkhardt P, Linares J, Naranjo R: [Necrolytic migratory erythema associated with glucagonoma]. Actas Dermosifiliogr; 2005 Apr;96(3):175-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Necrolytic migratory erythema associated with glucagonoma].
  • [Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.
  • Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.
  • We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.
  • The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.
  • [MeSH-major] Erythema / complications. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16476361.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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16. Stark I, Mensing CH, Sander CA: [Necrolytic migratory erythema in glucagonoma syndrome]. Hautarzt; 2008 Jan;59(1):50-3
Hazardous Substances Data Bank. CIPROFLOXACIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Necrolytic migratory erythema in glucagonoma syndrome].
  • The glucagonoma syndrome is a rare disease in which a typical skin lesion, necrolytic migratory erythema, is often one of the presenting symptoms.
  • Skin biopsies, laboratory studies and imaging confirmed the diagnosis of necrolytic migratory erythema as part of a glucagonoma syndrome.
  • [MeSH-major] Ciprofloxacin / administration & dosage. Erythema / diagnosis. Erythema / drug therapy. Glucagonoma / diagnosis. Glucagonoma / drug therapy
  • [MeSH-minor] Administration, Oral. Aged. Anti-Infective Agents / administration & dosage. Female. Humans. Necrosis / diagnosis. Necrosis / drug therapy. Syndrome. Treatment Outcome

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  • (PMID = 17549440.001).
  • [ISSN] 1432-1173
  • [Journal-full-title] Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete
  • [ISO-abbreviation] Hautarzt
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 5E8K9I0O4U / Ciprofloxacin
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17. Abreu Velez AM, Howard MS: Diagnosis and treatment of cutaneous paraneoplastic disorders. Dermatol Ther; 2010 Nov-Dec;23(6):662-75
MedlinePlus Health Information. consumer health - Skin Conditions.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and treatment of cutaneous paraneoplastic disorders.
  • Cutaneous signs of these disorders afford clinicians opportunities for early diagnosis and treatment.
  • We aim to succinctly review the recognition, diagnosis, and treatment of selected cutaneous paraneoplastic diseases.
  • Skin disorders that may be associated with paraneoplastic syndromes include: cutaneous metastases, tripe palms, Sweet's syndrome, glucagonoma, Paget's disease and extramammary Paget's disease, acanthosis nigricans, Birt-Hogg-Dube syndrome, basal cell nevus syndrome, Bazex syndrome (acrokeratosis paraneoplastica), carcinoid syndrome, Cowden's disease(multiple hamartoma syndrome), dermatomyositis, erythema gyratum repens, ichthyosis aquisita, von Recklinghausen's disease, pityriasis rotunda, pyoderma gangrenosum, Quincke's edema (angioedema and paraneoplastic uricaria), paraneoplastic pemphigus, Degos' disease, superior vena cava syndrome, Werner's syndrome, diffuse normolipemic plane xanthomas, and yellow nail syndrome.
  • [MeSH-major] Paraneoplastic Syndromes / diagnosis. Paraneoplastic Syndromes / therapy. Skin Diseases / diagnosis. Skin Diseases / therapy

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 21054710.001).
  • [ISSN] 1529-8019
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
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18. Dourakis SP, Alexopoulou A, Georgousi KK, Delladetsima JK, Tolis G, Archimandritis AJ: Glucagonoma syndrome: survival 21 years with concurrent liver metastases. Am J Med Sci; 2007 Sep;334(3):225-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma syndrome: survival 21 years with concurrent liver metastases.
  • A patient who survived for 21 years since initial discovery of glucagonoma with concurrent liver metastases is described.
  • Psychiatric symptoms, weight loss, necrolytic migratory erythema, diarrhea, and diabetes mellitus developed gradually after diagnosis of the tumor.
  • The longevity of this patient may be related to the slow tumor growth expressed histologically by ischemic necrosis of the malignant cells and in imaging by extensive tumor calcifications, a very rare finding in this type of the tumor.
  • [MeSH-major] Glucagonoma / pathology. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology

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  • (PMID = 17873541.001).
  • [ISSN] 0002-9629
  • [Journal-full-title] The American journal of the medical sciences
  • [ISO-abbreviation] Am. J. Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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19. Colović R, Matić S, Micev M, Grubor N, Latincić S: [Glucagonoma without glucagonoma syndrome]. Srp Arh Celok Lek; 2010 Mar-Apr;138(3-4):244-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Glucagonoma without glucagonoma syndrome].
  • INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.
  • They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.
  • In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.
  • CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.
  • During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.
  • Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.
  • CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.
  • Those two would probably result in discovery of more glucagonomas and other neuroendocrine tumours without characteristic clinical syndromes.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20499510.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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20. Ritz-Laser B, Mamin A, Brun T, Avril I, Schwitzgebel VM, Philippe J: The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression. Mol Endocrinol; 2005 Mar;19(3):759-70
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression.
  • We show here that Gata-4 and/or Gata-6 are not only expressed in the adult exocrine pancreas but also in glucagonoma and insulinoma cell lines, whereas Gata-5 is restricted to the exocrine pancreas.
  • During pancreas development, Gata-4 is expressed already at embryonic d 10.5 and colocalizes with early glucagon+ cells at embryonic d 12.5.
  • Gata-4 was able to transactivate the glucagon gene both in heterologous BHK-21 (nonislet Syrian baby hamster kidney) and in glucagon-producing InR1G9 cells.
  • Using gel-mobility shift assays, we identified a complex formed with nuclear extracts from InR1G9 cells on the G5 control element (-140 to -169) of the glucagon gene promoter as Gata-4.
  • Mutation of the GATA binding site on G5 abrogated the transcriptional activation mediated by Gata-4 and reduced basal glucagon gene promoter activity in glucagon-producing cells by 55%.
  • Furthermore, Gata-4 acted more than additively with Forkhead box A (hepatic nuclear factor-3) to trans-activate the glucagon gene promoter.
  • We conclude that, besides its role in endoderm differentiation, Gata-4 might be implicated in the regulation of glucagon gene expression in the fetal pancreas and that Gata activity itself may be modulated by interactions with different cofactors.
  • [MeSH-major] DNA-Binding Proteins / chemistry. Gene Expression Regulation. Glucagon / metabolism. Islets of Langerhans / metabolism. Transcription Factors / chemistry. Zinc Fingers
  • [MeSH-minor] Animals. Base Sequence. Binding Sites. Cell Differentiation. Cell Line. Cell Nucleus / metabolism. Chloramphenicol O-Acetyltransferase / metabolism. Cricetinae. Dose-Response Relationship, Drug. GATA4 Transcription Factor. GATA6 Transcription Factor. Humans. Mice. Microscopy, Fluorescence. Molecular Sequence Data. Mutation. Pancreas / embryology. Promoter Regions, Genetic. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tissue Distribution. Transcriptional Activation. Transfection


21. Mikkelsen CS, Mikkelsen DB, Vestergaard V, Clemmensen O, Nielsen HO, Bygum A: [Glucagonoma syndrome without diabetes mellitus]. Ugeskr Laeger; 2008 Nov 17;170(47):3876
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Glucagonoma syndrome without diabetes mellitus].
  • Computerised tomography and endoscopic ultrasound showed a solid tumour of the pancreas.
  • A blood sample showed an increased level of glucagon without diabetes.
  • Glucagonoma syndrome is characterized by glucagon overproduction, diabetes, depression, deep venous thrombosis and necrolytic migrating erythema.
  • Glucagonoma is frequently diagnosed late which increases the risk of metastases.
  • It is important not to rule out glucagonoma in patients with a relevant clinical picture but without diabetes.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • [CommentIn] Ugeskr Laeger. 2008 Dec 15;170(51):4241; author reply 4241 [19160469.001]
  • (PMID = 19014744.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Denmark
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22. de Herder WW: Biochemistry of neuroendocrine tumours. Best Pract Res Clin Endocrinol Metab; 2007 Mar;21(1):33-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biochemistry of neuroendocrine tumours.
  • Several circulating or urinary tumour markers can be used for the diagnosis and follow-up of functioning and clinically non-functioning neuroendocrine tumours of the pancreatic islet cells and intestinal tract.
  • Among the specific tumour markers are serotonin and its metabolites--e.g.
  • 5-hydroxyindoleacetic acid (5-HIAA)--in carcinoid tumours and the carcinoid syndrome, insulin and its precursors or breakdown products in insulinoma, and gastrin in gastrinoma.
  • Plasma vasointestinal polypeptide (VIP) determinations have been used in the diagnosis of VIPoma, plasma glucagon for glucagonoma, and serum somatostatin for somatostatinoma.
  • Among the tumour-non-specific markers are: chromogranins, neuron-specific enolase (NSE), alpha-subunits of the glycoprotein hormones, catecholamines, pancreatic polypeptide (PP), ghrelin and adrenomedullin.
  • [MeSH-major] Biomarkers, Tumor / analysis. Neuroendocrine Tumors / diagnosis
  • [MeSH-minor] Biomarkers / analysis. Carcinoid Tumor / diagnosis. Gastrinoma / diagnosis. Gastrins / analysis. Humans. Insulin / analysis. Insulin / metabolism. Insulinoma / diagnosis. Malignant Carcinoid Syndrome / diagnosis. Pancreatic Neoplasms / diagnosis. Serotonin / analysis. Serotonin / metabolism

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  • (PMID = 17382264.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Gastrins; 0 / Insulin; 333DO1RDJY / Serotonin
  • [Number-of-references] 49
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23. Dinc B, Sahin C: Metastatic glucagonoma. Eurasian J Med; 2009 Apr;41(1):70-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic glucagonoma.
  • We report a case of a very rare endocrine tumor of the pancreas.
  • Because the CA 19-9 and glucagon levels were high, and abdominal dynamic CT showed a mass in the pancreas body and metastatic lesions in the liver, the decision was made to operate.
  • The histopathology of the tumor was reported as a neuroendocrine tumor, which was concordant with glucagonoma.

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  • (PMID = 25610069.001).
  • [ISSN] 1308-8734
  • [Journal-full-title] The Eurasian journal of medicine
  • [ISO-abbreviation] Eurasian J Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Other-IDs] NLM/ PMC4261651
  • [Keywords] NOTNLM ; Glucagonoma / Liver / Metastases
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24. Lepage C, Ciccolallo L, De Angelis R, Bouvier AM, Faivre J, Gatta G, EUROCARE working group: European disparities in malignant digestive endocrine tumours survival. Int J Cancer; 2010 Jun 15;126(12):2928-34

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It was 58.1% for differentiated MDET and 8.1% for small-cell MDET (p < 0.001), 55.9% for patients under 65 and 37.0% for older patients.
  • Among well-differentiated pancreatic tumours, 5-year relative survival was 55.6% for insulinoma, 48.4% for gastrinoma, 33.4% for glucagonoma, 28.8% for carcinoid tumours and 49.9% for non-functioning tumours.
  • MDET differentiation, site, geographic area, age and sex, were independent prognostic factors.
  • Overall, in Europe approximately half of the patients with MDET survive 5 years after the initial diagnosis.
  • Prognosis varies with tumour differentiation, anatomic site and histological type.

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  • (PMID = 19569047.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Investigator] Aareleid T; Hédelin G; Velten M; Launoy G; Faivre J; Ziegler H; Tryggvadottir L; Berrino F; Allemani C; Baili P; Ciccolallo L; Gatta G; Lucca F; Micheli A; Sant M; Sowe S; Zigon G; Crosignani P; Contiero P; Conti E; Paci E; Crocetti E; De Lisi V; Serventi L; Falcini F; Zanetti R; Patriarca S; Rosso S; Capocaccia R; Carrani E; De Angelis R; Roazzi P; Santaquilani M; Grande E; Inghelmann R; Simonetti A; Tavilla A; Francisci S; Verdecchia A; Langmark F; Andersen A; Rachtan J; Zwierko M; Plesko I; Obsitnikova A; Pompe-Kirn V; Maja PZ; Izarzugaza I; Ardanaz E; Moreno C; Jundt G; Lutz JM; Bouchardy C; Godward S; Williams EM; Forman D; Verne J; Møller H; Bell J; Botha H; Lawrence G; Black RJ; Brewster DH; Steward JA
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25. King J, Quinn R, Glenn DM, Janssen J, Tong D, Liaw W, Morris DL: Radioembolization with selective internal radiation microspheres for neuroendocrine liver metastases. Cancer; 2008 Sep 1;113(5):921-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radioembolization with selective internal radiation microspheres for neuroendocrine liver metastases.
  • BACKGROUND: There are limited effective treatment options available and a poor 5-year survival for patients with inoperable neuroendocrine liver metastases (NETLMs).
  • Patients were monitored prospectively, and the response to treatment was measured by using cancer markers and tumor size on computed tomography imaging studies.
  • The site of the primary neuroendocrine tumor was the bronchus in 1 patient, the medullary thyroid in 2 patients, gastrointestinal in 15 patients, the pancreas in 8 patients, and of unknown origin in 8 patients.
  • The tumors were classified as vipoma (1 tumor), somatostatinoma (1 tumor), glucagonoma (2 tumors), large cell (3 tumors), carcinoid (25 tumors), and of unknown origin (2 tumors).
  • [MeSH-major] Brachytherapy / methods. Embolization, Therapeutic / methods. Liver Neoplasms / radiotherapy. Liver Neoplasms / secondary. Neuroendocrine Tumors / pathology

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  • [Copyright] (c) 2008 American Cancer Society.
  • (PMID = 18618495.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Yttrium Radioisotopes; U3P01618RT / Fluorouracil
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26. Akerström G, Hellman P: Surgery on neuroendocrine tumours. Best Pract Res Clin Endocrinol Metab; 2007 Mar;21(1):87-109
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  • [Title] Surgery on neuroendocrine tumours.
  • Neuroendocrine tumours of the gastrointestinal tract and pancreas present a major challenge to physicians in their recognition and treatment requirements, and surgical treatment of these tumours has become increasingly important for symptom palliation and survival.
  • For some carcinoid tumours the extent of surgery may depend on tumour size.
  • Midgut carcinoid is the most common cause of the carcinoid syndrome, requiring surgery for primary and mesenteric tumours to minimize the risk for abdominal complications but also for removal of liver metastases to palliate hormonal symptoms.
  • Among endocrine pancreatic tumours, insulinoma and gastrinoma often cause severe symptoms of hormone excess despite their inconspicuous size, but they can be successfully removed with improved pre- and intraoperative localization.
  • Other tumours--glucagonoma, VIPoma, and non-functioning endocrine pancreatic tumours--are often large or metastasizing, but generally require surgical debulking to alleviate hormonal symptoms and have favourable survival.
  • [MeSH-major] Neuroendocrine Tumors / surgery
  • [MeSH-minor] Algorithms. Carcinoid Tumor / pathology. Carcinoid Tumor / surgery. Gastrinoma / surgery. Glucagonoma / surgery. Humans. Insulinoma / surgery. Intestinal Neoplasms / surgery. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Models, Biological. Multiple Endocrine Neoplasia Type 1 / complications. Multiple Endocrine Neoplasia Type 1 / surgery. Nesidioblastosis / surgery. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery. Vipoma / surgery. Zollinger-Ellison Syndrome / surgery

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  • (PMID = 17382267.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 55
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27. Singh R, Basturk O, Klimstra DS, Zamboni G, Chetty R, Hussain S, La Rosa S, Yilmaz A, Capelli P, Capella C, Cheng JD, Adsay NV: Lipid-rich variant of pancreatic endocrine neoplasms. Am J Surg Pathol; 2006 Feb;30(2):194-200
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lipid-rich variant of pancreatic endocrine neoplasms.
  • Most pancreatic endocrine neoplasms (PENs) show characteristic and well-recognized endocrine morphology; however, a lipid-rich pattern, which can present a diagnostic problem in biopsies, has been reported, mostly as individual cases.
  • Some have been included in descriptions of the rare clear-cell variant associated with von Hippel-Lindau (VHL) syndrome.
  • The growth pattern was relatively diffuse, with vague compartmentalization of the cells by a delicate vasculature; prominent nesting was noted in only 4 cases.
  • Pathology reports indicated substantial diagnostic challenge in these cases; on biopsies, 1 case was originally diagnosed as adrenal cortical carcinoma, another as renal cell carcinoma, a third as solid-pseudopapillary tumor, and a fourth had a fine needle aspiration cytologic diagnosis of adenocarcinoma.
  • Clinically, as in conventional PENs, there appeared to be two distinct subsets: Two cases were familial or functional/syndromic (1 with VHL and the other with MEN-1 and glucagonoma syndrome) and occurred in younger adults (ages 41 and 47 years); the majority (n = 9) were nonfunctional/nonsyndromic and nonfamilial.
  • Immunohistochemically, markers implicated in VHL-associated neoplasia, including HIF-1alpha, inhibin, and Melan-A (in clear-cell PENs) and MUC6 (in serous cystadenomas) were mostly negative in lipid-rich PENs (1 of 10, 1 of 10, 0 of 10 and 0 of 10, respectively).
  • In conclusion, the lipid-rich pattern, reminiscent of adrenal cortical cells, represents a distinct subset of PENs.
  • The findings suggest that the pathogenesis of lipid-rich tumors may be different from the VHL-associated clear-cell variants of PENs.
  • [MeSH-major] Endocrine Gland Neoplasms / pathology. Lipids. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adrenocortical Carcinoma / pathology. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Carcinoma, Renal Cell / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Microscopy, Electron, Transmission. Middle Aged. Multiple Endocrine Neoplasia Type 1 / pathology. von Hippel-Lindau Disease / complications

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  • (PMID = 16434893.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lipids
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28. Butte JM, Montero PH, Solar A, Torres J, Olmos PR, Goñi I, Quintana JC, Martínez J, Llanos O: Cervical metastases of glucagonoma in a patient with multiple endocrine neoplasia type 1: report of a case. Surg Today; 2008;38(12):1137-43
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  • [Title] Cervical metastases of glucagonoma in a patient with multiple endocrine neoplasia type 1: report of a case.
  • Multiple endocrine neoplasia type 1 (MEN 1) is a syndrome characterized by tumors of the parathyroid glands, pancreatic islet cells, duodenum, and pituitary gland.
  • We report a case of cervical metastases of glucagonoma with MEN 1.
  • Computed tomography (CT) showed two hypervascular lesions in the tail of the pancreas and cervical ultrasound showed multiple hypoechogenic ovoid images in the neck.
  • A cervical CT scan confirmed two 15-mm lymph nodes in the left cervical region and 111In-DOTATOC imaging showed focal abnormal somatostatin expression in the pancreatic tail and the cervical nodes.
  • The patient had asymptomatic hypoglycemic episodes, with blood sugar levels as low as 30 mg/dl, which raised our suspicion of MEN 1 associated with pancreatic insulinoma.
  • Histopathological examination revealed 12 pancreatic tumors as well as metastases in four cervical lymph nodes.
  • A follow-up CT scan, 18 months after surgery, showed new tumors in the head of the pancreas and in the duodenal wall.
  • A pancreatoduodenectomy was performed and histopathological examination revealed nine nonfunctioning endocrine tumors in the pancreas, one tumor in the duodenal wall, and metastases in two peripancreatic lymph nodes.
  • [MeSH-major] Glucagonoma / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / pathology


29. Liu WJ, Zhao YP, Zhang TP, Liao Q, Cong L: [Clinical experience in diagnosis and treatment of glucagonoma]. Zhonghua Wai Ke Za Zhi; 2009 Mar 1;47(5):333-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical experience in diagnosis and treatment of glucagonoma].
  • OBJECTIVE: To study the diagnosis and treatment of glucagonoma.
  • METHODS: A retrospective review of glucagonoma cases was committed between June 1993 and July 2008 in Peking Union Medical College Hospital.
  • It was measured by sex, age, misdiagnosis, clinical symptoms, laboratory data, imaging studies, diagnosis, treatment procedures and so on.
  • RESULTS: The tumors of eleven cases were found in the tail, and one case was in the head of the pancreas at the same time.
  • Nine patients had the metastasis out of pancreas and all of them had the liver metastasis.
  • One case was a member of multiple endocrine neoplasia type 1 (MEN-1) syndromes.
  • The glucagon was detected by immunohistochemistry and was positive in five patients.
  • Multimodal treatments included tumor resection, chemoembolization, treated with somatostatin analogues and (or) radionuclides and so on were applied to all patients.
  • CONCLUSIONS: Glucagonoma is a rare pancreatic endocrine tumor.
  • Radical tumor surgery is used as the first choice.
  • [MeSH-major] Glucagonoma / diagnosis. Glucagonoma / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy

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  • (PMID = 19595005.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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30. Appetecchia M, Ferretti E, Carducci M, Izzo F, Carpanese L, Marandino F, Terzoli E: Malignant glucagonoma. New options of treatment. J Exp Clin Cancer Res; 2006 Mar;25(1):135-9
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  • [Title] Malignant glucagonoma. New options of treatment.
  • Few cases of malignant glucagonomas have been described in the literature.
  • In this paper we present a case of a 77-year-old woman with necrolytic migratory erythema and high plasma glucagon and chromogranin A levels caused by a neuroendocrine tumour.
  • An abdominal CT scan suggested a pancreatic lesion and two liver metastases.
  • The patient underwent pancreatic debulking and liver metastasectomy.
  • Histological and immunohistochemical investigations revealed a well differentiated neuroendocrine tumour with vascular invasion and scattered immunopositivity for somatostatin receptors.
  • Three months after surgery symptoms of disease recurred accompanied by hyperglucagonaemia and newly diagnosed liver lesions.
  • The patient was treated with octreotide (30 mg i.m. every 28 days) and interferon-alpha (6 MU s.cc 3 times per week) plus three cycles of hepatic chemoembolisation.
  • The patient is now asymptomatic with persistent hepatic disease and normal serum glucagon levels forty months after primary treatment.
  • So far, only few immunohistochemical studies are reported on malignant glucagonoma and combined treatment schedules.
  • We demonstrated, for the first time, a scattered immunopositivity for somatostatin receptors in a malignant glucagonoma.
  • A combined antiproliferative medical treatment and the hepatic chemoembolization have been able to control tumor growth and disease symptoms for a long time after surgery.
  • [MeSH-major] Glucagonoma / therapy
  • [MeSH-minor] Aged. Chromogranin A. Chromogranins / blood. Female. Glucagon / blood. Humans. Immunohistochemistry. Interferon-alpha / metabolism. Neuroendocrine Tumors / blood. Octreotide / pharmacology. Proglucagon / metabolism. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 16761630.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Interferon-alpha; 55963-74-1 / Proglucagon; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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31. Topham EJ, Child FJ: Exfoliative erythema of malnutrition with zinc and essential amino acid deficiency. Clin Exp Dermatol; 2005 May;30(3):235-7
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  • A similar clinical picture to necrolytic migratory erythema can be seen with zinc deficiency or protein malnutrition, often in patients with alcoholic liver disease, in the absence of glucagonoma.
  • The speed of clinical improvement following zinc replacement therapy, usually within days to weeks, is striking, confirming the clinical diagnosis.

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  • (PMID = 15807677.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acids, Essential; J41CSQ7QDS / Zinc
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32. Zhou C, Dhall D, Nissen NN, Chen CR, Yu R: Homozygous P86S mutation of the human glucagon receptor is associated with hyperglucagonemia, alpha cell hyperplasia, and islet cell tumor. Pancreas; 2009 Nov;38(8):941-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Homozygous P86S mutation of the human glucagon receptor is associated with hyperglucagonemia, alpha cell hyperplasia, and islet cell tumor.
  • OBJECTIVE: The goal of the study was to investigate the genetic and molecular basis of a novel syndrome of marked hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.
  • METHODS: The glucagon receptor (GCGR) gene and the glucagon gene were sequenced in a patient with hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.
  • RESULTS: The glucagon gene sequence was normal, but the GCGR sequencing uncovered a homozygous missense mutation, c.256C>T, p.P86S in the extracellular domain of GCGR.
  • When expressed in human embryonic kidney 293 cells, GCGR P86S localized to the plasma membrane but bound 96% less radiolabeled glucagon than WT GCGR.
  • The median effective concentration of glucagon-induced cyclic adenosine monophosphate production was 24 nmol/L for GCGR P86S but 2.4 nmol/L for WT GCGR.
  • The patient's alpha cells also express glucagonlike peptide 1 and pancreatic polypeptide.
  • CONCLUSIONS: We hereby report the first homozygous missense mutation in the human GCGR, which is associated with alpha cell hyperplasia and hyperglucagonemia.
  • This mutation lowers the receptor's affinity to glucagon and decreases cyclic adenosine monophosphate production with physiological concentrations of glucagon.
  • Thus, the P86S mutation in GCGR likely causes alpha cell hyperplasia and hyperglucagonemia.

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  • (PMID = 19657311.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK071870-04; United States / NIDDK NIH HHS / DK / K08 DK071870; United States / NIDDK NIH HHS / DK / DK071870; United States / NIDDK NIH HHS / DK / K08 DK071870-04
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Glucagon; 147336-22-9 / Green Fluorescent Proteins; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ NIHMS139678; NLM/ PMC2767399
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33. Ruiz-Tovar J, Priego P, Martínez-Molina E, Morales V, Sanjuanbenito A, Lobo E: Pancreatic neuroendocrine tumours. Clin Transl Oncol; 2008 Aug;10(8):493-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic neuroendocrine tumours.
  • INTRODUCTION: Pancreatic neuroendocrine tumours (PNT) are infrequent epithelial neoplasms associated with a better outcome than pancreatic adenocarcinoma.
  • There were 28 insulinomas, eight glucagonomas, three gastrinomas, one VIPoma and one carcinoid.
  • Enucleation was performed in 20 patients, distal pancreatectomy in 16, middle pancreatic resection in four, cephalic pancreatoduodenectomy in two and total pancreatoduodenectomy in one.
  • In six patients, the tumour was not resected.
  • RESULTS: Postoperative complication rate was 22%: six pancreatic fistulas, three intra-abdominal collections, one remnant pancreatitis and one pancreatic pseudocyst.
  • Five patients presented recurrences: three liver metastases and two pancreatic recurrences.
  • CONCLUSION: Conservative surgery of the pancreas is preferred, but aggressive surgery is indicated when the primary tumour can be controlled.
  • Despite of minimising pancreatic resection, there is a high complication rate, mainly pancreatic fistulas, though they can often be conservatively managed.
  • [MeSH-major] Neuroendocrine Tumors / mortality. Pancreatic Neoplasms / mortality
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Gastrinoma / pathology. Gastrinoma / surgery. Glucagonoma / pathology. Glucagonoma / surgery. Humans. Insulinoma / pathology. Insulinoma / surgery. Male. Middle Aged. Neoplasm Staging. Pancreatic Fistula / pathology. Pancreatic Fistula / surgery. Pancreaticoduodenectomy. Prognosis. Retrospective Studies. Survival Rate. Treatment Outcome. Vipoma / pathology. Vipoma / surgery

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  • (PMID = 18667380.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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34. Molino C, Fabbian F, Russo G, Cantelli S, Bortot A, Galdi A, Catizone L: [MEN type 1 and chronic renal failure: a rarely reported association]. G Ital Nefrol; 2007 Jan-Feb;24(1):79-82
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  • BACKGROUND: Multiple endocrine neoplasia type 1 (MEN 1), or Wermer's syndrome, is a rare autosomal dominant genetic syndrome characterized by tumors or hyperplasia involving the pituitary, parathyroid, and pancreatic islet cells.
  • Association between MEN 1 and nephrocalcinosis is well known, though data published in medical literature regarding Wermer's syndrome and chronic renal failure relation are still rare.
  • CASE: A 70-year-old Caucasian female patient had a history of primitive hyperparathyroidism, prolactinoma, glucagonoma, adrenal adenoma and pulmonary neuroendocrine neoplasia.
  • CONCLUSIONS: Although the association between renal failure and MEN 1 is rarely reported, patients affected by Wermer's syndrome have several risk factors of decreasing renal function such as hypertension, nephrolithiasis and diabetes mellitus.

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  • (PMID = 17342698.001).
  • [ISSN] 0393-5590
  • [Journal-full-title] Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia
  • [ISO-abbreviation] G Ital Nefrol
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
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35. Diaz AG, Lucas S, Ferraina P, Ferraro A, Puchulu F, Paes De Lima A, Maselli Mdel C, Gomez RM, Bruno OD: [Clinical experience in 37 cases of insulinoma]. Medicina (B Aires); 2006;66(6):499-504
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  • [Transliterated title] Experiencia clinica sobre 37 casos de insulinoma.
  • Insulinoma is the most frequent pancreatic islet cell tumor.
  • Diagnosis is established through demonstration of inappropriately elevated insulin serum concentrations in the presence of hypoglycemia.
  • Mean duration of symptoms before diagnosis was 2.7 +/- 2 years.
  • In 22 patients, a solitary tumor was excised (61.1%).
  • In 3 patients another tumour (glucagonoma) was found (1 of them with MEN 1).
  • [MeSH-major] Insulinoma. Pancreatic Neoplasms

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  • (PMID = 17240619.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin
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36. Virgolini I, Traub-Weidinger T, Decristoforo C: Nuclear medicine in the detection and management of pancreatic islet-cell tumours. Best Pract Res Clin Endocrinol Metab; 2005 Jun;19(2):213-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear medicine in the detection and management of pancreatic islet-cell tumours.
  • Over the last decade somatostatin receptor scintigraphy using various derivatives of long-acting somatostatin analogues has gained its place in the management of pancreatic islet-cell tumours.
  • Scintigraphy is based on the high-affinity binding of such somatostatin analogues to receptors over-expressed by these tumour types.
  • Following the introduction of (111)In-DTPA-D-Phe(1)-octreotide, clinical studies with radiolabelled DOTA-Tyr(3)-octreotide and DOTA-Tyr(3)-octreotate derivatives have shown considerable improvement of imaging results with increased tumour uptake.
  • One of the newer developments, (68)Ga-labelled DOTA-Tyr(3)-octreotide, has shown promising results in patients with pancreatic islet-cell tumours, based on the high-affinity binding to the somatostatin receptor subtype 2 in combination with positron emission tomography (PET) technology.
  • Other peptides--such as ligands for the gastrin/CCK2 receptors or vasoactive intestinal peptide (VIP)--have also been studied for imaging pancreatic cell tumours.
  • Whereas small-sized gastrinoma, somatostatinoma, glucagonoma, carcinoid and VIPoma are frequently detected by somatostatin receptor scintigraphy, insulinoma may escape detection due to reduced receptor expression.
  • When labelled with (90)Y or (177)Lu, some somatostatin analogues have been applied to patients in advanced stages of the disease.
  • [MeSH-major] Adenoma, Islet Cell / radionuclide imaging. Adenoma, Islet Cell / radiotherapy. Islets of Langerhans / radionuclide imaging. Pancreatic Neoplasms / radionuclide imaging. Pancreatic Neoplasms / radiotherapy

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  • (PMID = 15763696.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 51110-01-1 / Somatostatin
  • [Number-of-references] 56
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37. Berković MC, Altabas V, Herman D, Hrabar D, Goldoni V, Vizner B, Zjacić-Rotkvić V: A single-centre experience with octreotide in the treatment of different hypersecretory syndromes in patients with functional gastroenteropancreatic neuroendocrine tumors. Coll Antropol; 2007 Jun;31(2):531-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A single-centre experience with octreotide in the treatment of different hypersecretory syndromes in patients with functional gastroenteropancreatic neuroendocrine tumors.
  • The aim of this research was to assess the clinical and biochemical efficacy of the octreotide in the treatment of patients with various functional gastroenteropancreatic neuroendocrine tumors (GEP-NETs).
  • They were diagnosed with VIPoma, glucagonoma, gastrinoma, medullary thyroid carcinoma (solitary and as a part of MEN-II syndrome), pancreatic carcinoids (solitary and as a part of multiple endocrine neoplasia type-1 syndrome-MEN-1 syndrome) and midgut carcinoids.
  • The patients presented with Verner-Morrison, glucagonoma, Zollinger Ellison and carcinoid syndrome respectively.
  • All had a metastatic disease at the time of diagnosis and a positive octreoscan finding.
  • The results prove octreotide to be effective in reducing symptoms and biochemical markers associated with hypersecretory syndromes of GEP-NETs.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Neuroendocrine Tumors / drug therapy. Octreotide / therapeutic use. Pancreatic Neoplasms / drug therapy. Stomach Neoplasms / drug therapy. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Biomarkers, Tumor. Female. Humans. Male. Malignant Carcinoid Syndrome / drug therapy. Middle Aged. Treatment Outcome

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  • (PMID = 17847934.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; RWM8CCW8GP / Octreotide
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38. Lepage C, Rachet B, Coleman MP: Survival from malignant digestive endocrine tumors in England and Wales: a population-based study. Gastroenterology; 2007 Mar;132(3):899-904

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival from malignant digestive endocrine tumors in England and Wales: a population-based study.
  • BACKGROUND AND AIMS: Little is known about the prognosis of patients with malignant digestive endocrine tumors (MDETs), primarily because of their rarity.
  • METHODS: Survival from these tumors has been evaluated in a large, well-defined, national population.
  • Relative survival was estimated and the impact of age, sex, period, histology, and anatomic site modeled.
  • RESULTS: Among 4104 cases of MDETs, 21.2% were small cell tumors.
  • Five-year survival was 56.8% for well-differentiated tumors but only 5.2% for small cell tumors (P < .0001).
  • Survival was highest for large bowel tumors and lowest for esophageal tumors.
  • Among well-differentiated pancreatic tumors, 5-year relative survival was 49.2% for insulinomas, 39.9% for gastrinomas, 17.1% for glucagonomas, 26.3% for carcinoid tumors, and 29.3% for nonfunctioning tumors.
  • Gender, age at diagnosis, and anatomic site were independent prognostic factors.
  • Prognosis varies with tumor differentiation, anatomic site, and histologic type.
  • Early diagnosis is difficult; new therapeutic options appear to represent the best approach to improved prognosis.
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Age Factors. Aged. Aged, 80 and over. Cell Differentiation. England / epidemiology. Female. Follow-Up Studies. Humans. Incidence. Male. Middle Aged. Population Surveillance. Prognosis. Proportional Hazards Models. Registries / statistics & numerical data. Risk Assessment. Risk Factors. Sex Distribution. Sex Factors. Survival Analysis. Time Factors. Wales / epidemiology

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  • (PMID = 17383419.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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39. Krysiak R, Okopień B, Herman ZS: [Rare pancreatic endocrine tumors]. Przegl Lek; 2008;65(4):209-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Rare pancreatic endocrine tumors].
  • [Transliterated title] Rzadkie guzy endokrynne trzustki.
  • Functional pancreatic endocrine tumors other than gastrinoma and insulinoma are quite rare.
  • Some of these tumors may be part of multiple endocrine neoplasia type one (MEN-1) syndrome or phakomatoses.
  • Depending on their cell type, functional pancreatic endocrine tumors may cause distinct clinical endocrine syndromes, such as the 'glucagonoma syndrome', Verner-Morrison syndrome and the 'somatostatinoma syndrome'.
  • Currently, the only curative treatment for islet cell tumors is complete surgical resection.
  • The medical treatment of endocrine pancreatic tumours consists of somatostatin analogues, chemotherapy, and interferon-alpha.
  • The purpose of this manuscript is to provide an overview of the contemporary etiopathogenesis, diagnosis and treatment of rare pancreatic endocrine tumors.
  • [MeSH-major] Glucagonoma / diagnosis. Glucagonoma / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Somatostatinoma / diagnosis. Somatostatinoma / therapy. Vipoma / diagnosis. Vipoma / therapy
  • [MeSH-minor] Humans. Rare Diseases / diagnosis. Rare Diseases / therapy

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  • (PMID = 18724549.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 47
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40. Nakashima H, Komine M, Sasaki K, Mitsui H, Fujimoto M, Ihn H, Asahina A, Kikuchi K, Tamaki K: Necrolytic migratory erythema without glucagonoma in a patient with short bowel syndrome. J Dermatol; 2006 Aug;33(8):557-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Necrolytic migratory erythema without glucagonoma in a patient with short bowel syndrome.
  • While it is typically associated with glucagonoma, some cases of NME without glucagonoma have been reported.
  • Her laboratory data revealed essential amino acid deficiency and a slightly decreased serum zinc level, while her plasma glucagon level was low.
  • With diagnosis of non-glucagonoma-associated NME with malabsorption due to short-bowel syndrome, she was treated and improved by i.v. amino acid supplement.
  • Histological findings of NME include necrotic changes of keratinocytes in the upper epidermis, proliferation of those in the lower epidermis and inflammatory cell infiltration of upper dermis.
  • [MeSH-major] Erythema / etiology. Short Bowel Syndrome / complications
  • [MeSH-minor] Cell Differentiation. Cell Proliferation. Female. Humans. Keratinocytes / pathology. Keratinocytes / physiology. Keratins / metabolism. Middle Aged


41. Mizuno T, Hiraoka H, Yoshioka C, Takeda Y, Matsukane Y, Shimoyama N, Morimoto M, Hayashi T, Okuda M: Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog. Vet Dermatol; 2009 Feb;20(1):72-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog.
  • Based on histopathological findings, blood examinations and necropsy findings, the condition was diagnosed as superficial necrolytic dermatitis associated with a glucagon-secreting extrapancreatic neuroendocrine tumour.
  • Gross necropsy revealed tumour invasion into the spleen, liver, adrenal glands and mesenteric lymph nodes.
  • Immunohistochemical analysis of the neoplastic cells revealed that the tumour was a glucagonoma, consistent with earlier findings of persistent glucagonaemia and hypoaminoacidaemia.
  • [MeSH-major] Dermatitis / veterinary. Dog Diseases / pathology. Glucagonoma / veterinary

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  • (PMID = 19152590.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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42. Nishiuchi T, Imachi H, Murao K, Fujiwara M, Muraoka T, Kikuchi F, Nishiuchi Y, Kushida Y, Haba R, Ishida T: Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1). Endocrine; 2009 Aug;36(1):20-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1).
  • Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by tumors of the parathyroid glands, the anterior pituitary, and the endocrine pancreas.
  • He was admitted to our hospital because of recurrent hypoglycemia and a growth of pancreatic tumors.
  • He subsequently underwent surgery for the pancreatic tumors.
  • The majority of these tumor cells were immunohistochemically positive for insulin and negative for glucagon.
  • A few nodules showed immunohistochemical staining positivity for glucagon but they were negative for insulin.
  • Although it is uncommon for patients with MEN1 to exhibit insulinoma and glucagonoma, this case suggests the need for careful analysis of pancreatic tumors in patients with MEN1.
  • [MeSH-major] Glucagonoma / pathology. Insulinoma / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / pathology


43. Gutiérrez V, Cobo M, Olea D, García J, Ramírez C, Bautista D, Alcalde J: Glucagonoma with two pancreatic masses and pulmonary metastases as debut of MEN-1. Clin Transl Oncol; 2007 Oct;9(10):674-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma with two pancreatic masses and pulmonary metastases as debut of MEN-1.
  • This is a rare case of a patient with type 1 multiple endocrine neoplasia (MEN-1) syndrome.
  • The case is further unusual in that the glucagonoma debuted with two synchronic pancreatic masses at the time of diagnosis and with pulmonary metastases as the primary site of metastasis and not the more usual site of the liver.
  • [MeSH-major] Glucagonoma / diagnostic imaging. Lung Neoplasms / diagnostic imaging. Multiple Endocrine Neoplasia Type 1 / diagnostic imaging. Pancreatic Neoplasms / diagnostic imaging

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  • (PMID = 17974529.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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44. Radny P, Eigentler TK, Soennichsen K, Overkamp D, Raab HR, Viebahn R, Mueller-Horvart C, Sotlar K, Rassner G: Metastatic glucagonoma: treatment with liver transplantation. J Am Acad Dermatol; 2006 Feb;54(2):344-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic glucagonoma: treatment with liver transplantation.
  • Glucagonoma is a rare pancreatic endocrine tumor that is often both well developed and malignant at detection.
  • We hope to familiarize dermatologists and other specialists with this rare and potentially fatal disorder because early recognition of necrolytic migratory erythema, a clinical feature that may appear in patients with glucagonoma, can lead to possible cure, whereas delayed identification of the disease is associated with metastatic disease and a poor prognosis.
  • We report the case of a 57-year-old patient with a metastatic glucagon-producing tumor; necrolytic migratory erythema was diagnosed and was successfully treated by a multimodal intervention including liver transplantation.
  • Currently, 72 months after transplantation, our patient is in complete remission, which has been verified by somatostatin receptor scintigraphy monitoring, computed tomographic scanning and glucagon serum control.
  • Increased awareness of the clinical symptoms and visible polymorphic mucocutaneous and nonspecific histopathologic features of glucagonoma syndrome is needed to avoid unnecessary delay in the diagnosis of this syndrome.
  • [MeSH-major] Glucagonoma / secondary. Glucagonoma / surgery. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Liver Transplantation. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Glucagon / blood. Humans. Immunohistochemistry. Male. Middle Aged. Octreotide / administration & dosage. Pancreatectomy. Receptors, Somatostatin / metabolism. Splenectomy


45. Obi N, Katabami T, Obi R, Odanaka M, Sasano K, Tanaka Y: Primary malignant hepatic glucagonoma: an autopsy case. Endocr J; 2009;56(5):715-9
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  • [Title] Primary malignant hepatic glucagonoma: an autopsy case.
  • She displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (NME), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml).
  • Thus, we suspected a glucagonoma causing secondary diabetes.
  • However, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma.
  • At autopsy, the only tumor detected was the liver mass.
  • This was a large solid tumor (8 x 6 x 5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe.
  • Based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases.
  • Since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver.
  • [MeSH-major] Diabetes Mellitus, Type 2 / etiology. Glucagonoma / pathology. Liver Neoplasms / pathology

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  • (PMID = 19367016.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amino Acids
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46. Cheshire H, Stather P, Vorster J: Acquired acrodermatitis enteropathica due to zinc deficiency in a patient with pre-existing Darier's disease. J Dermatol Case Rep; 2009 Nov 28;3(3):41-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired acrodermatitis enteropathica due to zinc deficiency in a patient with pre-existing Darier's disease.
  • Typically these patches start near the body's orifices before migrating to other sites, however in this patient the presentation was atypical thus delaying the diagnosis.
  • OBSERVATIONS: We report a case of an atypical presentation of acrodermatitis enteropathica (AE) due to acquired zinc deficiency in a 65 year old female patient with a previous diagnosis of histologically confirmed Darier's disease.
  • Acrodermatitis enteropathica typically presents in infants, either due to an autosomal recessive genetic disorder, or after the cessation of breast feeding.
  • In adults acquired zinc deficiency can be caused by glucagonoma syndrome, poor nutritional state, intestinal malabsorption, nephrotic syndrome and after major trauma (i.e. burns or significant surgery).
  • In our patient low zinc levels confirmed hypozincaemia and the diagnosis of acrodermatitis enteropathica.
  • CONCLUSION: We believe this to be an unusual presentation of acrodermatitis enteropathica due to a probable dietary zinc deficiency in a lady with pre-existing Darier's disease which may possibly have influenced the uncharacteristic clinical presentation.

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  • (PMID = 21886729.001).
  • [ISSN] 1898-7249
  • [Journal-full-title] Journal of dermatological case reports
  • [ISO-abbreviation] J Dermatol Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Other-IDs] NLM/ PMC3157796
  • [Keywords] NOTNLM ; Darier's disease / acrodermatitis enteropathica / hair loss / mucous membranes / zinc
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47. Vanderlan WB, Zhang Z, Abouljoud MS: Duodenal enteroglucagonoma revealed by differential comparison of serum and tissue glucagon reactivity with Siemens' Double Glucagon Antibody and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon: a case report. J Med Case Rep; 2010;4:178

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Duodenal enteroglucagonoma revealed by differential comparison of serum and tissue glucagon reactivity with Siemens' Double Glucagon Antibody and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon: a case report.
  • INTRODUCTION: This case report demonstrates that the differential immunohistochemical reactivities of Siemens' Double Antibody Glucagon compared to DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon allow for pathologic distinction of enteral versus pancreatic glucagonoma.
  • He had a low serum glucagon level using Siemens' Double Antibody Glucagon, a clinical syndrome consistent with glucagon hypersecretion.
  • A periampullary mass biopsy proved to be a neuroendocrine tumor, with positive immunohistochemical reactivity to DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon.
  • CONCLUSIONS: Differential comparison of the immunohistochemical reactivities of Siemens' Double Antibody Glucagon and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon discerns enteroglucagon from pancreatic glucagon.

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  • (PMID = 20550685.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2896376
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48. Lu J, Herrera PL, Carreira C, Bonnavion R, Seigne C, Calender A, Bertolino P, Zhang CX: Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development. Gastroenterology; 2010 May;138(5):1954-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development.
  • BACKGROUND & AIMS: The tumor suppressor menin is recognized as a key regulator of pancreatic islet development, proliferation, and beta-cell function, whereas its role in alpha cells remains poorly understood.
  • The purpose of the current study was to address this issue in relation to islet tumor histogenesis.
  • METHODS: We generated alpha cell-specific Men1 mutant mice with Cre/loxP technology and carried out analyses of pancreatic lesions developed in the mutant mice during aging.
  • RESULTS: We showed that, despite the alpha-cell specificity of the GluCre transgene, both glucagonomas and a large amount of insulinomas developed in mutant mice older than 6 months, accompanied by mixed islet tumors.
  • Interestingly, the cells sharing characteristics of both alpha and beta cells were identified shortly after the appearance of menin-deficient alpha cells but well before the tumor onset.
  • Using a genetic cell lineage tracing analysis, we demonstrated that insulinoma cells were directly derived from transdifferentiating glucagon-expressing cells.
  • CONCLUSIONS: Our work shows cell transdifferentiation as a novel mechanism involved in islet tumor development and provides evidence showing that menin regulates the plasticity of differentiated pancreatic alpha cells in vivo, shedding new light on the mechanisms of islet tumorigenesis.
  • [MeSH-major] Cell Transdifferentiation. Cell Transformation, Neoplastic / metabolism. Glucagon / metabolism. Glucagon-Secreting Cells / metabolism. Glucagonoma / metabolism. Insulinoma / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins / deficiency
  • [MeSH-minor] Age Factors. Aging / metabolism. Aging / pathology. Animals. Biomarkers / metabolism. Cell Fusion. Cell Lineage. Cell Proliferation. Gene Deletion. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genotype. Insulin / metabolism. Insulin-Secreting Cells / metabolism. Insulin-Secreting Cells / pathology. Mice. Mice, Knockout. Phenotype. Transcription Factors / metabolism


49. Pierce RA, Spitler JA, Hawkins WG, Strasberg SM, Linehan DC, Halpin VJ, Eagon JC, Brunt LM, Frisella MM, Matthews BD: Outcomes analysis of laparoscopic resection of pancreatic neoplasms. Surg Endosc; 2007 Apr;21(4):579-86
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  • [Title] Outcomes analysis of laparoscopic resection of pancreatic neoplasms.
  • BACKGROUND: Experience with laparoscopic resection of pancreatic neoplasms remains limited.
  • The purpose of this study is to critically analyze the indications for and outcomes after laparoscopic resection of pancreatic neoplasms.
  • METHODS: The medical records of all patients undergoing laparoscopic resection of pancreatic neoplasms from July 2000 to February 2006 were reviewed.
  • RESULTS: Laparoscopic pancreatic resection was performed in 22 patients (M:F, 8:14) with a mean age of 56.3 +/- 15.1 years and mean body mass index (BMI) of 26.3 +/- 4.5 kg/m2.
  • Indications for pancreatic resection were cyst (1), glucagonoma (1), gastrinoma (2), insulinoma (3), metastatic tumor (2), IPMT (4), nonfunctioning neuroendocrine tumor (3), and mucinous/serous cystadenoma (6).
  • Mean tumor size was 2.4 +/- 1.6 cm.
  • Seven patients experienced a total of ten postoperative complications, including a urinary tract infection (UTI) (1), lower-extremity deep venous thrombosis (DVT) and pulmonary embolus (1), infected peripancreatic fluid collection (1), pancreatic pseudocyst (1), and pancreatic fistula (6).
  • Five pancreatic fistulas were managed by percutaneous drainage.
  • The reoperation rate was 4.5% and the overall pancreatic-related complication rate was 36.4%.
  • One patient developed pancreatitis and a pseudocyst 5 months postoperatively, which was managed successfully with a pancreatic duct stent.
  • CONCLUSIONS: Laparoscopic pancreatic resection is safe and feasible in selected patients with pancreatic neoplasms.
  • With a pancreatic duct leak rate of 27%, this problem remains an area of development for the minimally invasive technique.
  • [MeSH-major] Laparoscopy / methods. Pancreatectomy / methods. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Postoperative Complications / epidemiology

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  • (PMID = 17180287.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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50. 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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51. 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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  • 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.
  • Somatostatin receptors expression by immunohistochemistry with somatostatin receptor types 1-5 antibodies in tissue paraffin sections were studied and correlated with the histological diagnosis according to the WHO classification, location and functional status.
  • 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 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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52. Davies K, Conlon KC: Neuroendocrine tumors of the pancreas. Curr Gastroenterol Rep; 2009 Apr;11(2):119-27
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  • [Title] Neuroendocrine tumors of the pancreas.
  • Pancreatic endocrine tumors are rare neoplasms accounting for less than 5% of pancreatic malignancies.
  • They are broadly classified into either functioning tumors (insulinomas, gastrinomas, glucagonomas, VIPomas, and somatostatinomas) or nonfunctioning tumors.
  • The diagnosis of these tumors is difficult and requires a careful history and examination combined with laboratory tests and radiologic imaging.
  • Signs and symptoms are usually related to hormone hypersecretion in the case of functioning tumors and to tumor size or metastases with nonfunctioning tumors.
  • Surgical resection remains the treatment of choice even in the face of metastatic disease.
  • Further development of novel diagnostic and treatment modalities offers potential to greatly improve quality of life and prolong disease-free survival for patients with pancreatic endocrine tumors.
  • [MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms
  • [MeSH-minor] Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Catheter Ablation. Chemoembolization, Therapeutic / methods. Evidence-Based Medicine. Gastrins / secretion. Glucagon / secretion. Humans. Insulin / secretion. Quality of Life. Somatostatin / secretion. Survival Analysis. Treatment Outcome

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  • (PMID = 19281699.001).
  • [ISSN] 1534-312X
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins; 0 / Insulin; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon
  • [Number-of-references] 44
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53. Dadan J, Wojskowicz P, Wojskowicz A: Neuroendocrine tumors of the pancreas. Wiad Lek; 2008;61(1-3):43-7
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  • [Title] Neuroendocrine tumors of the pancreas.
  • The neuroendocrine tumors (NET) of the pancreas are very rare lesions with frequency of about 3 to 10 per 1 000 000 inhabitants.
  • The neuroendocrine tumors composes a heterogeneous group of tumors.
  • The gastro-entero-pancreatic tumors (GEP) constitute 70% of all NET and 2% of all digestive system tumors.
  • There have been several attempts to classify those lesions and since 2000 exists WHO classification which divides NET according to malignancy and histologic structure.
  • The most often NET of the pancreas are insulinoma, gastrinoma, glucagonoma, somatostatinoma, VIPoma.
  • There is a recommendation to assay hormonal activity, measure concentration of specific peptides, biogenic amines and hormones produced by NET cells to establish diagnosis.
  • Those tests are useful in monitoring treatment and in prognostication course of the disease.
  • Imaging methods especially useful in localization GEP-NET are: ultrasound (US), endoscopic ultrasound (EUS), somatostatin receptor scintigraphy (SRS), computer tomography (CT), magnetic resonance (MR) and angiography.
  • The most sensitive method in preoperative diagnosis seems to be EUS or less accessible intra ductal ultrasonography (IDUS).
  • Surgical treatment depends on progression of disease as well as on localization of tumor and consists in both radical methods and palliative operations.
  • Although NET of pancreas are very rare. they are still important diagnostic and therapeutic problem and requires interdisciplinary co-operation.
  • The neuroendocrine tumors should be treated in centers with highest rank of references.
  • [MeSH-major] Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Gastrinoma / diagnosis. Gastrinoma / metabolism. Gastrinoma / therapy. Glucagonoma / diagnosis. Glucagonoma / metabolism. Glucagonoma / therapy. Humans. Insulinoma / diagnosis. Insulinoma / metabolism. Insulinoma / therapy. Somatostatinoma / diagnosis. Somatostatinoma / metabolism. Somatostatinoma / therapy. Vipoma / diagnosis. Vipoma / metabolism. Vipoma / therapy

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  • (PMID = 18717042.001).
  • [ISSN] 0043-5147
  • [Journal-full-title] Wiadomości lekarskie (Warsaw, Poland : 1960)
  • [ISO-abbreviation] Wiad. Lek.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 30
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54. Wang HW, Breslin MB, Lan MS: Pdx-1 modulates histone H4 acetylation and insulin gene expression in terminally differentiated alpha-TC-1 cells. Pancreas; 2007 Mar;34(2):248-53
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  • [Title] Pdx-1 modulates histone H4 acetylation and insulin gene expression in terminally differentiated alpha-TC-1 cells.
  • OBJECTIVES: Islet-associated transcription factors play a critical role in regulating pancreatic endocrine cell differentiation and islet hormone gene expression.
  • Both alpha- and beta-cells differentiate from a common endocrine precursor cell.
  • Therefore, it is important to reveal the differential gene expression profiles between alpha- and beta-cells that can direct their terminal cell fates. alpha-TC-1 and beta-TC-1 are 2 terminally differentiated islet tumor cell lines derived from islets transformed by promoter-specific driven SV40 T antigen overexpression.
  • In this study, we demonstrated that Pdx-1 is a potent transcriptional regulator of endogenous insulin gene expression in alpha-TC-1 cells.
  • RESULTS: Differential transcription factor expression profiles of alpha-TC-1 and beta-TC-1 cells revealed that INSM-1 and Pdx-1 transcription factors were expressed exclusively in beta-TC-1 cells.
  • Overexpression of Ad-Pdx-1 in alpha-TC-1 cells induced insulin gene expression.
  • Chromatin immunoprecipitation assays in Ad-Pdx-1 alpha-TC-1 cells demonstrated Pdx-1 occupancy and the hyperacetylation of histone H4 in the insulin promoter region.
  • CONCLUSIONS: Collectively, these experiments revealed that Pdx-1 is a potent transcriptional regulator that is capable of modulating histone H4 acetylation and activates the insulin gene in a terminally differentiated glucagonoma cell line.
  • [MeSH-major] Glucagon-Secreting Cells / physiology. Histones / metabolism. Homeodomain Proteins / metabolism. Insulin / genetics. Insulin-Secreting Cells / physiology. Trans-Activators / metabolism
  • [MeSH-minor] Acetylation. Animals. Cell Differentiation. Cell Line, Tumor. Gene Expression / physiology. Mice. Mice, Transgenic. Pancreatic Neoplasms. Polymerase Chain Reaction. Promoter Regions, Genetic / physiology. Transcription Factors / genetics. Transcription, Genetic / physiology

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  • (PMID = 17312465.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK061436
  • [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 / Histones; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Trans-Activators; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein
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55. Gauthier BR, Gosmain Y, Mamin A, Philippe J: The beta-cell specific transcription factor Nkx6.1 inhibits glucagon gene transcription by interfering with Pax6. Biochem J; 2007 May 1;403(3):593-601
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  • [Title] The beta-cell specific transcription factor Nkx6.1 inhibits glucagon gene transcription by interfering with Pax6.
  • The transcription factor Nkx6.1 is required for the establishment of functional insulin-producing beta-cells in the endocrine pancreas.
  • Overexpression of Nkx6.1 has been shown to inhibit glucagon gene expression while favouring insulin gene activation.
  • Down-regulation resulted in the opposite effect, suggesting that absence of Nkx6.1 favours glucagon gene expression.
  • To understand the mechanism by which Nkx6.1 suppresses glucagon gene expression, we studied its effect on the glucagon gene promoter activity in non-islet cells using transient transfections and gel-shift analyses.
  • In glucagonoma cells transfected with an Nkx6.1-encoding vector, the glucagon promoter activity was reduced by 65%.
  • In BHK21 cells, Nkx6.1 inhibited by 93% Pax6-mediated activation of the glucagon promoter, whereas Cdx2/3 and Maf stimulations were unaltered.
  • Mutagenesis of the three potential AT-rich motifs within the G1 revealed that only the Pax6-binding site preferentially interacted with Nkx6.1.
  • Chromatin immunoprecipitation confirmed interaction of Nkx6.1 with the glucagon promoter and revealed a direct competition for binding between Pax6 and Nkx6.1.
  • A weak physical interaction between Pax6 and Nkx6.1 was detected in vitro and in vivo suggesting that Nkx6.1 predominantly inhibits glucagon gene transcription through G1-binding competition.
  • We suggest that cell-specific expression of the glucagon gene may only proceed when Nkx6.1, in combination with Pdx1 and Pax4, are silenced in early alpha-cell precursors.
  • [MeSH-major] Eye Proteins / antagonists & inhibitors. Glucagon / genetics. Glucagon-Secreting Cells / physiology. Homeodomain Proteins / physiology. Paired Box Transcription Factors / antagonists & inhibitors. Repressor Proteins / antagonists & inhibitors. Transcription, Genetic / drug effects
  • [MeSH-minor] Animals. Cell Line. Cricetinae. Promoter Regions, Genetic / drug effects. RNA, Messenger / antagonists & inhibitors

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  • (PMID = 17263687.001).
  • [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 / Eye Proteins; 0 / Homeodomain Proteins; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / RNA, Messenger; 0 / Repressor Proteins; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ PMC1876377
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56. Jabbour SA: Skin manifestations of hormone-secreting tumors. Dermatol Ther; 2010 Nov-Dec;23(6):643-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Skin manifestations of hormone-secreting tumors.
  • Dermatologists may see some of these skin lesions first, either before the endocrinologist, or even after the internist or specialist has missed the right diagnosis.
  • Because some skin lesions might reflect a life-threatening endocrine or metabolic disorder, identifying the underlying disorder is very important, so that patients can receive corrective rather than symptomatic treatment.
  • In this issue, we will review various hormone-secreting tumors, including pituitary disorders (Cushing's syndrome and acromegaly), hyperthyroidism, glucagonoma, carcinoid syndrome, mastocytosis, and hyperandrogenism.
  • We will focus on clinical manifestations, mainly cutaneous, followed by a brief discussion on how to make the diagnosis of each condition in addition to treatment options.
  • [MeSH-major] Hormones / secretion. Neoplasms / complications. Paraneoplastic Syndromes / etiology. Skin / pathology. Skin Diseases / etiology

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 21054708.001).
  • [ISSN] 1529-8019
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Hormones
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57. Fanelli CG, Porcellati F, Rossetti P, Bolli GB: Glucagon: the effects of its excess and deficiency on insulin action. Nutr Metab Cardiovasc Dis; 2006 Mar;16 Suppl 1:S28-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagon: the effects of its excess and deficiency on insulin action.
  • AIM: To review the role that glucagon plays in physiology, physiopathology and clinical medicine.
  • DATA SYNTHESIS: Glucagon assays employing specific radioimmunoassay (RIA) techniques are now widely used to characterize pathologic conditions where the effect of the excess or deficiency of glucagon on insulin actions might play a role.
  • Glucagon excess counteracts the action of insulin on glucose metabolism by stimulating glycogenolysis and gluconeogenesis.
  • Aside from glucagon excess in association with glucagonoma, glucagon excess is found in several metabolic disturbances.
  • In diabetes mellitus, hyperglycaemia is the consequence of the glycogenolytic and gluconeogenic effects of glucagon excess occurring in the setting of a relative insulin deficiency (i.e.
  • Type 2 diabetes), whereas excess of glucagon and absent insulin levels are typical features of diabetic ketoacidosis.
  • Although plasma glucagon levels of patients with diabetes are usually increased relative to the prevailing plasma glucose concentrations, it is a paradox that in those patients glucagon levels fail to rise when hypoglycaemia develops.
  • Since glucagon release is considered the primary defence against insulin-induced hypoglycaemia, the defective response of glucagon to hypoglycaemia may favour the development of severe hypoglycaemia.
  • Such defective response to hypoglycaemia in diabetes can be regarded as a condition of selective glucagon deficiency the mechanisms of which remain to be elucidated.
  • CONCLUSION: The most common condition associated with glucagon excess or deficiency is diabetes mellitus.
  • Glucagon excess contributes to hyperglycaemia whereas reduced glucagon response to insulin-induced hypoglycaemia promotes severe hypoglycaemia.
  • It is expected that drugs that are able to reduce glucagon secretion in concert with strategies directed to recover glucagon secretion to hypoglycaemia might contribute to improve the overall glycaemic control in diabetes.
  • [MeSH-major] Blood Glucose / metabolism. Diabetes Mellitus, Type 2 / metabolism. Glucagon / deficiency. Glucagon / pharmacology. Insulin / metabolism

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  • (PMID = 16530126.001).
  • [ISSN] 0939-4753
  • [Journal-full-title] Nutrition, metabolism, and cardiovascular diseases : NMCD
  • [ISO-abbreviation] Nutr Metab Cardiovasc Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 9007-92-5 / Glucagon
  • [Number-of-references] 57
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58. Tsimmerman IaS: [Neuroendocrine tumours of pancreas and gastrointestinal tract]. Klin Med (Mosk); 2009;87(12):7-13
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  • [Title] [Neuroendocrine tumours of pancreas and gastrointestinal tract].
  • This paper reviews data on benign and malignant neuroendocrine tumours of pancreas and gastrointestinal tract including insulinoma, glucagonoma, somatostatinoma, gastrinoma, carcinoid syndrome, and multiple endocrine neoplasms.
  • Their origin, prevalence, clinical manifestations, laboratory and instrumental diagnosis, surgical and medicamentous treatment are discussed.
  • [MeSH-major] Gastrointestinal Neoplasms. Neuroendocrine Tumors. Pancreatic Neoplasms
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Diagnosis, Differential. Diagnostic Imaging. Digestive System Surgical Procedures / methods. Humans. Prevalence. Russia / epidemiology

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  • (PMID = 20135878.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 39
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59. Henopp T, Anlauf M, Schmitt A, Schlenger R, Zalatnai A, Couvelard A, Ruszniewski P, Schaps KP, Jonkers YM, Speel EJ, Pellegata NS, Heitz PU, Komminoth P, Perren A, Klöppel G: Glucagon cell adenomatosis: a newly recognized disease of the endocrine pancreas. J Clin Endocrinol Metab; 2009 Jan;94(1):213-7
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  • [Title] Glucagon cell adenomatosis: a newly recognized disease of the endocrine pancreas.
  • BACKGROUND: Glucagon-producing tumors are either solitary neoplasms of the pancreas, occasionally associated with a glucagonoma syndrome, or multiple neoplasms associated with multiple endocrine neoplasia type 1 (MEN1).
  • We observed a previously undescribed multicentric glucagon-producing tumor disease that is not related to MEN1.
  • METHODS: Pancreatic tissue from four patients showing multiple neuroendocrine microadenomas and in two cases also macrotumors were screened for hormones using immunohistochemical and morphometric methods.
  • RESULTS: The pancreatic tissue from the four patients contained more than 870 microadenomas and 10 macrotumors, all of which expressed exclusively glucagon and none of which showed evidence of malignancy.
  • In addition, many islets were unusually large and showed glucagon cell hyperplasia.
  • There was no clinical or molecular evidence of any hereditary tumor disease, and changes in the MEN1 gene were only seen in individual tumors.
  • CONCLUSIONS: The findings are sufficiently distinctive to suggest a new neoplastic disease of the endocrine pancreas that we recommend calling glucagon cell adenomatosis.
  • Clinically, this disease may be an incidental finding, or it may lead to a glucagonoma syndrome.
  • [MeSH-major] Adenoma / pathology. Glucagon / secretion. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Cyclin-Dependent Kinase Inhibitor p27 / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Male. Proto-Oncogene Proteins / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics

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  • (PMID = 18957496.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 9007-92-5 / Glucagon; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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60. Yu R, Nissen NN, Dhall D, Heaney AP: Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature. Pancreas; 2008 May;36(4):428-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature.
  • We report a rare case of nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas.
  • The patient's clinical presentation, diagnosis, treatment, pancreas pathology, and follow-up are reviewed.
  • A 60-year-old patient was incidentally found to harbor a pancreatic mass with markedly elevated glucagon levels but without glucagonoma syndrome.
  • She was initially diagnosed with glucagonoma, and the tumor was resected.
  • Pathological examination demonstrated that the tumor was a nonfunctioning islet cell tumor and revealed nesidioblastosis and hyperplasia of alpha cells and microglucagonoma in the apparently normal surgical margin.
  • No pancreatic tumors recurred 36 months after surgery.
  • This is the third case of alpha-cell nesidioblastosis reported in the English literature.
  • Nesidioblastosis and hyperplasia of alpha cells should be considered in the differential diagnosis of hyperglucagonemia.
  • Somatostatin analog may be used to suppress glucagon secretion in alpha-cell hyperplasia.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Glucagonoma / pathology. Islets of Langerhans / pathology. Nesidioblastosis / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18437091.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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61. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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62. O'Grady HL, Conlon KC: Pancreatic neuroendocrine tumours. Eur J Surg Oncol; 2008 Mar;34(3):324-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic neuroendocrine tumours.
  • Pancreatic neuroendocrine tumours (PET) are rare neoplasms of the pancreas accounting for less than 5% of all primary pancreatic malignancies.
  • Included in this group are insulinomas, gastrinomas, glucagonoma and somatostatinomas.
  • Where a PET is not associated with a clinical syndrome due to hormone oversecretion, it is referred to as a non-functioning PET.
  • Non-functioning PETs are pancreatic tumours with endocrine differentiation but lack a clinical syndrome of hormone hypersecretion.
  • Presentation is related to the mass effect of the tumour with symptoms often non-specific.
  • [MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms
  • [MeSH-minor] Algorithms. Biomarkers, Tumor. Diagnostic Imaging. Humans. Neoplasm Metastasis. Prognosis

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  • (PMID = 17967523.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 74
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63. Stone SP, Buescher LS: Life-threatening paraneoplastic cutaneous syndromes. Clin Dermatol; 2005 May-Jun;23(3):301-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Life-threatening paraneoplastic cutaneous syndromes.
  • Paraneoplastic syndromes are diseases or symptom complexes associated with malignancy, usually internal.
  • In this article, we discuss the link between malignancy and such dermatologic disorders as acanthosis nigricans, acrokeratosis paraneoplastica of Bazex, dermatomyositis, erythema gyratum repens, necrolytic migratory erythema (glucagonoma syndrome), and paraneoplastic pemphigus and discuss, where such information is known, the mechanism by which these paraneoplastic diseases occur.
  • [MeSH-major] Paraneoplastic Syndromes / diagnosis. Skin Diseases / diagnosis
  • [MeSH-minor] Critical Illness. Erythema / diagnosis. Humans. Neoplasms / diagnosis. Pemphigus / diagnosis

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  • (PMID = 15896545.001).
  • [ISSN] 0738-081X
  • [Journal-full-title] Clinics in dermatology
  • [ISO-abbreviation] Clin. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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64. Fenkci SM, Fidan Yaylali G, Sermez Y, Akdam H, Sabir N, Kiraç S: Malign cystic glucagonoma presented with diabetic ketoacidosis: case report with an update. Endocr Relat Cancer; 2005 Jun;12(2):449-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malign cystic glucagonoma presented with diabetic ketoacidosis: case report with an update.
  • A 44-year-old woman was diagnosed with type II diabetes in 1998 and 1 year later she developed necrolytic migratory erythema, which is a specific skin lesion of glucagonoma.
  • During the clinical investigation, a nodular 6 cm mass in the distal pancreatic region and multiple cystic liver metastases were found.
  • She was operated on, and glucagonoma was detected and the long-acting, repeatable, octreotide treatment was started.
  • 3 years after resection of a pancreatic glucagonoma she presented to a hospital emergency department with diabetic ketoacidosis.
  • Despite somatostatin therapy the tumor had expanded in the liver.
  • [MeSH-major] Diabetic Ketoacidosis / diagnosis. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Erythema / complications. Erythema / diagnosis. Female. Humans. Liver Neoplasms / radionuclide imaging. Liver Neoplasms / secondary

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  • (PMID = 15947115.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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65. Chen HW, Chen HW, Su DH, Shun CT, Liu KL: Rare presentation of endocrine pancreatic tumor: a case of diffuse glucagonoma without metastasis and necrolytic migratory erythema. J Formos Med Assoc; 2005 May;104(5):363-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare presentation of endocrine pancreatic tumor: a case of diffuse glucagonoma without metastasis and necrolytic migratory erythema.
  • Glucagonoma is a very rare endocrine pancreatic tumor.
  • At diagnosis, most glucagonomas are malignant and often metastatic.
  • Suspicion of glucagonoma is based on characteristic presentations known as "glucagonoma syndrome".
  • Glucagonoma is often found in the pancreatic body and/or tail and is usually large enough to be localized by computed tomography.
  • We report a case of diffuse glucagonoma necrolytic migratory erythema (NME) in a 45-year-old man with mild diabetes mellitus, mild anemia, and weight loss over 1.5 years.
  • Diffused enlarged pancreas was noted on abdominal ultrasonography incidentally during a routine health check-up.
  • No enlarged lymph node or extrapancreatic tumor mass was found by several imaging studies.
  • Total pancreatectomy was performed, and the pathology revealed glucagon-producing islet cells and intrapancreatic vascular emboli of tumor cells.
  • Presentation of diffuse malignant glucagonoma with tumor emboli but no metastasis or NME is unusual.

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  • (PMID = 15959605.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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66. Pamuklar E, Semelka RC: MR imaging of the pancreas. Magn Reson Imaging Clin N Am; 2005 May;13(2):313-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MR imaging of the pancreas.
  • MR imaging is a valuable tool in the assessment of the full spectrum of pancreatic diseases.
  • MR imaging techniques are sensitive for the evaluation of pancreatic disorders in the following settings:.
  • (1) TI-weighted fat-suppressed and dynamic gadolinium-enhanced SGE imaging for the detection of chronic pancreatitis, ductal adeno-carcinoma, and islet-cell tumors;.
  • (2) T2-weighted fat-suppressed imaging and T2-weighted breath-hold imaging for the detection of islet-cell tumors;and (3) precontrast breath-hold SGE imaging for the detection of acute pancreatitis.
  • Relatively specific morphologic and signal intensity features permit characterization of acute pancreatitis,chronic pancreatitis, ductal adenocarcinoma, insulinoma, gastrinoma, glucagonoma, microcystic cystadenoma, macrocystic cystadenoma, and solid and papillary epithelial neoplasm.
  • MR imaging is effective as a problem-solving modality because it distinguishes chronic pancreatitis from normal pancreas and chronic pancreatitis with focal enlargement from pancreatic cancer in the majority of cases.MR imaging studies should be considered in the following settings:.
  • (2) in patients with prior CT imaging who have focal enlargement of the pancreas with no definable mass;.
  • (3) in patients in whom clinical history is worrisome for malignancy and in whom findings on CT imaging are equivocal or difficult to interpret; and (4) in situations requiring distinction between chronic pancreatitis with focal enlargement and pancreatic cancer.
  • Patients with biochemical evidence of islet-cell tumors should be examined by MR imaging as the first-line imaging modality because of the high sensitivity of MR imaging for detecting the presence of islet-cell tumors and determining the presence of metastatic disease.
  • [MeSH-major] Magnetic Resonance Imaging / methods. Pancreatic Diseases / diagnosis
  • [MeSH-minor] Contrast Media. Diagnosis, Differential. Humans. Image Enhancement / methods. Neoplasms, Glandular and Epithelial / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / secondary. Tomography, X-Ray Computed

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  • (PMID = 15935314.001).
  • [ISSN] 1064-9689
  • [Journal-full-title] Magnetic resonance imaging clinics of North America
  • [ISO-abbreviation] Magn Reson Imaging Clin N Am
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 56
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67. Lackner C, Dlaska D, Fuchsbichler A, Stumptner C, Gogg-Kamerer M, Zatloukal K, Denk H: p62 protein is expressed in pancreatic beta cells. J Pathol; 2005 Aug;206(4):402-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p62 protein is expressed in pancreatic beta cells.
  • Furthermore, p62 has recently been detected as a component of intracytoplasmic protein aggregates (inclusion bodies), which are hallmarks of a variety of chronic degenerative disorders, such as Parkinson's disease and Alzheimer's disease, but also of steatohepatitis.
  • Here we report that p62 and insulin are co-expressed in a diffuse fashion in beta cells in normal human pancreas as well as in primary chronic pancreatitis and in normal pancreas from mouse and swine.
  • In contrast, p62 protein is absent from, or only focally and very weakly expressed in, insulinomas, glucagonomas or non-functioning pancreatic neuroendocrine tumours or carcinomas that express insulin or other pancreatic as well as extrapancreatic hormones.
  • Although the biological function of p62 in beta cells is unknown, the co-expression of p62 and insulin in non-neoplastic beta cells suggests that, in the beta cell, p62 may play a role in specific insulin-related signalling.
  • Since p62 may also be involved in pro-apototic signal transduction, the loss of p62 expression in neuroendocrine neoplasms of the pancreas may render the tumour cells less sensitive to pro-apototic signals.
  • Further research is necessary to elucidate the role of p62 in beta cell-specific signal transduction.
  • [MeSH-minor] Animals. Antibodies, Neoplasm / immunology. Carcinoma, Neuroendocrine / chemistry. Carcinoma, Neuroendocrine / genetics. Chronic Disease. Cross Reactions / immunology. Female. Gene Expression / genetics. Glucagonoma / chemistry. Glucagonoma / genetics. Humans. Immunohistochemistry / methods. Insulinoma / chemistry. Insulinoma / genetics. Male. Mice. Pancreatic Neoplasms / chemistry. Pancreatic Neoplasms / genetics. Swine

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  • [Copyright] Copyright 2005 Pathological Society of Great Britain and Ireland
  • (PMID = 15926199.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibodies, Neoplasm; 0 / SQSTM1 protein, human
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68. Fendrich V, Bartsch DK: [Diagnosis and surgical management of neureondocrine pancreatic tumours]. Zentralbl Chir; 2010 Jun;135(3):210-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnosis and surgical management of neureondocrine pancreatic tumours].
  • [Transliterated title] Diagnostik und operative Therapie des Gastrinoms, Vipoms, Glukagonoms, Somatostatinoms und nichtfunktioneller endokriner Pankreastumoren.
  • The only chance of cure for patients with pancreatic endocrine tumours (PETs) is complete surgical removal not only of the primary tumour, but also of local or distant metastases.
  • This is true for gastrinomas, vipomas, glucagonomas, somatostatinomas and non-functional pancreatic endocrine tumours.
  • [MeSH-major] Hyperinsulinism / surgery. Insulinoma / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Laparoscopy. Lymph Node Excision. Male. Middle Aged. Minimally Invasive Surgical Procedures. Neoplasm Staging. Pancreas / pathology. Pancreas / surgery. Young Adult

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  • [Copyright] Georg Thieme Verlag Stuttgart, New York.
  • (PMID = 20549584.001).
  • [ISSN] 1438-9592
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
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69. Kitamura Y, Sato M, Hatamochi A, Yamazaki S: Necrolytic migratory erythema without glucagonoma associated with hepatitis B. Eur J Dermatol; 2005 Jan-Feb;15(1):49-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Necrolytic migratory erythema without glucagonoma associated with hepatitis B.
  • We report a case of necrolytic migratory erythema (NME) without glucagonoma associated with hepatitis B.
  • Although the most common cause of NME is a glucagon-secreting alpha-islet cell tumor of the pancreas, a dermatitis clinically and histologicaly identical to NME has been described in patients without glucagonoma.
  • We added some discussion on the terminology of this disease.

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  • (PMID = 15701595.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
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70. Yang J, Zhou GW, Chen X, Wei Y, Peng CH, Ning G, Li HW: [Diagnosis and treatment of multiple endocrine neoplasia type 1 related pancreatic endocrine tumors]. Zhonghua Wai Ke Za Zhi; 2009 Mar 1;47(5):329-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnosis and treatment of multiple endocrine neoplasia type 1 related pancreatic endocrine tumors].
  • OBJECTIVE: To summarize the experience on diagnosis and treatment of multiple endocrine neoplasia type 1 (MEN-1) related pancreatic endocrine tumors (PET).
  • The other patient was diagnosed as glucagonoma clinically.
  • [MeSH-major] Multiple Endocrine Neoplasia Type 1 / diagnosis. Multiple Endocrine Neoplasia Type 1 / surgery. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery


71. Qian ZY, Miao Y, Dai CC, Xu ZK, Liu XL: [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2005 Oct;27(5):572-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas].
  • OBJECTIVE: To investigate the feasibility and therapeutic results of multiple organ resection in patients with tumor of the body and tail of pancreas.
  • METHODS: The clinical and pathological data were analysed in 16 consecutive patients with neoplasm of the body and tail of pancreas from 1999 to 2004 retrospectively.
  • RESULTS: Multiple organ resection was performed in 6 cases of primary pancreatic adenocarcinoma of the body and tail (3 cases of pancreatic cancer, 2 cases of malignant glucagonoma, and 1 case of well-differentiated pancreatic stromal sarcoma) and 10 cases of extrapancreatic malignancy (4 cases of gastric cancer, 2 cases of gastric leiomyosarcoma, 1 case of duodenal cancer, and 3 cases of colon cancer of hepatic flexure).
  • Patients with primary pancreatic cancer or pancreatic stromal sarcoma died within 1 year.
  • Two patients with malignant glucagonoma died 51 and 39 months later.
  • [MeSH-major] Adenocarcinoma / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16274034.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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72. Hong J, Abudula R, Chen J, Jeppesen PB, Dyrskog SE, Xiao J, Colombo M, Hermansen K: The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro. Metabolism; 2005 Oct;54(10):1329-36
Hazardous Substances Data Bank. GLUCAGON .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro.
  • The influence of fatty acids on beta cell function has been well established whereas little is known about the role of fatty acids on alpha cell function.
  • The aim of our study was to investigate the short-term effects of chain length, spatial configuration, and degree of unsaturation of fatty acids on glucagon secretion from isolated mouse islets and alpha tumor cell 1 clone 6 cells (alpha TC1-6 cells).
  • Glucagon release was measured with different saturated and unsaturated fatty acids as well as cis and trans isomers of fatty acids at low and high glucose.
  • Palmitate (0.1-0.5 mmol/L) immediately stimulated glucagon release in a dose-dependent manner from both isolated islets and alpha TC 1-6 cells.
  • The longer chain length of saturated fatty acids, the higher glucagon responses were obtained.
  • The average fold increase in glucagon to saturated fatty acids (0.3 mmol/L) compared to control was octanoate 1.5, laurate 2.0, myristate 2.9, palmitate 5.4, and stearate 6.2, respectively.
  • Saturated fatty acids were more effective than unsaturated fatty acids in stimulating glucagon secretion.
  • Fatty acids immediately stimulate glucagon secretion from isolated mouse islets pancreatic alpha cells.
  • [MeSH-major] Fatty Acids / pharmacology. Glucagon / secretion

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  • (PMID = 16154432.001).
  • [ISSN] 0026-0495
  • [Journal-full-title] Metabolism: clinical and experimental
  • [ISO-abbreviation] Metab. Clin. Exp.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids; 0 / Insulin; 9007-92-5 / Glucagon
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73. Pinto Marín A, Hernández Agudo E, Feliú J, González Barón M: Pancreatic glucagonoma presenting as a pulmonary mass. Clin Transl Oncol; 2009 Jan;11(1):60-2
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic glucagonoma presenting as a pulmonary mass.
  • Glucagonoma is an uncommon disease, a neuroendocrine tumour that develops from glucagon-producing pancreatic cells.
  • They are usually slow-growing, but generally advanced at diagnosis, and metastatic disease is virtually incurable.
  • Liver is the most common site of metastatic disease.
  • We present the case of a 48-year-old man with a glucagonoma being diagnosed from a pulmonary mass.
  • This case had no liver affection in the whole evolution of the disease, and showed a particularly aggressive course, with very little response to all therapies administered, and a survival from diagnosis of just 16 months.
  • [MeSH-major] Glucagonoma / secondary. Lung Neoplasms / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diagnosis, Differential. Fatal Outcome. Humans. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 19155206.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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74. Mai VQ, Jones RC, Dickert JM, Clyde PW, Shakir KM: Plasma glucagon levels suppressed by a glucose load in a man with incidental pancreatic glucagonoma. Endocr Pract; 2007 Nov-Dec;13(7):780-4
Hazardous Substances Data Bank. GLUCAGON .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plasma glucagon levels suppressed by a glucose load in a man with incidental pancreatic glucagonoma.
  • OBJECTIVE: To describe a patient with a histologically proven pancreatic glucagonoma, noted incidentally during a follow-up visit for high aminotransferase levels, and to evaluate its autonomy with a standard 75-g oral glucose tolerance test.
  • METHODS: We present the results of a 2-hour oral glucose tolerance test, with plasma glucagon and blood glucose levels measured every 30 minutes after an oral glucose load.
  • In addition, we provide a brief review of the literature on the diagnosis and management of glucagonomas and the importance of long-term surveillance.
  • RESULTS: In our patient, who had a 1-year history of impaired fasting glucose, plasma glucagon levels were persistently suppressed to within the normal range after oral glucose challenge.
  • Octreotide scintigraphy revealed abnormal uptake in the pancreatic tail, and a 2.8-cm mass was removed at laparoscopic distal pancreatectomy.
  • Immunohistochemical staining of the tumor tissue showed intense reactivity for glucagon.
  • Plasma glucagon levels were reduced to <50 pg/mL postoperatively, and scintigraphic study at 4-month follow-up showed no residual uptake at the previous tumor site or elsewhere.
  • CONCLUSION: Glucagon-secreting pancreatic tumors are extremely rare.
  • A substantially elevated plasma level of glucagon is usually seen in patients with metastatic tumors.
  • In the early stage of a glucagonoma, however, the plasma glucagon level may be only modestly elevated and may still be susceptible to normal negative feedback inhibition.
  • We demonstrated plasma glucagon complete suppressibility after oral glucose challenge in a patient with a glucagonoma, the first such report in the literature.
  • [MeSH-major] Glucagon / blood. Glucagonoma / blood. Glucose Tolerance Test. Pancreatic Neoplasms / blood

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  • (PMID = 18194937.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins; 9007-92-5 / Glucagon; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase
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75. Shen HC, Ylaya K, Pechhold K, Wilson A, Adem A, Hewitt SM, Libutti SK: Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice. Endocrinology; 2010 Aug;151(8):4024-30
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice.
  • The pancreatic alpha- and beta-cells are critical components in regulating blood glucose homeostasis via secretion of glucagon and insulin, respectively.
  • Both cell types are typically localized in the islets of Langerhans.
  • The lack of suitable cell lines to study alpha- and beta-cells interactions have led us to develop an alpha-cell-specific Cre-expressing transgenic line utilizing a glucagon promoter sequence, the Glu-Cre transgenic mouse.
  • Here, we demonstrate that the Glu-Cre could specifically and efficiently excise floxed target genes in adult islet alpha-cells.
  • We further showed that deletion of the tumor suppressor gene, multiple endocrine neoplasia type 1 (Men1), in alpha-cells led to tumorigenesis.
  • However, to our surprise, the lack of Men1 in alpha-cells did not result in glucagonomas but rather beta-cell insulinomas.
  • Because deletion of the Men1 alleles was only present in alpha-cells, our data suggested that cross communication between alpha- and beta-cells contributes to tumorigenesis in the absence of Men1.
  • Together, we believed that the new model systems described here will allow future studies to decipher cellular interactions between islet alpha- and beta-cells in a physiological context.

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  • (PMID = 20555035.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Men1 protein, mouse; 0 / Proto-Oncogene Proteins; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ PMC2940531
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76. Vagefi PA, Razo O, Deshpande V, McGrath DJ, Lauwers GY, Thayer SP, Warshaw AL, Fernández-Del Castillo C: Evolving patterns in the detection and outcomes of pancreatic neuroendocrine neoplasms: the Massachusetts General Hospital experience from 1977 to 2005. Arch Surg; 2007 Apr;142(4):347-54
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evolving patterns in the detection and outcomes of pancreatic neuroendocrine neoplasms: the Massachusetts General Hospital experience from 1977 to 2005.
  • OBJECTIVE: To assess changing patterns in the detection and outcomes of pancreatic neuroendocrine neoplasms (PNENs).
  • Insulinomas were the most common type of functional neoplasm (33.3%), followed by gastrinomas and glucagonomas; 12 patients (7.1%) had multiple endocrine neoplasia type 1.
  • Of the neoplasms, 107 (63.7%) were located in the pancreatic body or tail.
  • [MeSH-major] Carcinoma, Neuroendocrine / diagnosis. Carcinoma, Neuroendocrine / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery. Pancreaticoduodenectomy / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Diagnosis, Differential. Female. Follow-Up Studies. Hospitals, General. Humans. Male. Massachusetts / epidemiology. Middle Aged. Retrospective Studies. Survival Rate / trends. Treatment Outcome

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  • [Cites] Arch Surg. 2006 Aug;141(8):765-9; discussion 769-70 [16924083.001]
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  • (PMID = 17438169.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK071329; United States / NCI NIH HHS / CA / P01 CA117969
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS519098; NLM/ PMC3979851
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77. Flodgren E, Olde B, Meidute-Abaraviciene S, Winzell MS, Ahrén B, Salehi A: GPR40 is expressed in glucagon producing cells and affects glucagon secretion. Biochem Biophys Res Commun; 2007 Mar 2;354(1):240-5
Hazardous Substances Data Bank. GLUCAGON .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GPR40 is expressed in glucagon producing cells and affects glucagon secretion.
  • The free fatty acid receptor, GPR40, has been coupled with insulin secretion via its expression in pancreatic beta-cells.
  • However, the role of GPR40 in the release of glucagon has not been studied and previous attempts to identify the receptor in alpha-cells have been unfruitful.
  • Using double-staining for glucagon and GPR40 expression, we demonstrate that the two are expressed in the same cells in the periphery of mouse islets.
  • In-R1-G9 hamster glucagonoma cells respond dose-dependently to linoleic acid stimulation by elevated phosphatidyl inositol hydrolysis and glucagon release and the cells become increasingly responsive to fatty acid stimulation when overexpressing GPR40.
  • Isolated mouse islets also secrete glucagon in response to linoleic acid, a response that was abolished by antisense treatment against GPR40.
  • This study demonstrates that GPR40 is present and active in pancreatic alpha-cells and puts further emphasis on the importance of this nutrient sensing receptor in islet function.
  • [MeSH-major] Glucagon / secretion. Glucagon-Secreting Cells / physiology. Receptors, G-Protein-Coupled / metabolism
  • [MeSH-minor] Animals. Cells, Cultured. Cricetinae. Female. Mice


78. Kazanjian KK, Reber HA, Hines OJ: Resection of pancreatic neuroendocrine tumors: results of 70 cases. Arch Surg; 2006 Aug;141(8):765-9; discussion 769-70
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resection of pancreatic neuroendocrine tumors: results of 70 cases.
  • HYPOTHESIS: Neuroendocrine tumors of the pancreas can be managed surgically with excellent outcomes.
  • PATIENTS: Seventy consecutive patients who underwent resection for pancreatic neuroendocrine tumors between January 1, 1990, and December 31, 2005.
  • RESULTS: Of the 70 patients, 50 (71.4%) had nonfunctional tumors.
  • Thirty-seven patients (52.9%) had neuroendocrine carcinomas and 13 (18.6%) had benign islet cell neoplasms.
  • Twenty patients had functional tumors.
  • Of these 20 patients, 16 had insulinomas, 2 had glucagonomas, and 2 had gastrinomas.
  • Patients undergoing enucleation as compared with those not undergoing enucleation were younger (mean age, 39 vs 51 years, respectively; P = .009) and had smaller tumors (mean tumor size, 2 vs 5 cm, respectively; P<.001).
  • With a median follow-up of 50 months, the 5-year actuarial survival for the patients with malignant neuroendocrine carcinomas (n = 37) was 77%, and all of the patients with functional tumors are alive.
  • CONCLUSIONS: This single-institutional case series demonstrates that pancreatic neuroendocrine tumors can be safely resected without mortality and with minimal morbidity.
  • The presence of lymphovascular invasion can be used to classify neuroendocrine tumors as malignant, and this appears to predict survival.
  • Patients with malignant tumors can expect long-term survival even in the setting of metastatic disease.
  • [MeSH-major] Neuroendocrine Tumors / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery. Pancreaticoduodenectomy / methods

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  • (PMID = 16924083.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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79. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroendocrine tumors and somatostatin: imaging techniques.
  • Tumors and metastases bearing the somatostatin receptor subtypes 2 (SSTR2) or SSTR5 can be visualized in vivo after injection of radiolabeled octapeptide somatostatin analogs like 111In-pentetreotide.
  • The sensitivity of 111In-pentetreotide scintigraphy for the detection of carcinoid tumors is 86-95%.
  • The sensitivity of 111In-pentetreotide scintigraphy for the detection of gastrinomas, vasoactive intestinal polypeptide-secreting tumors, and glucagonomas as well as clinically non-functioning lesions is 75-100%.
  • 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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80. Igaz P, Igaz I, Rácz K, Tulassay Z: [Hereditary tumours of the endocrine pancreas]. Orv Hetil; 2006 Feb 5;147(5):195-200
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  • [Title] [Hereditary tumours of the endocrine pancreas].
  • [Transliterated title] Az endokrin pancreas öröklódó daganatai.
  • The pathogenesis, diagnosis and therapy of tumours originating from the endocrine pancreas represent one of the most exciting challenges of contemporary medicine.
  • Some of these tumours appear as part of four hereditary syndromes (multiple endocrine neoplasia type 1 (MEN1), von Hippel-Lindau disease (VHL), neurofibromatosis type 1 and tuberous sclerosis) that are all inherited as autosomal dominant traits and result from mutations of tumour suppressor genes.
  • Considering its clinical relevance, MEN1 appears to be the most important among these four syndromes.
  • Tumours of the endocrine pancreas develop in 30-80% of patients carrying mutations of the MEN1 gene.
  • Gastrinomas are the most frequent functioning tumours in MEN1 patients, followed by insulinomas, whereas other tumors e.g. glucagonoma, VIP-oma, GRF-oma and somatostatinoma occur very rarely.
  • Tumours of the endocrine pancreas are infrequent in patients suffering from VHL, neurofibromatosis and tuberous sclerosis.
  • In this review article, the authors present a synopsis of tumours of the endocrine pancreas related to these hereditary syndromes underlining the clinical characteristics, diagnostical and therapeutical possibilities.
  • [MeSH-major] Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Gastrinoma / diagnosis. Gastrinoma / genetics. Glucagonoma / genetics. Humans. Insulinoma / diagnosis. Insulinoma / genetics. Mass Screening. Multiple Endocrine Neoplasia Type 1 / complications. Neurofibromatosis 1 / complications. Somatostatinoma / genetics. Tuberous Sclerosis / complications. Vipoma / genetics. von Hippel-Lindau Disease / complications

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  • (PMID = 16509219.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Number-of-references] 50
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81. Goudet P, Murat A, Binquet C, Cardot-Bauters C, Costa A, Ruszniewski P, Niccoli P, Ménégaux F, Chabrier G, Borson-Chazot F, Tabarin A, Bouchard P, Delemer B, Beckers A, Bonithon-Kopp C: Risk factors and causes of death in MEN1 disease. A GTE (Groupe d'Etude des Tumeurs Endocrines) cohort study among 758 patients. World J Surg; 2010 Feb;34(2):249-55
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  • [Title] Risk factors and causes of death in MEN1 disease. A GTE (Groupe d'Etude des Tumeurs Endocrines) cohort study among 758 patients.
  • METHODS: Overall, 758 symptomatic MEN1 patients were identified through the GTE network (Groupe d'étude des Tumeurs Endocrines), which involves French and Belgian genetics laboratories responsible for MEN1 diagnosis and 80 clinical reference centers.
  • Female gender, family history of MEN1, and recent diagnosis were associated with a lower risk of death.
  • Compared with nonaffected patients, those with thymic tumors (hazard ratio [HR] = 4.64, 95% CI = 1.73-12.41), glucagonomas-vipomas-somatostatinomas (HR = 4.29, 95% CI = 1.54-11.93), nonfunctioning pancreatic tumors (HR = 3.43, 95% CI = 1.71-6.88), and gastrinoma (HR = 1.89, 95% CI = 1.09-3.25) had a higher risk of death after adjustment for age, gender, and diagnosis period.
  • The increased risk of death among patients with adrenal tumors was not significant, but three patients died from aggressive adrenal tumors.
  • Pituitary tumors, insulinomas, and bronchial tumors did not increase the risk of death.
  • CONCLUSIONS: The prognosis of MEN1 disease has improved since 1980.
  • Thymic tumors and duodenopancreatic tumors, including nonsecreting pancreatic tumors, increased the risk of death.
  • Rare but aggressive adrenal tumors may also cause death.

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  • (PMID = 19949948.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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82. 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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83. Krause W: Skin diseases in consequence of endocrine alterations. Aging Male; 2006 Jun;9(2):81-95
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  • There, knowledge of skin alterations is important not only for dermatologists, but also for endocrinologists and other physicians, because a clinical diagnosis of the underlying disease is often possible.
  • These include acanthosis nigricans, diseases due to alterations of androgen metabolism, carcinoid syndrome, diseases due to alterations of corticosteroid metabolism, diseases in association with diabetes mellitus, diseases due to alterations of estrogen metabolism, genetic syndromes including dermatological and endocrine symptoms, the glucagonoma syndrome, diseases due to dysfunctions of growth hormone secretion, diseases in association with Merkel cells of the skin, diseases due to dysfunctions of the thyroid gland, diseases to alteration of vitamin D metabolism, and vitiligo and disorders of pigmentation.
  • [MeSH-minor] Androgens / deficiency. Androgens / secretion. Estrogens / deficiency. Estrogens / secretion. Glucagonoma / etiology. Malignant Carcinoid Syndrome / etiology. Thyroid Hormones / deficiency. Thyroid Hormones / secretion. Vitamin D / secretion. Vitiligo / etiology

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  • (PMID = 16916743.001).
  • [ISSN] 1368-5538
  • [Journal-full-title] The aging male : the official journal of the International Society for the Study of the Aging Male
  • [ISO-abbreviation] Aging Male
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Thyroid Hormones; 1406-16-2 / Vitamin D
  • [Number-of-references] 71
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84. 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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85. Lewis RB, Lattin GE Jr, Paal E: Pancreatic endocrine tumors: radiologic-clinicopathologic correlation. Radiographics; 2010 Oct;30(6):1445-64
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  • [Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
  • Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.
  • They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and glucagonoma are the most common functioning PETs.
  • Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.
  • At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.
  • Cystic change, calcification, and necrosis are common in large tumors, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller tumors.
  • Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such tumors have a poor prognosis.
  • Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

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  • [Copyright] © RSNA, 2010.
  • (PMID = 21071369.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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86. Igaz P: MEN1 clinical background. Adv Exp Med Biol; 2009;668:1-15
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  • Multiple endocrine neoplasia Type 1 (MEN1) is a rare hereditary tumor syndrome predisposing to tumor development in several endocrine organs.
  • Its major manifestations include hyperparathyroidism, tumors of endocrine pancreas and pituitary.
  • Beside these three, several other endocrine (adrenocortical, foregut carcinoid) and nonendocrine (lipoma, angiofibroma, collagenoma, ependymoma, meningioma) tumors have been described to be associated with this syndrome.
  • Both familial and sporadic forms of the disease are known.
  • The diagnosis of MEN1 can be established if two of the three major manifestations are found in the same patient, whereas the diagnosis of familial MEN1 requires one MEN1 patient and a first degree relative with at least one MEN1 manifestation.
  • Both benign (parathyroid, anterior pituitary) and malignant (gastrinoma, glucagonoma) lesions may develop in MEN1 patients.
  • Regular surveillance of MEN1 gene mutation carriers is necessary to reveal disease manifestations.
  • Several diagnostic modalities can be used to screen for and to examine MEN1-related tumors.
  • The therapy of MEN1-associated tumors requires specific approach in some cases, as multiple tumors and recurrence is frequently observed.
  • [MeSH-minor] Adult. Child. Child, Preschool. Diagnosis, Differential. Genetic Predisposition to Disease. Genetic Testing. Humans. Middle Aged. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2a / pathology. Multiple Endocrine Neoplasia Type 2a / physiopathology. Mutation. Young Adult

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  • (PMID = 20175448.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Jabbour SA, Davidovici BB, Wolf R: Rare syndromes. Clin Dermatol; 2006 Jul-Aug;24(4):299-316
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare syndromes.
  • Dermatologists may also encounter patients presenting with skin lesions that reflect an underlying endocrine disorder not commonly seen in daily practice.
  • Some of these endocrine disorders include glucagonoma, neurofibromatosis type 1, McCune-Albright syndrome, multiple endocrine neoplasia, the Carney complex, carcinoid tumors, and mastocytosis.
  • The clinical syndrome classically associated with glucagonoma includes necrolytic migratory erythema, weight loss, diabetes mellitus, anemia, cheilitis, venous thrombosis, and neuropsychiatric symptoms.
  • Other presenting features include freckling, peripheral neurofibromas, Lisch nodules, bone abnormalities, tumors, neurologic abnormalities and hypertension.
  • McCune-Albright syndrome is characterized by café-au-lait spots, polyostotic fibrous dysplasia, sexual precocity, and hyperfunction of multiple endocrine glands.
  • The syndrome also includes mucosal neuromas, typically involving the lips and tongue, intestinal ganglioneuromas and a marfanoid habitus.
  • Multiple endocrine neoplasia type 1 is an autosomal dominant predisposition to tumors of the parathyroid glands (four-gland hyperplasia), anterior pituitary, and pancreatic islet cells; hence, the mnemonic device of the "3 Ps"; multiple cutaneous lesions (angiofibromas and collagenomas) are frequent in patients with multiple endocrine neoplasia type 1.
  • Carney complex may be viewed as a form of multiple endocrine neoplasia because affected patients often have tumors of two or more endocrine glands, including primary pigmented nodular adrenocortical disease (some with Cushing's syndrome), pituitary adenoma, testicular neoplasms, thyroid adenoma or carcinoma, and ovarian cysts.
  • Additional unusual manifestations include psammomatous melanotic schwannoma, breast ductal adenoma, and a rare bone tumor, osteochondromyxoma.
  • Carcinoid syndrome is the term applied to a constellation of symptoms mediated by various humoral factors elaborated by some carcinoid tumors; the major manifestations are diarrhea, flushing, bronchospasm, and cardiac valvular lesions.
  • Mast cell diseases include all disorders of mast cell proliferation.
  • [MeSH-minor] Female. Humans. Male. Syndrome

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  • (PMID = 16828412.001).
  • [ISSN] 0738-081X
  • [Journal-full-title] Clinics in dermatology
  • [ISO-abbreviation] Clin. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 155
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88. Tomita T, Masuzaki H, Iwakura H, Fujikura J, Noguchi M, Tanaka T, Ebihara K, Kawamura J, Komoto I, Kawaguchi Y, Fujimoto K, Doi R, Shimada Y, Hosoda K, Imamura M, Nakao K: Expression of the gene for a membrane-bound fatty acid receptor in the pancreas and islet cell tumours in humans: evidence for GPR40 expression in pancreatic beta cells and implications for insulin secretion. Diabetologia; 2006 May;49(5):962-8
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  • [Title] Expression of the gene for a membrane-bound fatty acid receptor in the pancreas and islet cell tumours in humans: evidence for GPR40 expression in pancreatic beta cells and implications for insulin secretion.
  • AIMS/HYPOTHESIS: G protein-coupled receptor 40 (GPR40) is abundantly expressed in pancreatic beta cells in rodents, where it facilitates glucose-induced insulin secretion in response to mid- to long-chain fatty acids in vitro.
  • METHODS: GPR40 mRNA expression in the human pancreas, pancreatic islets and islet cell tumours was analysed using TaqMan PCR.
  • The estimated mRNA copy number for the GPR40 gene in pancreatic islets was comparable to those for genes encoding sulfonylurea receptor 1, glucagon-like peptide 1 receptor and somatostatin receptors, all of which are known to be expressed abundantly in the human pancreatic islet.
  • A large amount of GPR40 mRNA was detected in insulinoma tissues, whereas mRNA expression was undetectable in glucagonoma or gastrinoma.
  • The GPR40 mRNA level in the pancreas correlated with the insulinogenic index, which reflects beta cell function (r=0.82, p=0.044), but not with glucose levels during the OGTT, the insulin area under the OGTT curve or the index for the homeostasis model assessment of insulin resistance (HOMA-IR).
  • CONCLUSIONS/INTERPRETATION: The present study provides evidence for GPR40 gene expression in pancreatic beta cells and implicates GPR40 in insulin secretion in humans.
  • [MeSH-major] Insulin / secretion. Insulinoma / genetics. Pancreatic Neoplasms / genetics. Receptors, G-Protein-Coupled / genetics


89. Jarufe NP, Coldham C, Orug T, Mayer AD, Mirza DF, Buckels JA, Bramhall SR: Neuroendocrine tumours of the pancreas: predictors of survival after surgical treatment. Dig Surg; 2005;22(3):157-62
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  • [Title] Neuroendocrine tumours of the pancreas: predictors of survival after surgical treatment.
  • AIMS: Neuroendocrine tumours of pancreatic and duodenal origin (NETP) are rare and we present a significant experience from a single centre.
  • RESULTS: Twenty-four patients had functioning tumours (16 insulinomas, 3 gastrinomas, 2 somatostatinomas, 1 vipoma, 1 glucagonoma and 1 carcinoid tumour).
  • [MeSH-major] Neuroendocrine Tumors / surgery. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16043962.001).
  • [ISSN] 0253-4886
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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90. Siegel R, Linse R, Rau B: [The question of surgical therapy for necrolytic migratory erythema, a cutaneous disease]. Chirurg; 2006 Jun;77(6):535-8
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  • [Title] [The question of surgical therapy for necrolytic migratory erythema, a cutaneous disease].
  • Its underlying cause is usually a pancreatic islet cell tumour with marked glucagon secretion.
  • The glucagonoma syndrome is characterised by pancreatic neuroendocrine neoplasm, NME, and diabetes mellitus.
  • We present a case of glucagonoma syndrome in a 58-year-old woman with a history of recurrent cutaneous manifestations who was referred for surgical resection of a pancreatic neoplasm after the NME was finally diagnosed.
  • We discuss diagnostic methods, differential diagnosis, and therapeutic management of this disease.
  • [MeSH-major] Erythema / etiology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes

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  • [Cites] Int J Dermatol. 2004 Jan;43(1):12-8 [14693015.001]
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  • (PMID = 16362349.001).
  • [ISSN] 0009-4722
  • [Journal-full-title] Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen
  • [ISO-abbreviation] Chirurg
  • [Language] ger
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Germany
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91. Resmini E, Minuto F, Colao A, Ferone D: Secondary diabetes associated with principal endocrinopathies: the impact of new treatment modalities. Acta Diabetol; 2009 Jun;46(2):85-95
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  • Indeed, impaired glucose tolerance (IGT) and overt diabetes mellitus are frequently associated with acromegaly and hypercortisolism (Cushing syndrome).
  • The increased cardiovascular morbidity and mortality associated with acromegaly and Cushing syndrome may partly be a consequence of increased insulin resistance that normally accompanies hormone excess.
  • The prevalence of diabetes mellitus and that of IGT in acromegaly is reported to range 16-56%, whereas the degree of glucose tolerance seems correlated with circulating growth hormone (GH) levels, age, and disease duration.
  • Therapy with somatostatin analogues (SSAs) induce control of GH and IGF-I excess in the majority of patients, but their inhibitory effect on pancreatic insulin secretion might complicate the overall effect of this treatment on glucose tolerance.
  • Hypercortisolism produces visceral obesity, insulin resistance, and dyslipidemia that together with hypertension, hypercoagulability, and ventricular morphologic and functional abnormalities increase cardiovascular risk, and persist up to 5 years after resolution of hypercortisolism.
  • In Cushing syndrome the prevalence of diabetes varies between 20 and 50%, but probably this prevalence is underestimated, as not always an oral glucose tolerance test is performed in the presence of an apparently normal fasting glycaemia.
  • Again, disease duration, rather than hormone levels, seems to be the major determinant in the occurrence of systemic complications in Cushing syndrome.
  • Due to the impact they have on mortality and morbidity in both acromegaly and Cushing syndrome, these complications should be treated aggressively.
  • In patients with neuroendocrine tumours (NETs) the occurrence of altered glucose tolerance may be due to a decreased insulin secretion, like it happens in patients who underwent pancreatic surgery and in those with pheochromocytoma, or to an altered counterbalance between hormones, such as in patients with glucagonoma and somatostatinoma.
  • Moreover, SSAs represent a valid therapeutic choice in the symptomatic treatment of NETs, and also in this case the medical therapy of the primary disease, may have a significant impact on the prevalence of glucose metabolism imbalance.
  • [MeSH-minor] Cushing Syndrome / complications. Gluconeogenesis. Glucose Tolerance Test. Human Growth Hormone / physiology. Humans. Hypoglycemic Agents / therapeutic use. Insulin / therapeutic use. Insulin Resistance. Liver / physiology. Prevalence. Risk Factors

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  • (PMID = 19322513.001).
  • [ISSN] 1432-5233
  • [Journal-full-title] Acta diabetologica
  • [ISO-abbreviation] Acta Diabetol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / Insulin; 12629-01-5 / Human Growth Hormone
  • [Number-of-references] 73
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92. Mohnike K, Blankenstein O, Pfuetzner A, Pötzsch S, Schober E, Steiner S, Hardy OT, Grimberg A, van Waarde WM: Long-term non-surgical therapy of severe persistent congenital hyperinsulinism with glucagon. Horm Res; 2008;70(1):59-64
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  • [Title] Long-term non-surgical therapy of severe persistent congenital hyperinsulinism with glucagon.
  • Intravenous infusions of glucagon are used as immediate treatment to stabilize euglycemia in affected newborns.
  • OBJECTIVE: To review the efficacy and safety of long-term subcutaneous glucagon infusion as a potential therapeutic option for blood glucose stabilization in infants with severe CHI without the need of additional intravenous glucose or immediate surgical intervention.
  • METHOD: Retrospective review of 9 children with CHI who received continuous subcutaneous infusion of glucagon for weeks or months.
  • Glucagon was added to octreotide to replace octreotide-induced suppression of endogenous glucagon secretion, thereby liberating glucose by stimulation of hepatic glycogenolysis.
  • In 3 cases, a stabilized formulation of glucagon was used to prevent glucagon crystallization that frequently occurs in smaller volumes.
  • RESULTS: Introduction of glucagon allowed the reduction or discontinuation of central glucose infusion in all children studied.
  • In 2 patients, glucagon was introduced due to recurrent hypoglycemia despite subtotal pancreatectomy.
  • In 3 children, subcutaneous glucagon was continuously administered for 1-4 years leading to stable euglycemia.
  • As a possible side effect, 2 children developed erythema necrolyticum, which resolved after discontinuation of the glucagon infusion.
  • This has been described before in glucagonoma.
  • CONCLUSION: In this retrospective series, combination therapy of low-dose octreotide and subcutaneous glucagon infusion has been effective in preventing hypoglycemic episodes in severe CHI.
  • [MeSH-major] Congenital Hyperinsulinism / drug therapy. Gastrointestinal Agents / administration & dosage. Glucagon / administration & dosage. Octreotide / administration & dosage

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18493152.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Gastrointestinal Agents; 9005-79-2 / Glycogen; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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93. Melen-Mucha G, Lawnicka H, Kierszniewska-Stepien D, Komorowski J, Stepien H: The place of somatostatin analogs in the diagnosis and treatment of the neuoroendocrine glands tumors. Recent Pat Anticancer Drug Discov; 2006 Jun;1(2):237-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The place of somatostatin analogs in the diagnosis and treatment of the neuoroendocrine glands tumors.
  • Similarly, these drugs are also very effective in the treatment of TSH-secreting adenomas.
  • The introduction of these drugs into therapy of the functional neuroendocrine tumors of the gastrointestinal tract was a crucial step in the treatment.
  • Octreotide and lanreotide are the drugs of choice in the treatment of patients with: VIPoma, glucagonoma and carcinoid syndrome.
  • Somatostatin receptor scintigraphy with OctreoScan has been recommended as the best imaging technique in these tumors in the localization and staging procedure.
  • SS analogs, coupled to radioisotope or cytotoxic drugs, create another class of SS molecules, very promising in the therapy of the endocrine glands tumors and in other tumors.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Neuroendocrine Tumors / diagnosis. Neuroendocrine Tumors / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

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  • (PMID = 18221040.001).
  • [ISSN] 1574-8928
  • [Journal-full-title] Recent patents on anti-cancer drug discovery
  • [ISO-abbreviation] Recent Pat Anticancer Drug Discov
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 190
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94. Simonenko VB, Dulin PA, Makanin MA: [Somatostatin analogues in treatment of gastrointestinal and pancreatic neuroendocrine tumors]. Klin Med (Mosk); 2006;84(4):4-8
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  • [Title] [Somatostatin analogues in treatment of gastrointestinal and pancreatic neuroendocrine tumors].
  • Sandostatin therapy is indicated to patients with functionally active neuroendocrine tumors of the stomach, duodenum, small bowel, or appendix.
  • Glucagonomas, vipomas, and, to a lesser degree, gastrinomas and metastatic insulinomas are examples of functionally active endocrine pancreatic tumors that should be treated with sandostatin.
  • Other syndromes, which should be treated with octreotide, include ectopic secretion of adrenocorticotropic hormone in Cushing syndrome, oncogenic osteomalacia, and hypercalciemia resulting from ectopic secretion of parathyroid-like peptide.
  • In patients with an advanced carcinoid syndrome, the starting dose of sandostatin (ocreotide) is 150 mcgr administered three times a day in hypordermic injections during 10 to 14 days, after which sandostatin LAR is administered in a dose of 20 mg once a month.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Gastrointestinal Neoplasms / drug therapy. Neuroendocrine Tumors / drug therapy. Pancreatic Neoplasms / drug therapy. Somatostatin / analogs & derivatives

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  • (PMID = 16755846.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin
  • [Number-of-references] 25
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95. Warner RR: Enteroendocrine tumors other than carcinoid: a review of clinically significant advances. Gastroenterology; 2005 May;128(6):1668-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enteroendocrine tumors other than carcinoid: a review of clinically significant advances.
  • Only relatively recently has there been an increased clinical recognition and characterization of the heterogeneous group of rare gastroenteropancreatic neuroendocrine neoplasms.
  • This review summarizes the derivation of these tumors and the advances in their diagnosis and treatment over the past decade and a half.
  • They are varied in their biological behavior and clinical courses and, depending on their cell type, can produce different hormones causing distinct clinical endocrine syndromes (insulinoma [hypoglycemia], gastrinoma [Zollinger-Ellison syndrome (ZES)], vasoactive intestinal peptideoma [VIPoma], watery diarrhea, hypokalemia-achlorhydria [WDHA], glucagonoma [glucagonoma syndrome], and so forth).
  • In addition to surgery for cure or palliation (by excision and a variety of other cytoreductive techniques), they each are treated with anti-hormonal agents or drugs targeted to each tumor's specific product or its effects.
  • Because of their usual slow rate of growth it is recommended that, even when they are advanced and incurable, unlike in patients with common and more malignant cancers, patients with neuroendocrine tumors often can be palliated and appear to survive longer when managed with an active approach using sequential multimodality treatment.
  • [MeSH-major] Carcinoma, Neuroendocrine. Gastrointestinal Neoplasms
  • [MeSH-minor] Carcinoid Tumor. Humans

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  • (PMID = 15887158.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 222
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96. Gotthardt M, Béhé MP, Grass J, Bauhofer A, Rinke A, Schipper ML, Kalinowski M, Arnold R, Oyen WJ, Behr TM: Added value of gastrin receptor scintigraphy in comparison to somatostatin receptor scintigraphy in patients with carcinoids and other neuroendocrine tumours. Endocr Relat Cancer; 2006 Dec;13(4):1203-11
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  • [Title] Added value of gastrin receptor scintigraphy in comparison to somatostatin receptor scintigraphy in patients with carcinoids and other neuroendocrine tumours.
  • As gastrin-binding CCK(2) receptors are also expressed on a variety of other neuroendocrine tumours (NET), we compared GRS to somatostatin receptor scintigraphy (SRS) in patients with NET.
  • SRS and GRS were performed within 21 days in a series of 60 consecutive patients with NET.
  • Of the 60 evaluable patients, 51 had carcinoid tumours, 3 gastrinomas, 2 glucagonomas, 1 insulinoma and 3 paragangliomas.
  • The overall tumour-detection rate was 73.7% for GRS and 82.1% for SRS.
  • Based on the number of tumour sites detected and the degree of uptake, GRS performed better than SRS in 13 patients (21.7%), equivalent images were obtained in 18 cases (30.0%) and SRS performed better in 24 (40.0%) cases.
  • In six of the SRS positive patients, 18 additional sites of tumour involvement could be detected.
  • Overall, GRS detected additional tumour sites in 20% of the patients.
  • GRS should be performed in selected patients as it may provide additional information in patients with NET with equivocal or absent somatostatin uptake.
  • [MeSH-major] Carcinoid Tumor / radionuclide imaging. Neuroendocrine Tumors / radionuclide imaging. Receptor, Cholecystokinin B / metabolism. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Glucagonoma / radionuclide imaging. Humans. Indium Radioisotopes. Insulinoma / radionuclide imaging. Male. Middle Aged. Octreotide / analogs & derivatives. Paraganglioma / radionuclide imaging. Pentetic Acid / analogs & derivatives. Prognosis. Radiopharmaceuticals

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  • (PMID = 17158765.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Indium Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptor, Cholecystokinin B; 0 / Receptors, Somatostatin; 142694-57-3 / SDZ 215-811; 7A314HQM0I / Pentetic Acid; RWM8CCW8GP / Octreotide
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97. Nijs E, Callahan MJ, Taylor GA: Disorders of the pediatric pancreas: imaging features. Pediatr Radiol; 2005 Apr;35(4):358-73; quiz 457
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  • [Title] Disorders of the pediatric pancreas: imaging features.
  • The purpose of this manuscript is to provide an overview of the normal development of the pancreas as well as pancreatic pathology in children.
  • Diagnostic imaging plays a major role in the evaluation of the pancreas in infants and children.
  • Familiarity with the range of normal appearance and the diseases that commonly affect this gland is important for the accurate and timely diagnosis of pancreatic disorders in the pediatric population.
  • These include pancreas divisum, annular pancreas, agenesis of the dorsal pancreatic anlagen and ectopic pancreatic tissue.
  • Syndromes that can manifest pancreatic pathology include: Beckwith Wiedemann syndrome, von Hippel-Lindau disease and autosomal dominant polycystic kidney disease.
  • Children and adults with cystic fibrosis and Shwachman-Diamond syndrome frequently present with pancreatic insufficiency.
  • In younger children, unexplained pancreatic injury must always alert the radiologist to potential child abuse.
  • Pancreatic pseudocysts are a complication of trauma, but can also be seen in the setting of acute or chronic pancreatitis from other causes.
  • Primary pancreatic neoplasms are rare in children and are divided into exocrine tumors such as pancreatoblastoma and adenocarcinoma and into endocrine or islet cell tumors.
  • Islet cell tumors are classified as functioning (insulinoma, gastrinoma, VIPoma and glucagonoma) and nonfunctioning tumors.
  • Solid-cystic papillary tumor is probably the most common pancreatic tumor in Asian children.
  • Although quite rare, secondary tumors of the pancreas can be associated with certain primary malignancies.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Diseases / diagnosis
  • [MeSH-minor] Adult. Child. Humans. Infant. Pancreas / abnormalities. Pancreas / anatomy & histology. Pancreatic Neoplasms / diagnosis

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  • (PMID = 15536562.001).
  • [ISSN] 0301-0449
  • [Journal-full-title] Pediatric radiology
  • [ISO-abbreviation] Pediatr Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 50
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98. Oberg K: Pancreatic endocrine tumors. Semin Oncol; 2010 Dec;37(6):594-618
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic endocrine tumors.
  • Pancreatic endocrine tumors have been steadily growing in incidence and prevalence during the last two decades, showing an incidence of 4-5/1,000,000 population.
  • They represent a heterogeneous group with very varying tumor biology and prognosis.
  • About half of the patients present clinical symptoms and syndromes related to substances released from the tumors (Zollinger-Ellison syndrome, insulinoma, glucagonoma, etc) and the other half are so-called nonfunctioning tumors mainly presenting with symptoms such as obstruction, jaundice, bleeding, and abdominal mass.
  • Ten percent to 15% of the pancreatic endocrine tumors are part of an inherited syndrome such as multiple endocrine neoplasia type 1 (MEN-1), von Hippel-Lindau (VHL), neurofibromatosis, or tuberousclerosis.
  • The diagnosis is based on histopathology demonstrating neuroendocrine features such as positive staining for chromogranin A and specific hormones such as gastrin, proinsulin, and glucagon.
  • Moreover, the biochemical diagnosis includes measurement of chromogranins A and B or specific hormones such as gastrin, insulin, glucagon, and vasoactive intestinal polypeptide (VIP) in the circulation.
  • Surgery is still one of the cornerstones in the management of pancreatic endocrine tumors, but curative surgery is rarely obtained in most cases because of metastatic disease.
  • Cytotoxic drugs, biological agents, such as somatostatin analogs, alpha interferons, mammalian target of rapamycin (mTOR) inhibitors and tyrosine kinase inhibitors are routinely used.
  • Tumor-targeted radioactive treatment is available in many centres in Europe and is effective in patients with tumors that express high content of somatostatin receptors type 2 and 5.
  • In the future, treatment will be based on tumor biology and molecular genetics with the aim of so-called personalized medicine.
  • [MeSH-major] Pancreatic Neoplasms
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Biological Therapy / methods. Biomarkers, Tumor. Humans. Neoplastic Syndromes, Hereditary / diagnosis. Neoplastic Syndromes, Hereditary / therapy. Pancreatectomy. Paraneoplastic Endocrine Syndromes / diagnosis. Paraneoplastic Endocrine Syndromes / therapy

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21167379.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
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99. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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100. Shen XX, Li HL, Hong J, Xiao J, Pan L, Li GW: [The role of syntaxin1A/synaptosome-associated protein-25 in reversing hyperglycemia-induced alpha cell toxicity]. Zhonghua Yi Xue Za Zhi; 2009 Mar 31;89(12):851-4
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  • [Title] [The role of syntaxin1A/synaptosome-associated protein-25 in reversing hyperglycemia-induced alpha cell toxicity].
  • OBJECTIVE: To investigate the effects of reversal of hyperglycemic toxicity on the synthesis and secretion of glucagon by the alpha cells and the possible mechanisms thereof.
  • METHODS: Mouse glucagonoma cells of the line TC1-6 were cultured in medium containing 5.5 mmol/L glucose for 10 days (low glucose group, LG), in medium containing 25 mmol/L glucose for 10 days (high glucose group, HG), in medium with 25 mmol/L glucose for 5 days and then in medium with 5.5 mmol/L glucose for 5 days (high-low glucose group, HL group), or in medium with 5.5 mmol/L glucose for 5 days and then in medium with 25 mmol/L glucose for 5 days (LH group), Radioimmunoassay was used to detect the glucagon concentration in the supernatant.
  • RT-PCR was used to detect the mRNA expression of glucagon in the TC1-6 cells.
  • (1) The glucagon level of the HG/LG group was lower than that of the HG group by 29% (P < 0.05). (2) The glucagon mRNA expression level in the TC1-6 cells of the HG/HL group was significantly lower than that of the HG group by (52.6 +/- 2.8)% (P < 0.05). (3) The syntaxin1A and SNAP-25 expression levels in the TC1-6 cells of the HG group were significantly higher than those of the LG group by 36% and 69% respectively (both P < 0.05), and the syntaxin1A and SNAP-25 expression levels in the TC1-6 cells of the HG/LG group were significantly lower than those of the HG group by 49% and 56% respectively (both P < 0.05).
  • CONCLUSION: After removing the high glucose toxicity the abnormal glucagon secretion by the alpha-cells can be ameliorated obviously, and the expression levels of syntaxin1A and SNAP-25 proteins that promote the secretion of glucagon are reduced accordingly.
  • [MeSH-major] Glucagon / secretion. Hyperglycemia / metabolism. Islets of Langerhans / cytology. Synaptosomal-Associated Protein 25 / metabolism. Syntaxin 1 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival. Gene Expression. Mice. Signal Transduction

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  • (PMID = 19595128.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Snap25 protein, mouse; 0 / Stx1a protein, mouse; 0 / Synaptosomal-Associated Protein 25; 0 / Syntaxin 1; 9007-92-5 / Glucagon
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