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6. 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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  • [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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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. 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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9. 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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10. 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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16. 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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  • [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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17. 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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  • [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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18. Kallichanda N, Tsai S, Stabile BE, Buslon V, Delgado DL, French SW: Histogenesis of solid pseudopapillary tumor of the pancreas: the case for the centroacinar cell of origin. Exp Mol Pathol; 2006 Oct;81(2):101-7
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  • [Title] Histogenesis of solid pseudopapillary tumor of the pancreas: the case for the centroacinar cell of origin.
  • Solid pseudopapillary tumor (SPT) is an unusual pancreatic neoplasm of low malignant potential that most frequently occurs in young women.
  • The tumor is indolent, with long patient survival, even in the presence of extension into adjacent organs and metastases.
  • Histologically, it is a solid and cystic tumor with a prominent vascular network and degenerative pseudopapillae formation.
  • Herein, we report a case of solid pseudopapillary tumor in a 41-year-old female in which the tumor cells immunohistochemically and ultrastructurally suggest a centroacinar cell origin.
  • The tumor cells and the normal centroacinar cells stained positive for alpha-antitrypsin (alpha-AT), CD10, cyclin D1 and NSE.
  • Ultrastructural examination shows similarities in nuclear shape, nucleoli location and cytoplasmic contents between neoplastic cells and normal centroacinar cells of the pancreas.
  • Based on both immunohistochemical and ultrastructural features, we propose that the centroacinar cell is the origin of SPT.
  • [MeSH-major] Carcinoma, Papillary / pathology. Islets of Langerhans / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Cyclin D1 / analysis. Female. Humans. Neprilysin / analysis. Phosphopyruvate Hydratase / analysis. alpha 1-Antitrypsin / analysis

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  • (PMID = 16916512.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Grant] United States / PHS HHS / / P50-019991
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha 1-Antitrypsin; 136601-57-5 / Cyclin D1; EC 3.4.24.11 / Neprilysin; EC 4.2.1.11 / Phosphopyruvate Hydratase
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19. Dubova EA, Shchegolev AI, Mishnev OD, Egorov VI: [Solid pseudopapillary tumor of the pancreas]. Arkh Patol; 2008 Jan-Feb;70(1):49-52
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  • [Title] [Solid pseudopapillary tumor of the pancreas].
  • The paper reviews the data available in the literature and describes the authors' observation of solid pseudopapillary tumor of the pancreas in a 33-year-old woman.
  • Microscopically, the tumor, 2.5 x 2.5 x 2 cm in size, appeared predominantly as solid areas and solitary pseudopapillae comprising monomorphic round and oval cells with a light cytoplasm and round nuclei.
  • Immunohistochemical study revealed diffuse cytoplasmic tumor cell staining in response to vimentin, alpha-antitrypsin, neuronspecific enolase, and cytokeratin 18; focal expression of synaptophysin and CD117; a negative reaction with antibodies to epithelial membrane antigen, S-100 protein, cytokeratins 7, 8, and 19, and CD57.
  • Progesterone receptors were detectable in the nuclei of solitary tumor cells and the reaction with estrogen receptor was negative.
  • [MeSH-major] Carcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18368811.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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20. 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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21. Abreu Velez AM, Howard MS: Diagnosis and treatment of cutaneous paraneoplastic disorders. Dermatol Ther; 2010 Nov-Dec;23(6):662-75
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  • [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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22. Tapia B, Ahrens W, Kenney B, Touloukian R, Reyes-Múgica M: Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature. Pediatr Dev Pathol; 2008 Sep-Oct;11(5):384-90
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  • [Title] Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature.
  • Primary epithelial tumors of the pancreas are extremely uncommon in children, and among these, acinar cell carcinoma (ACC) is the most rare.
  • The histologic diagnosis of ACC was supported by both immunohistochemistry and electron microscopy.
  • Despite its rarity, ACC should be kept in the differential diagnosis of pediatric pancreatic exocrine tumors.
  • We also provide a comparison with an example of solid pseudopapillary tumor, another relatively infrequent epithelial tumor of the pancreas in the young.
  • We review the relevant literature addressing the clinical and pathologic features of ACC and its distinction from other pancreatic neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Pancreatic Cyst / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Child. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Pancreatectomy. Treatment Outcome. alpha 1-Antitrypsin / metabolism

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  • (PMID = 19006424.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
  • [Number-of-references] 37
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23. Patel M, Fine DR: Fibrogenesis in the pancreas after acinar cell injury. Scand J Surg; 2005;94(2):108-11
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  • [Title] Fibrogenesis in the pancreas after acinar cell injury.
  • Fibrosis within the pancreas is a key feature of chronic pancreatitis and pancreatic cancer.
  • It has now been well demonstrated that following injury to acinar cells, pancreatic stellate cell activation, migration and proliferation is the key mediator of this process.
  • The pancreatic stellate cell is likely to play an important role in maintaining the normal extracellular matrix; we speculate that the dysregulation of this process is an important factor in chronic pancreatitis.
  • [MeSH-major] Pancreas / cytology. Pancreas / pathology
  • [MeSH-minor] Apoptosis / physiology. Apoptosis Regulatory Proteins. Chronic Disease. Fibrosis. Humans. Membrane Glycoproteins / metabolism. Metalloproteases / physiology. Pancreatitis / physiopathology. TNF-Related Apoptosis-Inducing Ligand. Transforming Growth Factor beta / physiology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16111091.001).
  • [ISSN] 1457-4969
  • [Journal-full-title] Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society
  • [ISO-abbreviation] Scand J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; EC 3.4.- / Metalloproteases
  • [Number-of-references] 22
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4. Erkan M, Kleeff J, Gorbachevski A, Reiser C, Mitkus T, Esposito I, Giese T, Büchler MW, Giese NA, Friess H: Periostin creates a tumor-supportive microenvironment in the pancreas by sustaining fibrogenic stellate cell activity. Gastroenterology; 2007 Apr;132(4):1447-64
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  • [Title] Periostin creates a tumor-supportive microenvironment in the pancreas by sustaining fibrogenic stellate cell activity.
  • BACKGROUND & AIMS: Pancreatic cancer creates desmoplasia by stimulating stellate cells (PSCs), thereby influencing tumor aggressiveness.
  • The aim of this study was to analyze the impact of the PSC-specific matrix protein periostin on tumor responses to radiochemotherapy.
  • METHODS: PSCs and cancer cells in primary and metastatic lesions of patients treated with or without neoadjuvant radiochemotherapy were evaluated by immunohistochemistry.
  • Interactions between PSCs and cancer cells and the effects of periostin in modulating cellular responses under conditions of hypoxia, starvation, and radiochemotherapy were assessed by immunoblotting and by growth, clonogenicity, and invasion assays.
  • Stromal cells were the only source of periostin in the pancreas and in metastatic sites.
  • Cancer cell supernatants stimulated periostin secretion from PSCs.
  • Recombinant periostin increased alpha-smooth muscle actin, periostin, collagen-1, fibronectin, and transforming growth factor-beta1 expression while decreasing PSC invasiveness.
  • In cancer cells, periostin stimulated growth and conferred resistance to starvation and hypoxia.
  • CONCLUSIONS: Once stimulated by cancer cells, PSCs remain active via an autocrine periostin loop even under radiotherapy and produce excessive extracellular matrix proteins, creating a tumor-supportive microenvironment.
  • Increased periostin expression may therefore reflect a more aggressive tumor phenotype.
  • [MeSH-major] Cell Adhesion Molecules / genetics. Gene Expression Regulation, Neoplastic. Pancreas / pathology. Pancreatic Neoplasms / metabolism. RNA, Messenger / genetics
  • [MeSH-minor] Actins / biosynthesis. Actins / drug effects. Actins / genetics. Biomarkers, Tumor / genetics. Cell Line, Tumor. Collagen Type I / drug effects. Collagen Type I / genetics. Collagen Type I / metabolism. Densitometry. Disease Progression. Fibronectins / biosynthesis. Fibronectins / drug effects. Fibronectins / genetics. Fibrosis / pathology. Gene Silencing. Humans. Immunoblotting. Immunohistochemistry. Microscopy, Fluorescence. Neoplasm Metastasis. Polymerase Chain Reaction. RNA, Small Interfering / genetics. Recombinant Proteins / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Stromal Cells / pathology. Survival Rate. Transforming Growth Factor beta1 / biosynthesis. Transforming Growth Factor beta1 / drug effects. Transforming Growth Factor beta1 / genetics

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  • (PMID = 17408641.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / Collagen Type I; 0 / Fibronectins; 0 / POSTN protein, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Transforming Growth Factor beta1
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25. Hirabayashi K, Nakamura N, Kajiwara H, Hori S, Kawaguchi Y, Yamashita T, Dowaki S, Imaizumi T, Osamura RY: Perivascular epithelioid cell tumor (PEComa) of the pancreas: immunoelectron microscopy and review of the literature. Pathol Int; 2009 Sep;59(9):650-5
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  • [Title] Perivascular epithelioid cell tumor (PEComa) of the pancreas: immunoelectron microscopy and review of the literature.
  • A perivascular epithelioid tumor (PEComa) is a rare tumor probably arising from the perivascular epithelioid cells.
  • Only three cases of pancreatic PEComa have been reported in the English-language literature.
  • The present report describes an extremely rare case of pancreatic PEComa.
  • A 47-year-old Japanese woman complained of lower abdominal pain and a well-demarcated solid tumor was found in the pancreatic head.
  • There was a well-demarcated, solid tumor measuring 17 mm in the pancreatic head.
  • The tumor was composed of a diffuse proliferation of epithelioid tumor cells with many blood vessels but no adipose tissue.
  • The tumor cells expressed HMB45 and alpha-smooth muscle actin.
  • Ultrastructurally, the tumor cells possessed many membrane-bound granules that were positive for HMB45 on immunoelectron microscopy.
  • [MeSH-major] Epithelioid Cells / ultrastructure. Pancreatic Neoplasms / ultrastructure. Perivascular Epithelioid Cell Neoplasms / ultrastructure
  • [MeSH-minor] Actins / metabolism. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Female. Humans. Immunohistochemistry / methods. Melanoma-Specific Antigens. Melanosomes / ultrastructure. Middle Aged. Neoplasm Proteins / metabolism. Pancreaticoduodenectomy. Treatment Outcome

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  • (PMID = 19712133.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / ACTA2 protein, human; 0 / Actins; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins
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26. Lo HA, Sun LN, Chen CF, Wang D, Zhang HP: Ischemia-reperfusion of the pancreas induced hyperresponsiveness of the airways in rats. Transplant Proc; 2009 Jan-Feb;41(1):63-6
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  • [Title] Ischemia-reperfusion of the pancreas induced hyperresponsiveness of the airways in rats.
  • OBJECTIVES: Ischemia-reperfusion (I/R) of the rat pancreas induced acute pancreatitis with systemic inflammatory response syndrome.
  • Activated inflammatory cells sequestered in the lung and the proteases released from the inflammatory pancreas both could induce lung inflammation and lung injury.
  • METHODS: Ischemia of the pancreas was induced by clamping the gastroduodenal and the splenic artery for 2 hours followed by reperfusion for 6 hours.
  • The pulmonary function test of Penh was used to reflect the airway responses. mRNA expression of iNOS and tumor necrosis factor-alpha (TNFalpha) in the lung tissue were measured by real time polymerase chain reactions.
  • RESULTS: This protocol resulted in significant elevations of the blood concentrations of nitric oxide, hydroxyl radical, amylase, TNFalpha, and white cells among the I/R group.
  • Pulmonary function data showed that I/R of the pancreas induced significant increases in the responses to methacholine challenge: Penh was significantly increased in the I/R group compared with the sham group.
  • Lavage white cells were significantly increased in the I/R group.
  • CONCLUSIONS: I/R of the pancreas induced systemic inflammatory responses and increased white cell sequestration in the lung.
  • Hyperresponsive responses in the airways of the reperfusion group may be due to airways inflammation, which increased white cell sequesteration in the lung and the expressions iNOS and TNFalpha inflammatory mediators in lung tissues.
  • [MeSH-major] Pancreas / physiopathology. Reperfusion Injury / physiopathology

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  • (PMID = 19249477.001).
  • [ISSN] 0041-1345
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nitrates; 0 / Nitrites; 0W5ETF9M2K / Methacholine Chloride; 31C4KY9ESH / Nitric Oxide; EC 3.2.1.- / Amylases
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27. 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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28. Nishida A, Andoh A, Inatomi O, Fujiyama Y: Interleukin-32 expression in the pancreas. J Biol Chem; 2009 Jun 26;284(26):17868-76
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  • [Title] Interleukin-32 expression in the pancreas.
  • We studied IL-32 expression in human pancreatic tissue and pancreatic cancer cell lines.
  • IL-32 was weakly immunoexpressed by pancreatic duct cells.
  • In the inflamed lesions of chronic pancreas, the ductal expression of IL-32 was markedly increased.
  • A strong expression of IL-32alpha was detected in the pancreatic cancer cells.
  • In pancreatic cancer cell lines (PANC-1, MIA PaCa-2, and BxPC-3 cells), the expression of IL-32 mRNA and protein was enhanced by IL-1beta, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha.
  • An inhibitor of phosphatidylinositol 3-kinase (LY294002) significantly suppressed the IL-1beta-, IFN-gamma- and TNF-alpha-induced IL-32 mRNA expression.
  • The blockade of NF-kappaB and activated protein-1 activation markedly suppressed the IL-1beta-, IFN-gamma-, and/or TNF-alpha-induced IL-32 mRNA expression.
  • Furthermore, IL-32-specific small interfering RNA significantly decreased the uptake of [3H]thymidine and increased the annexin V-positive population (apoptotic cells) in PANC-1 cells.
  • Pancreatic duct cells are the local source of IL-32, and IL-32 may play an important role in inflammatory responses and pancreatic cancer growth.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Gene Expression Regulation, Neoplastic. Interleukins / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Apoptosis. Blotting, Northern. Blotting, Western. Cell Proliferation. Cells, Cultured. Electrophoretic Mobility Shift Assay. Enzyme-Linked Immunosorbent Assay. Humans. Immunoenzyme Techniques. Interferon-gamma / genetics. Interferon-gamma / metabolism. Interleukin-1beta / genetics. Interleukin-1beta / metabolism. NF-kappa B / antagonists & inhibitors. NF-kappa B / genetics. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism. Transfection. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19386602.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL32 protein, human; 0 / Interleukin-1beta; 0 / Interleukins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Other-IDs] NLM/ PMC2719425
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29. 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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  • [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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30. Sanlioglu AD, Dirice E, Elpek O, Korcum AF, Balci MK, Omer A, Griffith TS, Sanlioglu S: High levels of endogenous tumor necrosis factor-related apoptosis-inducing ligand expression correlate with increased cell death in human pancreas. Pancreas; 2008 May;36(4):385-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High levels of endogenous tumor necrosis factor-related apoptosis-inducing ligand expression correlate with increased cell death in human pancreas.
  • OBJECTIVES: Type 1 diabetes (T1D) has been characterized by the T cell-mediated destruction of pancreatic beta cells.
  • Although various members of the tumor necrosis factor (TNF) family, such as Fas ligand or TNF, have recently been implicated in the development of T1D, the lack of TNF-related apoptosis-inducing ligand (TRAIL) expression or function facilitates the onset of T1D.
  • Thus, the goal of the present study was to investigate the expression profiles of TRAIL and its receptors in human pancreas.
  • RESULTS: Acinar cells displayed high levels of TRAIL and death receptor 4, but only low levels of death receptor 5.
  • In contrast, only TRAIL and TRAIL decoy receptors (DcR1, DcR2) were detected in ductal cells.
  • High levels of TRAIL expression in pancreas correlated with increased number of apoptotic cells.
  • CONCLUSIONS: Although the expression of TRAIL decoy receptors might be necessary for defense from TRAIL-induced apoptosis, high levels of TRAIL may provide protection for Langerhans islets from the immunological attack of cytotoxic T cells.
  • [MeSH-major] Apoptosis / physiology. Cell Death / physiology. Pancreas / cytology. Pancreas / physiology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 18437085.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tumor Necrosis Factor-alpha
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36. Thirabanjasak D, Basturk O, Altinel D, Cheng JD, Adsay NV: Is serous cystadenoma of the pancreas a model of clear-cell-associated angiogenesis and tumorigenesis? Pancreatology; 2009;9(1-2):182-8
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  • [Title] Is serous cystadenoma of the pancreas a model of clear-cell-associated angiogenesis and tumorigenesis?
  • BACKGROUND: Similar to the other von Hippel-Lindau (VHL)-related tumors such as renal cell carcinomas and capillary hemangioblastomas, serous cystadenomas (SCAs) of the pancreas are also characterized by clear cells.
  • Over the years, we have also noticed that the tumor epithelium shows a prominent capillary network.
  • METHODS: Eighteen cases of SCA were reviewed histologically, and immunohistochemical analysis was performed for CD31 and vascular endothelial growth factor (VEGF) as well as the molecules implicated in clear-cell tumorigenesis: GLUT-1, hypoxia-inducible factor-1 (HIF-1alpha), and carbonic anhydrase IX (CA IX).
  • RESULTS: There was an extensively rich capillary network that appears almost intraepithelially in all cases of SCA, which was confirmed by CD31 stain that showed, on average, 26 capillaries per every 100 epithelial cells.
  • Among the clear-cell tumorigenesis markers, CA IX was detected in all cases, GLUT-1 and HIF-1alpha in most cases.
  • CONCLUSION: As in other VHL-related clear-cell tumors, there is a prominent capillary network immediately adjacent to the epithelium of SCA, confirming that the clear-cell- angiogenesis association is also valid for this tumor type.
  • Molecules implicated in clear-cell tumorigenesis are also consistently expressed in SCA.
  • More importantly, SCA may also serve as a model of clear-cell-associated angiogenesis and tumorigenesis, and the information gained from this tumor type may also be applicable to other clear-cell tumors.

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  • [Copyright] Copyright 2008 S. Karger AG, Basel and IAP.
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  • (PMID = 19077470.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA101936; United States / NCI NIH HHS / CA / CA101936
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Glucose Transporter Type 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC2835376
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37. Marrache F, Tu SP, Bhagat G, Pendyala S, Osterreicher CH, Gordon S, Ramanathan V, Penz-Osterreicher M, Betz KS, Song Z, Wang TC: Overexpression of interleukin-1beta in the murine pancreas results in chronic pancreatitis. Gastroenterology; 2008 Oct;135(4):1277-87
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  • [Title] Overexpression of interleukin-1beta in the murine pancreas results in chronic pancreatitis.
  • BACKGROUND & AIMS: Chronic pancreatitis is a significant cause of morbidity and a known risk factor for pancreatic adenocarcinoma.
  • Interleukin-1beta is a proinflammatory cytokine involved in pancreatic inflammation.
  • We sought to determine whether targeted overexpression of interleukin-1beta in the pancreas could elicit localized inflammatory responses and chronic pancreatitis.
  • RESULTS: Three transgenic lines were generated, and in each line the pancreas was atrophic and occasionally showed dilation of pancreatic and biliary ducts secondary to proximal fibrotic stenosis.
  • Pancreatic histology showed typical features of chronic pancreatitis.
  • There was evidence for increased acinar proliferation and apoptosis, along with prominent expression of tumor necrosis factor-alpha; chemokine (C-X-C motif) ligand 1; stromal cell-derived factor 1; transforming growth factor-beta1; matrix metallopeptidase 2, 7, and 9; inhibitor of metalloproteinase 1; and cyclooxygenase 2.
  • Older mice displayed acinar-ductal metaplasia but did not develop mouse pancreatic intraepithelial neoplasia or tumors.
  • CONCLUSIONS: Overexpression of interleukin-1beta in the murine pancreas induces chronic pancreatitis.
  • Elastase sshIL-1beta mice consistently develop severe chronic pancreatitis and constitute a promising model for studying chronic pancreatitis and its relationship with pancreatic adenocarcinoma.

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  • (PMID = 18789941.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA093405; United States / NCI NIH HHS / CA / R01 CA120979-03; United States / NCI NIH HHS / CA / U54 CA126513; United States / NCI NIH HHS / CA / R01 CA093405-07A1; United States / NCI NIH HHS / CA / CA093405-07A1; United States / NCI NIH HHS / CA / CA120979-03; United States / NCI NIH HHS / CA / U54 CA126513-03; United States / NCI NIH HHS / CA / CA126513-03; United States / NCI NIH HHS / CA / R01 CA120979
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1beta; EC 3.4.21.36 / Pancreatic Elastase
  • [Other-IDs] NLM/ NIHMS73579; NLM/ PMC2707078
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38. Suzuki Y, Sugiyama M, Abe N, Fujioka Y, Atomi Y: Immunohistochemical similarities between pancreatic mucinous cystic tumor and ovarian mucinous cystic tumor. Pancreas; 2008 Jan;36(1):e40-6
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] Immunohistochemical similarities between pancreatic mucinous cystic tumor and ovarian mucinous cystic tumor.
  • OBJECTIVE: Pancreatic mucinous cystic tumor (MCT(P)) and ovarian mucinous cystic tumor (MCT(O)) show common features.
  • However, there are few studies showing a comparison of both types of tumor.
  • We immunohistochemically studied both types of tumor to clarify their characteristics.
  • The tumors were immunohistochemically examined using antibodies against female sex hormone receptors (estrogen receptor, progesterone receptor, and alpha-inhibin), pancreatobiliary tissue markers (carbohydrate antigen 19-9 and DUPAN2) and cell cycle regulators (p27kip1 and phosphorylated retinoblastoma).
  • Samples from 7 female patients with invasive pancreatic ductal carcinoma (DC), 8 female patients with normal pancreatic tissue, and 10 patients with normal ovarian tissue were also examined.
  • RESULTS: In the tumor epithelial cells, the expressions of DUPAN2 and p27/kip1 were similar between MCT(P) (38% and 88%, respectively) and MCT(O) (14% and 76%, respectively), but significantly different between both tumors and DC (100% and 0%).
  • In the stromal cells, the expressions of estrogen receptor, progesterone receptor, alpha-inhibin, and p27/kip1 were similar between MCT(P) (63%, 75%, 50%, and 63%, respectively) and MCT(O) (57%, 71%, 81%, and 57%, respectively), but significantly different between both tumors and DC (0%, 0%, 0%, and 0%, respectively).
  • A frequent p27/kip1 expression level was associated with nonaggressive progression of both tumors.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / chemistry. Cystadenocarcinoma, Mucinous / chemistry. Cystadenoma, Mucinous / chemistry. Immunohistochemistry. Ovarian Neoplasms / chemistry. Pancreatic Neoplasms / chemistry
  • [MeSH-minor] Adult. Aged. Cyclin-Dependent Kinase Inhibitor p27 / analysis. Epithelial Cells / chemistry. Female. Humans. Inhibins / analysis. Middle Aged. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis

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  • (PMID = 18192871.001).
  • [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 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / inhibin-alpha subunit; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 57285-09-3 / Inhibins
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39. Crucitti A, Grossi U, Giustacchini P, Tomaiuolo PM, Bellantone R: Solid pseudopapillary tumor of the pancreas in children: report of a case and review of the literature. Updates Surg; 2010 Aug;62(1):69-72
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • [Title] Solid pseudopapillary tumor of the pancreas in children: report of a case and review of the literature.
  • Solid pseudopapillary tumor (SPT) of the pancreas is an infrequent neoplasm of low malignant potential, first described by Frantz in 1933 and representing less than 3% of all exocrine tumors.
  • A 15-year-old girl with a 12 × 14 × 10 cm solid mass growing from the tail and the body of the pancreas, involving spleen, left adrenal gland and kidney, stomach and some bowel loops, was referred for surgical treatment.
  • Histopathological examination revealed that the tumor was a 14-cm well-circumscribed solid mass, with pseudopapillary cell architecture, showing strong cellular immunoreactivity for alpha-1 antitrypsin, vimentin, neurone-specific enolase, progesterone receptors and in part to CD10 and CAM 5.2, but not to sinaptofisin and chromogranin.
  • A 24-month post-surgical follow-up after successful surgical resection showed no evidence of recurrent disease.
  • High survival rates can be achieved in most cases, warranting aggressive treatments even in metastatic disease.
  • [MeSH-major] Pancreatic Neoplasms

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  • (PMID = 20845104.001).
  • [ISSN] 2038-131X
  • [Journal-full-title] Updates in surgery
  • [ISO-abbreviation] Updates Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
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40. Aydede H, Erhan Y, Ikgül O, Cilaker S, Sakarya A, Vatansever S: Effect of portal vein occlusion on the pancreas: an experimental model. World J Surg; 2006 Jun;30(6):1000-6
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  • [Title] Effect of portal vein occlusion on the pancreas: an experimental model.
  • BACKGROUND: The effects of portal vein occlusion on the pancreas are not clearly understood.
  • Therefore, we studied histomorphological changes induced in the rat pancreas by various periods of portal vein occlusion.
  • The pancreas was removed immediately after sham laparotomy in Group I and immediately after clamp release in Groups II-IV.
  • Pancreatic tissue specimens were subjected to histochemical analysis for cell typing and diagnosis, immunohistochemical analysis for identification of the inflammatory markers tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), endothelial nitric oxide synthase (eNOS), and inducible NOS (iNOS), and TUNEL analysis was carried out for identification of apoptotic cells.
  • RESULTS: Histochemistry revealed signs of inflammation in pancreatic tissue from rats subjected to portal vein occlusion.
  • Immunohistochemistry revealed that the expression of proinflammatory cytokines TNF-alpha and IL-1beta and the oxidative damage indicator iNOS in rat pancreatic tissue increased progressively with the duration of portal vein occlusion.
  • CONCLUSION: We conclude that portal vein occlusion triggers an inflammatory response in the pancreas that worsens the longer the occlusion lasts.
  • [MeSH-major] Pancreas / pathology. Pancreatitis / physiopathology. Portal Vein / pathology
  • [MeSH-minor] Animals. Apoptosis. Constriction, Pathologic / physiopathology. Female. Immunohistochemistry. In Situ Nick-End Labeling. Interleukin-1beta / analysis. Nitric Oxide Synthase Type II / analysis. Nitric Oxide Synthase Type III / analysis. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16736328.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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41. Huber SA, Sartini D: Roles of tumor necrosis factor alpha (TNF-alpha) and the p55 TNF receptor in CD1d induction and coxsackievirus B3-induced myocarditis. J Virol; 2005 Mar;79(5):2659-65
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  • [Title] Roles of tumor necrosis factor alpha (TNF-alpha) and the p55 TNF receptor in CD1d induction and coxsackievirus B3-induced myocarditis.
  • Giving C57BL/6 mice 10(4) PFU of coxsackievirus B3 (H3 variant) fails to induce myocarditis, but increasing the initial virus inoculum to 10(5) or 10(6) PFU causes significant cardiac disease.
  • Tumor necrosis factor alpha (TNF-alpha) concentrations in the heart were increased in all infected mice, but cytokine levels were highest in mice given the larger virus inocula.
  • TNF-alpha(-/-) and p55 TNF receptor-negative (TNFR(-/-)) mice developed minimal myocarditis compared to B6;129 or C57BL/6 control mice. p75 TNFR(-/-) mice were as disease susceptible as C57BL/6 animals.
  • No significant differences in virus titers in heart or pancreas were observed between the groups, but C57BL/6 and p75 TNFR(-/-) animals showed 10-fold more inflammatory cells in the heart than p55 TNFR(-/-) mice, and the cell population was comprised of high concentrations of CD4(+) gamma interferon-positive and Vgamma4(+) cells.
  • Cardiac endothelial cells isolated from C57BL/6 and p75 TNFR(-/-) mice upregulate CD1d, the molecule recognized by Vgamma4(+) cells, but infection of TNF(-/-) or p55 TNFR(-/-) endothelial cells failed to upregulate CD1d.
  • Infection of C57BL/6 endothelial cells with a nonmyocarditic coxsackievirus B3 variant, H310A1, which is a poor inducer of TNF-alpha, failed to elicit CD1d expression, but TNF-alpha treatment of H310A1-infected endothelial cells increased CD1d levels to those seen in H3-infected cells.
  • TNF-alpha treatment of uninfected endothelial cells had only a modest effect on CD1d expression, suggesting that optimal CD1d upregulation requires both infection and TNF-alpha signaling.

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  • (PMID = 15708985.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / P01 AI045666; United States / NHLBI NIH HHS / HL / R01 HL058583; United States / NHLBI NIH HHS / HL / HL58583; United States / NIAID NIH HHS / AI / P01 AI45666
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC548425
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42. Dinc B, Sahin C: Metastatic glucagonoma. Eurasian J Med; 2009 Apr;41(1):70-2

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  • [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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43. Kolb-van Harten P, Rosien U, Klöppel G, Layer P: Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression. Pancreatology; 2007;7(4):370-2
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  • [Title] Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression.
  • We report a case of acinar cell carcinoma of the pancreas associated with excessively elevated levels of serum alpha-fetoprotein (>32,000 ng/ml).
  • Abdominal computed tomography scan revealed a large pancreatic mass with infiltration of the splenic artery.
  • This regimen was associated with clinical improvement and dramatic decreases in both tumor size and serum alpha-fetoprotein.
  • [MeSH-major] Carcinoma, Acinar Cell / metabolism. Pancreatic Neoplasms / metabolism. alpha-Fetoproteins / metabolism

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  • [Copyright] 2007 S. Karger AG, Basel and IAP
  • (PMID = 17703084.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha-Fetoproteins; 0W860991D6 / Deoxycytidine; 50SG953SK6 / Mitomycin; B76N6SBZ8R / gemcitabine
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44. Vakiani E, Young RH, Carcangiu ML, Klimstra DS: Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases. Am J Surg Pathol; 2008 Oct;32(10):1540-5
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  • [Title] Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases.
  • We report 4 cases of acinar cell carcinoma of the pancreas, 3 presenting as metastases in the ovary, the first report of this circumstance, which may pose a broad differential diagnosis and caused significant diagnostic difficulty in all the cases.
  • In 3 cases, the ovarian tumors were detected before the pancreatic tumor; in 1 case, a large abdominal mass and ovarian tumors were discovered synchronously.
  • The ovarian tumors were large, solid, white-tan on gross examination, and bilateral in 3 cases; the single case involving only 1 ovary had 2 discrete masses of tumor.
  • Two cases had a predominant acinar growth pattern of cells with brightly eosinophilic, granular cytoplasm.
  • In 2 cases, the pattern was predominantly solid-cribriform with areas of comedolike necrosis, and the cells had pale eosinophilic, finely granular cytoplasm.
  • The main differential diagnostic consideration was well-differentiated neuroendocrine neoplasm (carcinoid tumor); positive immunostaining with antibodies against chymotrypsin and trypsin and negative immunostaining with antibodies against synaptophysin and chromogranin helped exclude this diagnosis.
  • We observed focal alpha-inhibin immunostaining in 2 cases, which may represent a potential diagnostic pitfall, as a Sertoli cell tumor or unusual granulosa cell tumor may also enter the differential diagnosis.
  • Inclusion of antibodies against the pancreatic enzymes chymotrypsin and trypsin in the immunohistochemical panel is critical in establishing the correct diagnosis and should be considered when evaluating ovarian tumors with architectural (mainly acinar) and cytologic (granular eosinophilic cytoplasm) characteristics that should bring a metastatic acinar cell carcinoma into consideration.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Ovarian Neoplasms / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 18724247.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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45. Li YH, Huang ZW, Xue P, Guo J, He FQ, You Z, Wang ZR: [Effects of Chaiqin Chengqi Decoction on activation of nuclear factor-kappaB in pancreas of rats with acute necrotizing pancreatitis]. Zhong Xi Yi Jie He Xue Bao; 2008 Feb;6(2):180-4
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  • [Title] [Effects of Chaiqin Chengqi Decoction on activation of nuclear factor-kappaB in pancreas of rats with acute necrotizing pancreatitis].
  • Blood sample was collected from abdominal vein for examination and the pancreatic tissue samples were taken for making pathology section 6 hours later.
  • The pancreatic tissue (HE staining) was observed by light microscope.
  • The content of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) was detected with the method of enzyme-linked immunosorbent assay, and the activation of nuclear factor-kappaB (NF-kappaB) in pancreas was detected by immunohistochemical method.
  • RESULTS: Compared with the SO group, there was dramatic increase in the white blood cell (WBC) counts and AMY level in the ANP group (P<0.05, P<0.01).
  • The integral optical density of NF-kappaB p65 positive cells of pancreas in CQCQD-treated group was lower than that in the ANP group (P<0.05).
  • CONCLUSION: CQCQD can reduce the content of serum TNF-alpha and IL-6, depress the activation of NF-kappaB, and lessen the pancreatic lesions.
  • [MeSH-major] Drugs, Chinese Herbal / therapeutic use. NF-kappa B / metabolism. Pancreas / metabolism. Pancreatitis, Acute Necrotizing / drug therapy. Phytotherapy
  • [MeSH-minor] Animals. Female. Interleukin-6 / blood. Male. Random Allocation. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 18241655.001).
  • [ISSN] 1672-1977
  • [Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
  • [ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Chai Qin Cheng Qi decoction; 0 / Drugs, Chinese Herbal; 0 / Interleukin-6; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha
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46. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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47. Korkolis DP, Aggeli C, Plataniotis GD, Gontikakis E, Zerbinis H, Papantoniou N, Xinopoulos D, Apostolikas N, Vassilopoulos PP: Successful en bloc resection of primary hepatocellular carcinoma directly invading the stomach and pancreas. World J Gastroenterol; 2009 Mar 7;15(9):1134-7
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  • [Title] Successful en bloc resection of primary hepatocellular carcinoma directly invading the stomach and pancreas.
  • Multivisceral surgical resection for cure was successfully performed in a 70-year-old man suffering from a primary hepatocellular carcinoma (HCC) associated with direct invasion to the stomach and pancreas.
  • The patient presented with gastric outlet obstruction, upper abdominal pain and a history of chronic liver disease due to hepatitis B virus (HBV) infection.
  • Upper gastrointestinal (GI) endoscopy revealed an infiltrating tumor protruding through the gastric wall and obliterating the lumen.
  • Computer tomograghy (CT) and magnetic resonance imaging (MRI) scan demonstrated a 15-cm tumor in the left lateral segment of the liver with invasion to the stomach and pancreas.
  • Alpha-foetoprotein (AFP) levels and liver function tests were normal.
  • Pathology revealed a poorly differentiated, giant cell HCC involving the stomach and pancreas.
  • Disease-free margins of resection were achieved.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Liver Neoplasms / surgery. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery

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  • (PMID = 19266609.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2655177
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48. Santini D, Poli F, Lega S: Solid-papillary tumors of the pancreas: histopathology. JOP; 2006;7(1):131-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solid-papillary tumors of the pancreas: histopathology.
  • A solid-pseudopapillary tumor is an uncommon and "enigmatic" pancreatic neoplasm, and the term encompasses the two most conspicuous histological features: solid and pseudopapillary areas.
  • Histologically, solid-pseudopapillary tumors are generally characterized by solid areas alternating with a pseudopapillary pattern, and cystic spaces which are the results of degenerative changes occurring in the solid neoplasm.
  • Its immunohistochemical pattern is very distinctive and neoplastic cells are consistently vimentin-, CD10- and CD56-positive.
  • Some cases express focal positivity for alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase and synaptophysin.
  • Endocrine and pancreatic enzyme markers are absent; the origin of solid-pseudopapillary tumors has not yet been clarified.
  • Many investigators favor the theory that solid-pseudopapillary tumors originate from multipotent primordial cells while others suggest an extra-pancreatic origin from genital ridge angle-related cells.
  • Solid-pseudopapillary tumors appear as a low malignancy tumor and only a small number of cases recur or develop metastases after resection.
  • [MeSH-major] Carcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antigens, CD56 / analysis. Cell Proliferation. Humans. Immunohistochemistry. Neoplasm Invasiveness. Neprilysin / analysis. Receptors, Progesterone / analysis. Vimentin / analysis

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  • (PMID = 16407635.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Receptors, Progesterone; 0 / Vimentin; EC 3.4.24.11 / Neprilysin
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49. 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
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  • [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


50. Liu XN, Huo TT, Wang WZ: [Protective effect of shenfu injection against ischemia-reperfusion injury due to pancreas transplantation in rats]. Zhongguo Zhong Xi Yi Jie He Za Zhi; 2006 Jun;26 Suppl:111-5
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  • [Title] [Protective effect of shenfu injection against ischemia-reperfusion injury due to pancreas transplantation in rats].
  • OBJECTIVE: To investigate the protective effect of Shenfu Injection against ischemia-reperfusion (I/R) injury due to pancreas transplantation in rats, and explore its possible mechanism.
  • Except I/R group, the rats in the other groups were intravenous injected with Shenfu Injection (SF,10 mg/kg), Hongshen Injection (HS, 9 mg/kg) and Fuzi Injection (FZ 1 mg/kg) respectively at the day and 30 minutes before pancreas transplantation performed in the SF group, HS group and FZ group, respectively.
  • The blood glucose was detected before and after reperfusion, and 2 hours later after reperfusion, the contents of serum nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha), the concentrations of malondialdehyde (MDA) , superoxide dismutase (SOD) , and myeloperoxidase (MPO) in the transplanted pancreas tissues were detected.
  • The cell apoptosis of the transplanted pancreas tissue was determined by TUNEL, and the bcl-2 and Bax protein expression was determined by Western blot.
  • RESULTS: After reperfusion, the levels of blood glucose and TNF-alpha decreased and the concentration of NO increased in the SF group, HS group and FZ group, compared with those in the I/R group.
  • CONCLUSION: Shenfu Injection can protect L/R injury due to pancreas transplantation in rats, the possible mechanism may be related to promoting activity of SOD, increasing synthesis of endogenous NO, decreasing the excretion of TNF-alpha, alleviating conglutination and aggregation of polymorphonuclear neutrophils (PMNs) in pancreas, as well as up-regulating Bcl-2 gene expression and down-regulating the Bax gene expression.

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  • (PMID = 17569364.001).
  • [ISSN] 1003-5370
  • [Journal-full-title] Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine
  • [ISO-abbreviation] Zhongguo Zhong Xi Yi Jie He Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Protective Agents; 0 / Shen-Fu; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; 4Y8F71G49Q / Malondialdehyde; EC 1.15.1.1 / Superoxide Dismutase
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51. Toyoda E, Doi R, Koizumi M, Kami K, Ito D, Mori T, Fujimoto K, Nakajima S, Wada M, Imamura M: Analysis of E-, N-cadherin, alpha-, beta-, and gamma-catenin expression in human pancreatic carcinoma cell lines. Pancreas; 2005 Mar;30(2):168-73
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  • [Title] Analysis of E-, N-cadherin, alpha-, beta-, and gamma-catenin expression in human pancreatic carcinoma cell lines.
  • OBJECTIVES: Cadherins are cell surface glycoproteins that mediate Ca2+-dependent, homophilic cell-cell adhesion.
  • The classic cadherins interact with either beta-catenin or gamma-catenin, which is bound to alpha-catenin that links the complex to the actin cytoskeleton.
  • The aim of this study was to analyze the expressions of E- and N-cadherins and catenins in human pancreatic cancer cell lines.
  • METHODS: We examined the expression of cadherins and catenins in 7 human pancreatic cancer cells by RT-PCR, Western blotting, and immunocytochemistry.
  • RESULTS: E-cadherin was expressed in all cell lines except for MIAPaCa-2, whereas N-cadherin was expressed in Capan-2, CFPAC-1, BxPC-3, and PANC-1.
  • The alpha-, beta-, and gamma-catenins were expressed and cadherins/beta-catenin interactions were detected in all cadherin-expressing cells.
  • CONCLUSION: The decreased or loss of cadherins and catenins expression could be involved in the tumor progression and metastasis, although these events may occur in in vivo conditions by interaction between cancer cells and extracellular matrices.
  • [MeSH-major] Adenocarcinoma / physiopathology. Cadherins / genetics. Catenins / genetics. Pancreatic Neoplasms / physiopathology
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. RNA, Messenger / analysis. alpha Catenin / genetics. alpha Catenin / metabolism. beta Catenin / genetics. beta Catenin / metabolism. gamma Catenin / genetics. gamma Catenin / metabolism

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  • (PMID = 15714139.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Catenins; 0 / RNA, Messenger; 0 / alpha Catenin; 0 / beta Catenin; 0 / gamma Catenin
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52. Lu L, Zhang Q, Pu LJ, Xu XW, Zhang RY, Zhang JS, Hu J, Yang ZK, Lü AK, Ding FH, Shen J, Chen QJ, Lou S, Fang DH, Shen WF: Elevation of tumor necrosis factor-alpha, interleukin-1beta and interleukin-6 levels in aortic intima of Chinese Guizhou minipigs with streptozotocin-induced diabetes. Chin Med J (Engl); 2007 Mar 20;120(6):479-84
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  • [Title] Elevation of tumor necrosis factor-alpha, interleukin-1beta and interleukin-6 levels in aortic intima of Chinese Guizhou minipigs with streptozotocin-induced diabetes.
  • BACKGROUND: Large animal models with toxin-mediated pancreatic damage have been used extensively in researches with respect to diabetes mellitus and cardiovascular diabetic complications.
  • The present study aimed to establish Chinese Guizhou minipig models with streptozotocin (STZ)-induced diabetes and characterize the animal models by analyzing inflammatory cytokine levels in aortic wall, such as tumor necrosis factor (TNF)-alpha, interleukin-1beta (IL-1beta) and interleukin-6 (IL-6).
  • Oral glucose tolerance test (OGTT) was performed before and one month after STZ administration and serum concentrations of alanine transaminase, asparagine transaminase, albumin, blood urea nitrogen, creatinine, lipids and white blood cell count were measured before and six months later.
  • Animals in both groups were euthanized after six months and pancreas was examined immunohistochemically for islet beta cells.
  • Aortic intima of diabetic minipigs and controls was analyzed for TNF-alpha level in tissue conditioned medium by Western blot.
  • TNF-alpha, IL-1beta and IL-6 mRNA levels in aortic intima were assayed by reverse transcription and polymerase chain reaction (RT-PCR).
  • The normal pancreas had many irregular sized islets and small clusters of islet beta cells, while in pancreas of diabetic minipigs islet beta cells almost disappeared.
  • Western blot demonstrated dramatically increased TNF-alpha level in aotic intima conditioned medium, and significant elevation of TNF-alpha, IL-1beta and IL-6 mRNA levels was revealed by RT-PCR.
  • Inflammatory cytokines (TNF-alpha, IL-1beta and IL-6) significantly elevated in aortic intima of diabetic minipigs.
  • [MeSH-major] Aorta / chemistry. Diabetes Mellitus, Experimental / immunology. Interleukin-1beta / blood. Interleukin-6 / blood. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Animals. Glucose Tolerance Test. Immunohistochemistry. Male. Pancreas / pathology. Streptozocin. Swine. Swine, Miniature

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  • (PMID = 17439741.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 5W494URQ81 / Streptozocin
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53. Sawai H, Okada Y, Funahashi H, Matsuo Y, Takeyama H, Manabe T: Anaplastic carcinoma of the pancreas with squamous features: report of a case and immunohistochemical study. Med Sci Monit; 2005 Nov;11(11):CS65-8
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  • [Title] Anaplastic carcinoma of the pancreas with squamous features: report of a case and immunohistochemical study.
  • BACKGROUND: Anaplastic carcinomas of the pancreas are rare aggressive tumors with survival measurable in weeks.
  • Many terms have been applied used to describe these tumors, and anaplastic foci are identified in ductal adenocarcinomas and in ectopic pancreata, but are not the dominant pattern of growth.
  • We herein present our experience with a case of anaplastic carcinoma of the pancreas with squamous features in order that allowed us to delineate the clinicopathologic and immunohistochemical features of this rare entity.
  • CASE REPORT: According to imaging findings, the 77-year-old Japanese man was diagnosed as the malignant pancreatic tumor, and underwent a surgical resection.
  • Histopathologically, anaplastic tumor cells showed focal ductal and squamous features infiltrated into pancreatic parenchyma, extrapancreatic fatty tissue, and stomach.
  • The tumor cells showed strong reactivity for cytokeratin, alpha-SMA, vimentin, NSE, and S-100 protein.
  • Although immunoreactivity against p53 was negative, strong positive immunostaining for proliferating cell nuclear antigen and interleukin-1 receptor type I (IL-1RI) was observed in a the majority of tumor cells, while the alpha6 integrin subunit was predominantly strong expressed in the adenocarcinomatous lesion.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma / diagnosis. Integrins / analysis. Pancreatic Neoplasms / diagnosis. Receptors, Interleukin-1 / analysis
  • [MeSH-minor] Aged. Carcinoma, Squamous Cell / diagnosis. Fatal Outcome. Humans. Immunohistochemistry. Male. Peritoneal Neoplasms / diagnosis. Peritoneal Neoplasms / secondary. Prognosis

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  • (PMID = 16258403.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Integrins; 0 / Receptors, Interleukin-1
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54. Cao D, Antonescu C, Wong G, Winter J, Maitra A, Adsay NV, Klimstra DS, Hruban RH: Positive immunohistochemical staining of KIT in solid-pseudopapillary neoplasms of the pancreas is not associated with KIT/PDGFRA mutations. Mod Pathol; 2006 Sep;19(9):1157-63
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  • [Title] Positive immunohistochemical staining of KIT in solid-pseudopapillary neoplasms of the pancreas is not associated with KIT/PDGFRA mutations.
  • Solid-pseudopapillary neoplasms of the pancreas are uncommon neoplasms of low malignant potential and of uncertain histogenesis.
  • A small percentage of patients develop metastatic disease and some succumb to disease.
  • The management of patients with metastatic disease or unresectable tumor, and patients who are just not good surgical candidates is problematic.
  • Successful treatment of metastatic and unresectable gastrointestinal stromal tumors with KIT kinase inhibitor, imatinib mesylate (Gleevec), makes it intriguing to look at the status of KIT in solid-pseudopapillary neoplasms of the pancreas.
  • Of the 50 (50%) solid-pseudopapillary neoplasms, 25 showed diffuse expression (in >50% neoplastic cells) of KIT and additional five (10%) cases showed focal staining (in 10-50% neoplastic cells).
  • Expression of KIT was not associated with tumor behavior and prognosis.
  • Experience in gastrointestinal stromal tumors and other tumors have shown that mutation-mediated activation of KIT or PDGFRA is a prerequisite for clinical response with imatinib mesylate.
  • Thus, lack of mutations in KIT or PDGFRA in solid-pseudopapillary neoplasms suggests that imatinib mesylate is less likely to be effective in the treatment for patients with metastatic disease or unresectable tumor, and patients who are just not good surgical candidates.
  • [MeSH-major] Carcinoma, Papillary / metabolism. Mutation. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / metabolism. Cell Count. Child. DNA Mutational Analysis. Female. Humans. Immunohistochemistry / methods. Male. Middle Aged. Survival Rate

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  • [Copyright] Published online 16 June 2006.
  • (PMID = 16778826.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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55. Serra S, Salahshor S, Fagih M, Niakosari F, Radhi JM, Chetty R: Nuclear expression of E-cadherin in solid pseudopapillary tumors of the pancreas. JOP; 2007;8(3):296-303
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  • [Title] Nuclear expression of E-cadherin in solid pseudopapillary tumors of the pancreas.
  • CONTEXT: Solid pseudopapillary tumors of the pancreas are rare and have recently been shown to harbor mutations of the beta-catenin gene with resultant nuclear localization of beta-catenin protein to the nucleus.
  • OBJECTIVE: To explore the protein expression of E-cadherin in a series of solid pseudopapillary tumors of the pancreas.
  • PARTICIPANTS: Eighteen cases of solid pseudopapillary tumors of the pancreas.
  • Tissue cores from normal pancreas were used as controls and for orientation purposes.
  • MAIN OUTCOME MEASURES: The slides were stained with the following commercially available antibodies: CD10, CD56, vimentin, alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase, chromogranin, synaptophysin, beta-catenin and E-cadherin.
  • RESULTS: All the tumors were CD10, vimentin, alpha-1-antitrypsin and alpha-1-antichymotrypsin diffusely positive (50% or more of the tumor cells staining) and CD56 showed focal positivity in all cases with 5-10% of tumor cells displaying immunolabeling.
  • Similarly, E-cadherin protein was localized to the nucleus in all 18 cases, with loss of the characteristic membranous decoration of cells.
  • CONCLUSION: This study is the first demonstration of aberrant nuclear localization of E-cadherin protein in solid pseudopapillary tumors of the pancreas.
  • Whilst the exact mechanism is not know and nuclear E-cadherin is not related to tumor aggression, this staining pattern may be of diagnostic value in concert with beta-catenin staining.
  • [MeSH-major] Cadherins / analysis. Carcinoma, Papillary / chemistry. Cell Nucleus / chemistry. Pancreatic Neoplasms / chemistry

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  • (PMID = 17495358.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Cadherins; 0 / beta Catenin; EC 3.4.24.11 / Neprilysin
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56. Aleksic T, Baumann B, Wagner M, Adler G, Wirth T, Weber CK: Cellular immune reaction in the pancreas is induced by constitutively active IkappaB kinase-2. Gut; 2007 Feb;56(2):227-36
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  • [Title] Cellular immune reaction in the pancreas is induced by constitutively active IkappaB kinase-2.
  • The aim of the present study was to analyse the consequences of ectopic IkappaB kinase-2 (IKK2) activation in the pancreas of mice.
  • METHODS: Transgenic mice were generated using an inducible genetic system (tet system) to conditionally overexpress a gain of function mutant of IKK2 (tetO-IKK2-EE) in the pancreas.
  • To achieve transgene expression in the pancreas, these animals were crossed with CMV-rtTA mice that are known to express the rtTA protein in the pancreas.
  • RESULTS: In these double transgenic animals, doxycycline treatment induced expression of IKK2-EE (IKK2(CA)) in pancreatic acinar cells resulting in moderate activation of the IkappaB kinase complex, as measured by the immune complex kinase assay, and up to 200-fold activation of the transgene expression cassette, as detected by luciferase assay.
  • IKK2(CA) expression in the pancreas had a mosaic appearance.
  • Increased mRNA levels of tumour necrosis factor alpha and RANTES were detected in pancreatic acinar cells.
  • However, only minor damage to pancreatic tissue was observed.
  • CONCLUSIONS: Our observations suggest that the role of IKK2 activation in pancreatic acini is to induce leucocyte infiltration, but at a moderate level of activation it is not sufficient to induce pancreatic damage in mice.
  • The IKK2(CA) induced infiltrations resemble those observed in autoimmune pancreatitis, indicating a role for IKK2/NF-kappaB in this disease.
  • IKK2(CA) in pancreatic acinar cells increases tissue damage of secretagogue induced experimental pancreatitis underlining the proinflammatory role of the IKK/NF-kappaB pathway in this disease.
  • [MeSH-major] I-kappa B Kinase / immunology. Immunity, Cellular / immunology. Pancreas / immunology
  • [MeSH-minor] Animals. B-Lymphocytes / immunology. Ceruletide / immunology. Chemokine CCL5 / analysis. Doxycycline / immunology. Enzyme Activation. Gene Expression / genetics. Immunohistochemistry / methods. Luciferases / metabolism. Macrophages / immunology. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Mice, Transgenic. NF-kappa B / genetics. NF-kappa B / metabolism. RNA, Messenger / analysis. Transgenes / immunology. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16870717.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokine CCL5; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 888Y08971B / Ceruletide; EC 1.13.12.- / Luciferases; EC 2.7.11.10 / I-kappa B Kinase; N12000U13O / Doxycycline
  • [Other-IDs] NLM/ PMC1856776
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57. Ji Y, Wang XN, Lou WH, Sujie A, Tan YS, Jin DY: Serous cystic neoplasms of the pancreas: a clinicopathologic and immunohistochemical analysis. Chin J Dig Dis; 2006;7(1):39-44
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  • [Title] Serous cystic neoplasms of the pancreas: a clinicopathologic and immunohistochemical analysis.
  • OBJECTIVE: To clarify whether the various subtypes of serous cystic neoplasms (SCNs) of the pancreas can be distinguished from each other by marker profiles.
  • METHODS: The immunoprofiles of 13 SCNs were defined by using antibodies against cytoskeletal, neuroendocrine, hormone receptor, and mucin markers.
  • In addition, we examined the expression of calrentinin and alpha-inhibin.
  • RESULTS: SCN included 7 cases of serous microcystic adenomas (SMA), 3 cases of serous oligocystic ill-defined adenomas (SOIA), 1 case of solid serous adenoma (SSA), 1 case of von Hippel-Lindau-associated cystic neoplasm (VHL-CN), and 1 case of serous cystadenocarcinoma (SCC).
  • Other markers that were commonly expressed in the SCNs were alpha-inhibin (85%), MUC1 (69%) and MUC6 (77%).
  • CONCLUSION: The results suggest that, despite their biologic differences, the various types of SCNs have the same (or a very similar) cell type and may therefore have a common direction of differentiation.
  • A centroacinar origin is supported by the finding that a number of SCNs share MUC1 and MUC6 expression with pancreatic centroacinar cells.
  • Alpha-inhibin, and MUC6 may be regarded as new markers for this type of pancreatic tumor.
  • [MeSH-major] Cystadenoma, Serous / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor. Female. Humans. Immunohistochemistry. Male. Middle Aged. Tomography, X-Ray Computed


58. Minakawa K, Oka K, Nihei T, Sando N, Oikawa H, Toda J, Hosokawa Y, Matsumoto T, Yanagisawa A: Pancreatic endocrine tumor with partial acinar cell differentiation. APMIS; 2006 Oct;114(10):720-5
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  • [Title] Pancreatic endocrine tumor with partial acinar cell differentiation.
  • We examined a 70-year-old woman in whom a pancreatic endocrine tumor with partial acinar cell differentiation had been diagnosed.
  • The tumor was located in the pancreatic tail and measured 12.5 x 9.5 x 8 cm.
  • The neoplastic cells had large, irregular, oval nuclei; prominent eosinophilic nucleoli; and abundant eosinophilic cytoplasm with many fine granules.
  • The cells had proliferated in islet-like solid medullary, trabecular, acinar, and papillary patterns.
  • Most neoplastic cells were strongly positive for synaptophysin.
  • 10 to 25% of the neoplastic cells were positive for alpha1-antitrypsin.
  • Neuroendocrine and zymogen granules were simultaneously observed in the cytoplasm of the same neoplastic cells at the ultrastructural level.
  • The tumor may be considered an amphicrine tumor.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Islet Cell / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pancreas / pathology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Biopsy, Needle. Cytoplasmic Granules / ultrastructure. Female. Humans. Immunohistochemistry. Secretory Vesicles / ultrastructure. Synaptophysin / analysis. Synaptophysin / metabolism. alpha 1-Antitrypsin / analysis. alpha 1-Antitrypsin / metabolism

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  • (PMID = 17004975.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Synaptophysin; 0 / alpha 1-Antitrypsin
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59. Deng M, Chen PC, Xie S, Zhao J, Gong L, Liu J, Zhang L, Sun S, Liu J, Ma H, Batra SK, Li DW: The small heat shock protein alphaA-crystallin is expressed in pancreas and acts as a negative regulator of carcinogenesis. Biochim Biophys Acta; 2010 Jul-Aug;1802(7-8):621-31
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  • [Title] The small heat shock protein alphaA-crystallin is expressed in pancreas and acts as a negative regulator of carcinogenesis.
  • In the present study, we have re-examined the distribution of alphaA-crystallin in various normal human and mouse tissues and found that the normal pancreas expresses a moderate level of alphaA-crystallin.
  • Moreover, alphaA-crystallin is found significantly downregulated in 60 cases of pancreatic carcinoma of different types than it is in 11 normal human pancreas samples.
  • Finally, expression of alphaA-crystallin in a pancreatic cancer cell line, MiaPaCa, results in retarded cell migration.
  • Together, these results suggest that alphaA-crystallin seems to negatively regulate pancreatic carcinogenesis.

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  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20434541.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY015765; United States / NEI NIH HHS / EY / R01 EY018380; United States / NEI NIH HHS / EY / 1R01 EY015765; United States / NEI NIH HHS / EY / 1R01 EY018380
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Heat-Shock Proteins; 0 / alpha-Crystallin A Chain
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60. Robinson K, Vona-Davis L, Riggs D, Jackson B, McFadden D: Peptide YY attenuates STAT1 and STAT3 activation induced by TNF-alpha in acinar cell line AR42J. J Am Coll Surg; 2006 May;202(5):788-96
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  • [Title] Peptide YY attenuates STAT1 and STAT3 activation induced by TNF-alpha in acinar cell line AR42J.
  • BACKGROUND: STAT1 and STAT3, members of the cytoplasmic family of signal transducers and activators of transcription factors (STAT), have been associated with numerous inflammatory pathologies, including inflammatory bowel disease, hepatitis, and acute lung injury.
  • But little is known about their role in the pancreas.
  • We hypothesized that tumor necrosis factor (TNF)-alpha would induce STAT1 and STAT3, and PYY would attenuate their transcription factor binding.
  • STUDY DESIGN: Rat pancreatic acinar cells were treated with recombinant TNF-alpha (200 ng/mL); PYY (3-36; 500 pM) was added 30 minutes post-TNF-alpha treatment.
  • Cells were harvested at 2 hours, and nuclear protein and conditioned media were extracted.
  • RESULTS: Amylase production was considerably increased (p < 0.05) as early as 5 minutes after addition of exogenous TNF-alpha and remained elevated for 24 hours.
  • A notable increase (p < 0.05) in the production of cytokines interleukin (IL)-1beta, IL-4, IL-6, IL-10, and TNF-alpha was observed with TNF-alpha treatment; production was reduced with PYY.
  • TNF-alpha substantially upregulated STAT1 and STAT3 (two-fold or greater); PYY downregulated their binding activity to control levels.
  • Results from both the electrophoretic mobility shift assay- and the ELISA-based assays verified STAT1 and STAT3 responses to TNF-alpha and PYY.
  • CONCLUSIONS: In pancreatic acinar cells, TNF-alpha activated STAT1 and STAT3, known mediators of inflammatory cytokines.
  • Interestingly, PYY attenuated their protein/DNA binding, which may have an impact on development of the disease.
  • [MeSH-major] Pancreas / cytology. Peptide YY / pharmacology. STAT1 Transcription Factor / drug effects. STAT3 Transcription Factor / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Amylases / metabolism. Animals. Cell Line. Cytokines / metabolism. Enzyme-Linked Immunosorbent Assay. In Vitro Techniques. Rats. STAT4 Transcription Factor / drug effects. STAT4 Transcription Factor / metabolism. STAT5 Transcription Factor / drug effects. STAT5 Transcription Factor / metabolism. STAT6 Transcription Factor / drug effects. STAT6 Transcription Factor / metabolism. Signal Transduction

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  • (PMID = 16648019.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / STAT4 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / STAT6 Transcription Factor; 0 / Stat1 protein, rat; 0 / Stat3 protein, rat; 0 / Tumor Necrosis Factor-alpha; 106388-42-5 / Peptide YY; EC 3.2.1.- / Amylases
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61. Desgrosellier JS, Barnes LA, Shields DJ, Huang M, Lau SK, Prévost N, Tarin D, Shattil SJ, Cheresh DA: An integrin alpha(v)beta(3)-c-Src oncogenic unit promotes anchorage-independence and tumor progression. Nat Med; 2009 Oct;15(10):1163-9
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  • [Title] An integrin alpha(v)beta(3)-c-Src oncogenic unit promotes anchorage-independence and tumor progression.
  • Integrins regulate adhesion-dependent growth, survival and invasion of tumor cells.
  • In particular, expression of integrin alpha(v)beta(3) is associated with progression of a variety of human tumors.
  • Here we reveal a previously undescribed adhesion-independent role for integrin alpha(v)beta(3) in pancreatic cancer and other carcinomas.
  • Specifically, alpha(v)beta(3) expressed in carcinoma cells enhanced anchorage-independent tumor growth in vitro and increased lymph node metastases in vivo.
  • These effects required recruitment of c-Src to the beta(3) integrin cytoplasmic tail, leading to c-Src activation, Crk-associated substrate (CAS) phosphorylation and tumor cell survival that, unexpectedly, was independent of cell adhesion or focal adhesion kinase (FAK) activation.
  • Pharmacological blockade of c-Src kinase activity or decreased expression of endogenous alpha(v)beta(3) integrin or c-Src not only inhibited anchorage-independent growth but also suppressed metastasis in vivo, yet these manipulations did not affect tumor cell migration or invasion.
  • These data define an unexpected role for an integrin as a mediator of anchorage independence, suggesting that an alpha(v)beta(3)-c-Src signaling module may account for the aggressive behavior of integrin alpha(v)beta(3)-expressing tumors in humans.

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  • (PMID = 19734908.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA095262-06; United States / NCI NIH HHS / CA / CA129660-02; United States / NCI NIH HHS / CA / T32 CA121938; United States / NCI NIH HHS / CA / CA050286-20; United States / NCI NIH HHS / CA / R01 CA095262; United States / NCI NIH HHS / CA / R37 CA050286; United States / NCI NIH HHS / CA / R01 CA045726-23; United States / NCI NIH HHS / CA / CA123774; United States / NCI NIH HHS / CA / R37 CA050286-20; United States / NCI NIH HHS / CA / F32 CA123774; United States / NCI NIH HHS / CA / R21 CA129660; United States / NCI NIH HHS / CA / CA95262; United States / NCI NIH HHS / CA / R01 CA095262-06; United States / NCI NIH HHS / CA / CA129660; United States / NCI NIH HHS / CA / R21 CA129660-02; United States / NCI NIH HHS / CA / P01 CA078045-06A10004; United States / NCI NIH HHS / CA / P01 CA078045; United States / NHLBI NIH HHS / HL / HL57900; United States / NCI NIH HHS / CA / R01 CA045726; United States / NCI NIH HHS / CA / CA045726-23; United States / NHLBI NIH HHS / HL / P01 HL057900; United States / NCI NIH HHS / CA / CA78045; United States / NCI NIH HHS / CA / CA45726; United States / NCI NIH HHS / CA / CA078045-06A10004
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibronectins; 0 / Integrin alphaVbeta3; 0 / Ki-67 Antigen; 0 / RNA, Small Interfering; 147336-22-9 / Green Fluorescent Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2 / src-Family Kinases
  • [Other-IDs] NLM/ NIHMS125908; NLM/ PMC2759406
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62. Liao DJ, Wang Y, Wu J, Adsay NV, Grignon D, Khanani F, Sarkar FH: Characterization of pancreatic lesions from MT-tgf alpha, Ela-myc and MT-tgf alpha/Ela-myc single and double transgenic mice. J Carcinog; 2006 Jul 05;5:19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of pancreatic lesions from MT-tgf alpha, Ela-myc and MT-tgf alpha/Ela-myc single and double transgenic mice.
  • In order to identify good animal models for investigating therapeutic and preventive strategies for pancreatic cancer, we analyzed pancreatic lesions from several transgenic models and made a series of novel findings.
  • Female MT-tgf alpha mice of the MT100 line developed pancreatic proliferation, acinar-ductal metaplasia, multilocular cystic neoplasms, ductal adenocarcinomas and prominent fibrosis, while the lesions in males were less severe.
  • MT-tgf alpha-ES transgenic lines of both sexes developed slowly progressing lesions that were similar to what was seen in MT100 males.
  • In both MT100 and MT-tgf alpha-ES lines, TGF alpha transgene was expressed mainly in proliferating ductal cells.
  • Ela-myc transgenic mice with a mixed C57BL/6, SJL and FVB genetic background developed pancreatic tumors at 2-7 months of age, and half of the tumors were ductal adenocarcinomas, similar to what was reported originally by Sandgren et al 1.
  • However, in 20% of the mice, the tumors metastasized to the liver.
  • MT100/Ela-myc and MT-tgf alpha-ES/Ela-myc double transgenic mice developed not only acinar carcinomas and mixed carcinomas as previously reported but also various ductal-originated lesions, including multilocular cystic neoplasms and ductal adenocarcinomas.
  • The double transgenic tumors were more malignant and metastasized to the liver at a higher frequency (33%) compared with the Ela-myc tumors.
  • Sequencing of the coding region of p16ink4, k-ras and Rb cDNA in small numbers of pancreatic tumors did not identify mutations.
  • The short latency for tumor development, the variety of tumor morphology and the liver metastases seen in Ela-myc and MT-tgf alpha/Ela-myc mice make these animals good models for investigating new therapeutic and preventive strategies for pancreatic cancer.

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  • (PMID = 16822304.001).
  • [ISSN] 1477-3163
  • [Journal-full-title] Journal of carcinogenesis
  • [ISO-abbreviation] J Carcinog
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100864
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC1559682
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63. Ringel J, Jesnowski R, Moniaux N, Lüttges J, Ringel J, Choudhury A, Batra SK, Klöppel G, Löhr M: Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma. Cancer Res; 2006 Sep 15;66(18):9045-53
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  • [Title] Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma.
  • To understand the role of ADAM17/tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) in pancreatic ductal adenocarcinoma (PDAC), we investigated its expression, function, and in vitro regulation.
  • ADAM17/TACE mRNA was expressed in 3 of 10 normal pancreatic tissues, 6 of 8 samples from patients with chronic pancreatitis, 10 of 10 PDAC tissues, and 9 of 9 pancreatic cancer cell lines, but it was absent in primary duct epithelial cells.
  • Immunohistochemical staining revealed positive cancer cells in 8 of 10 PDACs but no staining of ducts in normal pancreas.
  • ADAM17/TACE was found in 0 of 16 pancreatic intraepithelial neoplasia (PanIN)-1A lesions, 1 of 30 PanIN-1B lesions, 2 of 13 PanIN-2 lesions but, in 13 of 15 PanIN-3 lesions, associated with PDAC.
  • Western blot, flow cytometry, and confocal microscopy analyses showed the aberrant expression of ADAM17/TACE protein in pancreatic cancer cell lines.
  • The proteolytic activity of ADAM17/TACE, assessed by the release of TNF-alpha, was inhibited by TNF-alpha protease inhibitor.
  • Furthermore, ADAM17/TACE mRNA expression was down-regulated in pancreatic cancer cells arrested in G2-M phase as well as in a time-dependent manner after TNF-alpha and interleukin-6 incubation.
  • [MeSH-major] ADAM Proteins / biosynthesis. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Cycle / genetics. Cell Growth Processes / genetics. Cell Line, Tumor. Disease Progression. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Immunohistochemistry. Neoplasm Invasiveness. Pancreatitis, Chronic / enzymology. Pancreatitis, Chronic / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16982746.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA772712
  • [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 / RNA, Messenger; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
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64. 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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  • [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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65. Lin YC, Lee PH, Yao YT, Hsiao JK, Sheu JC, Chen CH: Alpha-fetoprotein-producing pancreatic acinar cell carcinoma. J Formos Med Assoc; 2007 Aug;106(8):669-72
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  • [Title] Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.
  • A 47-year-old man with chronic hepatitis B had progressive elevated alpha-fetoprotein of 2 years' duration.
  • A pancreatic tail tumor, instead of liver tumor, was detected.
  • He underwent elective distal pancreatectomy and splenectomy and the pathology turned out to be acinar cell carcinoma of the pancreas.
  • Serum level of alpha-fetoprotein returned to normal soon after surgery.
  • Alpha-fetoprotein is commonly used as a tumor marker to screen for hepatocellular carcinoma in high-risk patients.
  • However, elevated alpha-fetoprotein could occur in a much rarer disease, acinar cell carcinoma of the pancreas.

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  • (PMID = 17711801.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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66. Li Z, Fallon J, Mandeli J, Wetmur J, Woo SL: The oncopathic potency of Clostridium perfringens is independent of its alpha-toxin gene. Hum Gene Ther; 2009 Jul;20(7):751-8
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  • [Title] The oncopathic potency of Clostridium perfringens is independent of its alpha-toxin gene.
  • Hypoxia in solid tumors is a major obstacle in conventional treatment because of inefficient delivery of therapeutic agents to the lesions, but offers the potential for anaerobic bacterial colonization that can lead to tumor destruction.
  • We have previously reported a recombinant Clostridium perfringens (Cp) strain constructed by deletion of the superoxide dismutase (sod) gene and insertion of the Panton-Valentine leukocidin (PVL) gene, Cp/sod(-)/PVL, which showed elevated oxygen sensitivity, tumor selectivity, and oncopathic potency in an orthotopic model of pancreatic cancer in immune-competent and syngeneic mice, and that led to substantial prolongation of animal survival.
  • A major limitation to Cp/sod(-)/PVL in clinical applications is that it expresses phospholipase C (plc), the alpha-toxin and the major virulence determinant in Cp that is causative in the development of gas gangrene.
  • Intravenous injection of Cp/plc(-)/sod(-)/PVL spores led to a significant survival advantage in tumor-bearing mice with the same efficacy as Cp/sod(-)/PVL, indicating that the oncopathic potency of Cp is independent of a functional plc gene.
  • Consequently, Cp/plc(-)/sod(-)/PVL is a novel oncopathic bacterial agent for the effective treatment of pancreatic cancer and other poorly vascularized tumors, with a substantially enhanced safety profile, which is essential for the development of translational studies in the future.

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  • [CommentIn] NIH Guide Grants Contracts. 2016 Jul 29;:NOT-OD-16-124 [27483554.001]
  • [RetractionIn] Hum Gene Ther. 2010 Mar;21(3):363 [20235840.001]
  • [CommentIn] Fed Regist. 2016 Jul 25;81(142):48426-48427 [27737274.001]
  • (PMID = 19298132.001).
  • [ISSN] 1557-7422
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-120017
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Calcium-Binding Proteins; EC 3.1.4.- / Type C Phospholipases; EC 3.1.4.3 / alpha toxin, Clostridium perfringens
  • [Other-IDs] NLM/ PMC2829288
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67. 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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  • [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 / radionuclide imaging. Lung Neoplasms / radionuclide imaging. Multiple Endocrine Neoplasia Type 1 / radionuclide imaging. Pancreatic Neoplasms / radionuclide 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] Spain
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68. Hameed O, Xu H, Saddeghi S, Maluf H: Hepatoid carcinoma of the pancreas: a case report and literature review of a heterogeneous group of tumors. Am J Surg Pathol; 2007 Jan;31(1):146-52
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  • [Title] Hepatoid carcinoma of the pancreas: a case report and literature review of a heterogeneous group of tumors.
  • Hepatoid carcinomas are tumors that display, at least focally, cytologic and/or architectural features of hepatocellular carcinoma.
  • We report a case of hepatoid carcinoma of the pancreas that developed in a 41-year-old woman in association with a pancreatic endocrine carcinoma.
  • The fine needle aspiration material was characterized by the presence of monotonous, small-to-medium sized tumor cells with round nuclei and finely granular chromatin, intermixed with more atypical tumor cells displaying larger nuclei with coarse clumped chromatin, prominent nucleoli, and moderate amounts of foamy cytoplasm.
  • The excised specimen displayed a poorly differentiated pancreatic endocrine carcinoma associated with well-defined islands of larger tumor cells growing in a perisinusoidal pattern which, based on their immunohistochemical profile and the demonstration of bile, proved to represent a hepatoid component.
  • This case and prior examples in the literature suggest that hepatoid carcinomas of the pancreas appear to be a heterogeneous group of tumors (pure or associated with another histologic component) that are often associated with early liver metastasis and a short survival, although those arising as a component of endocrine tumors seem to fare slightly better.
  • Hepatoid carcinoma of the pancreas should be included in the differential diagnosis of pancreatic tumors composed of large eosinophilic cells.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Carcinoma, Islet Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Fatal Outcome. Female. Humans. Immunohistochemistry. Neoplasms, Multiple Primary. Tomography, X-Ray Computed. alpha-Fetoproteins / analysis

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  • (PMID = 17197931.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
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69. Kamohara H, Takahashi M, Ishiko T, Ogawa M, Baba H: Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-alpha and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor. Int J Oncol; 2007 Sep;31(3):627-32
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  • [Title] Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-alpha and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor.
  • Pancreatic carcinoma is one of the most lethal of the gastrointestinal malignant tumors.
  • We previously reported that CXCL-8 was produced by a variety of human carcinoma cells and tissues, and that CXCL-8 promoted proliferation in pancreatic carcinoma cells (SUIT-2).
  • In the present study, we analyzed whether various cytokines affect cell proliferation by CXCL-8 expression in pancreas carcinoma cells.
  • All examined pancreatic carcinoma cells expressed CXCL-8 and TNFRII mRNA constitutively in RPMI-1640 medium without FBS.
  • TNF-alpha, LIF, IL-1beta, IL-6, IL-8, or IFN-beta enhanced the expression of CXCL-8 mRNA, but IL-10 did not in Hs-700T cells.
  • Actinomycin D suppressed and cycloheximide augmented CXCL-8 mRNA which was induced by TNF-alpha or not.
  • The half-life of CXCL-8 mRNA was 36.5 min by TNF-alpha and 35.2 min by no stimulation.
  • In our previous study, LIF promoted cell growth in Hs-700T cells.
  • Addition of recombinant CXCL-8 did not induce cell growth of Hs-700T.
  • Anti-CXCL-8 IgG significantly suppressed cell growth.
  • CXCL-8 would act as an autocrine growth factor in Hs-700T cells, which expressed CXCL-8 mRNA highly without stimulation.
  • Curcumin (diferuloylmethane), NF-kappaB inhibitor, suppressed cell proliferation in Hs-700T cells.
  • These results suggest that CXCL-8 plays a pivotal role in progression of pancreatic cancer, and its expression is influenced by inflammatory cytokines in pancreatic tumor microenvironment.
  • [MeSH-major] Interleukin-8 / metabolism. Leukemia Inhibitory Factor / metabolism. Pancreatic Neoplasms / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cycloheximide / pharmacology. Cytokines / metabolism. Dactinomycin / pharmacology. Humans. Immunoglobulin G / chemistry. Inflammation. Intercellular Signaling Peptides and Proteins / metabolism. RNA, Messenger / metabolism. Time Factors

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  • (PMID = 17671691.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cytokines; 0 / Immunoglobulin G; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interleukin-8; 0 / Leukemia Inhibitory Factor; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 1CC1JFE158 / Dactinomycin; 98600C0908 / Cycloheximide
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70. Marsh WL, Colonna J, Yearsley M, Bloomston M, Frankel WL: Calponin is expressed in serous cystadenomas of the pancreas but not in adenocarcinomas or endocrine tumors. Appl Immunohistochem Mol Morphol; 2009 May;17(3):216-9
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  • [Title] Calponin is expressed in serous cystadenomas of the pancreas but not in adenocarcinomas or endocrine tumors.
  • The diagnosis of serous microcystic adenoma (SMA) is usually straightforward.
  • For small biopsies and/or unusual variants, the differential diagnosis includes other pancreatic or metastatic neoplasms showing cystic or clear cell features.
  • We evaluated immunostains for potential use in the diagnosis of SMA.
  • Additionally, microarrays previously constructed from 56 pancreatic adenocarcinomas (PACs) and 64 pancreatic endocrine tumors (PENs) were studied.
  • The microarrays were stained with calponin, chromogranin, CD10, alpha-inhibin, and monoclonal neuron-specific enolase (m-NSE).
  • For SMAs, staining was seen with calponin (85.2%), alpha-inhibin (96.2%), and m-NSE (96.2%).
  • Staining for alpha-inhibin was absent in PACs and present in 4.1% of PENs; whereas immunoreactivity for m-NSE was present in 26.8% of PACs and 73.7% of PENs.
  • An immunohistochemical profile of staining with calponin, alpha-inhibin, and m-NSE and absent staining with chromogranin supports the diagnosis of SMA, and distinguishes SMA from PAC and PEN.
  • Calponin and alpha-inhibin are the most useful positive markers for SMA, and are negative in most entities in the differential diagnosis.

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  • (PMID = 19391217.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Microfilament Proteins; 0 / calponin; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins; EC 4.2.1.11 / Phosphopyruvate Hydratase
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71. Guerrero J, Tobar N, Cáceres M, Espinoza L, Escobar P, Dotor J, Smith PC, Martínez J: Soluble factors derived from tumor mammary cell lines induce a stromal mammary adipose reversion in human and mice adipose cells. Possible role of TGF-beta1 and TNF-alpha. Breast Cancer Res Treat; 2010 Jan;119(2):497-508
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  • [Title] Soluble factors derived from tumor mammary cell lines induce a stromal mammary adipose reversion in human and mice adipose cells. Possible role of TGF-beta1 and TNF-alpha.
  • In carcinomas such as those of breast, pancreas, stomach, and colon, cancer cells support the expansion of molecular and cellular stroma in a phenomenon termed desmoplasia, which is characterized by a strong fibrotic response.
  • In the case of breast tissue, in which stroma is mainly a fatty tissue, this response presumably occurs at the expense of the adipose cells, the most abundant stromal phenotype, generating a tumoral fibrous structure rich in fibroblast-like cells.
  • In this study, we aimed to determine the cellular mechanisms by which factors present in the media conditioned by MDA-MB-231 and MCF-7 human breast cancer cell lines induce a reversion of adipose cells to a fibroblastic phenotype.
  • We demonstrated that soluble factors generated by these cell lines stimulated the reversion of mammary adipose phenotype evaluated as intracellular lipid content and expression of C/EBP alpha and PPAR gamma.
  • We also demonstrated that exogenous TGF-beta 1 and TNF-alpha exerts a similar function.
  • The participation of both growth factors, components of media conditioned by tumoral mammary cells, on the expression and nuclear translocation of C/EBP alpha and PPAR gamma was tested in 3T3-L1 cells by interfering with the inhibitory effects of media with agents that block the TGF-beta 1 and TNF-alpha activity.
  • These results allow us to postulate that TGF-beta 1 and TNF-alpha present in this media are in part responsible for this phenotypic reversion.
  • [MeSH-major] Adipocytes / metabolism. Breast Neoplasms / metabolism. Cell Transdifferentiation. Fibroblasts / metabolism. Transforming Growth Factor beta1 / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] 3T3-L1 Cells. Animals. Blotting, Western. CCAAT-Enhancer-Binding Proteins / metabolism. Cell Line, Tumor. Cell Size. Culture Media, Conditioned / metabolism. Female. Humans. Immunohistochemistry. Mice. PPAR gamma / metabolism. Phenotype. Recombinant Proteins / metabolism. Signal Transduction

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  • (PMID = 19649705.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / CEBPA protein, mouse; 0 / Culture Media, Conditioned; 0 / PPAR gamma; 0 / Recombinant Proteins; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha
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72. Rooney S, Ryan MF: Effects of alpha-hederin and thymoquinone, constituents of Nigella sativa, on human cancer cell lines. Anticancer Res; 2005 May-Jun;25(3B):2199-204
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  • [Title] Effects of alpha-hederin and thymoquinone, constituents of Nigella sativa, on human cancer cell lines.
  • The separate effects of alpha-hederin and thymoquinone, the two principal bioactive constituents of Nigella sativa, on four human cancer cell lines [A549 (lung carcinoma), HEp-2 (larynx epidermoid carcinoma), HT-29 (colon adenocarcinoma) and MIA PaCa-2 (pancreas carcinoma)] were investigated.
  • Alpha-hederin was also examined as a pro-drug.
  • Alpha-hederin and thymoquinone separately induced a dose- and time-dependent effect on the cell lines tested.
  • HEp-2 cells were the most sensitive, exhibiting apoptosis with a higher incidence following thymoquinone treatment.
  • Pre-treatment of cells with alpha-hederin, followed by thymoquinone or cisplatin, did not enhance the cytotoxicity or apoptosis induced by either drug.
  • So, the membrane-perforating properties associated with saponins, here represented by alpha-hederin, enhance neither cytotoxicity nor apoptosis of these cancer cells.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Apoptosis / drug effects. Cell Line, Tumor. Colonic Neoplasms / drug therapy. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. HT29 Cells. Humans. Inhibitory Concentration 50. Laryngeal Neoplasms / drug therapy. Lung Neoplasms / drug therapy. Necrosis. Nigella sativa / chemistry. Pancreatic Neoplasms / drug therapy. Prodrugs / pharmacology

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  • (PMID = 16158964.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Drugs, Chinese Herbal; 0 / Prodrugs; 0 / Saponins; 27013-91-8 / alpha-hederin; 490-91-5 / thymoquinone; 6SMK8R7TGJ / Oleanolic Acid
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73. Jäggi F, Cabrita MA, Perl AK, Christofori G: Modulation of endocrine pancreas development but not beta-cell carcinogenesis by Sprouty4. Mol Cancer Res; 2008 Mar;6(3):468-82
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  • [Title] Modulation of endocrine pancreas development but not beta-cell carcinogenesis by Sprouty4.
  • Depending on cell type and the particular RTK, Spry proteins exert dual functions: They can either repress RTK-mediated signaling pathways, mainly by interfering with the Ras/Raf/mitogen-activated protein kinase pathway or sustaining RTK signal transduction, for example by sequestering the E3 ubiquitin-ligase c-Cbl and thus preventing ubiquitylation, internalization, and degradation of RTKs.
  • Here, by the inducible expression of murine Spry4 in pancreatic beta cells, we have assessed the functional role of Spry proteins in the development of pancreatic islets of Langerhans in normal mice and in the Rip1Tag2 transgenic mouse model of beta-cell carcinogenesis. beta cell-specific expression of mSpry4 provokes a significant reduction in islet size, an increased number of alpha cells per islet area, and impaired islet cell type segregation.
  • Functional analysis of islet cell differentiation in cultured PANC-1 cells shows that mSpry4 represses adhesion and migration of differentiating pancreatic endocrine cells, most likely by affecting the subcellular localization of the protein tyrosine phosphatase PTP1B.
  • In contrast, transgenic expression of mSpry4 during beta-cell carcinogenesis does not significantly affect tumor outgrowth and progression to tumor malignancy.
  • Rather, tumor cells seem to escape mSpry4 transgene expression.
  • [MeSH-major] Insulin-Secreting Cells / physiology. Islets of Langerhans / physiology. Nerve Tissue Proteins / physiology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA Primers. Disease Progression. Gene Expression Regulation, Neoplastic. Glucose Tolerance Test. Humans. Mice. Mice, Inbred C57BL. Mice, Transgenic. Nuclear Pore Complex Proteins / genetics. Polymerase Chain Reaction. RNA-Binding Proteins / genetics. Receptor Protein-Tyrosine Kinases / metabolism. Signal Transduction

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  • (PMID = 18337453.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AGFG1 protein, human; 0 / DNA Primers; 0 / Nerve Tissue Proteins; 0 / Nuclear Pore Complex Proteins; 0 / RNA-Binding Proteins; 0 / Spry4 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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74. Williard DE, Twait E, Yuan Z, Carter AB, Samuel I: Nuclear factor kappa B-dependent gene transcription in cholecystokinin- and tumor necrosis factor-alpha-stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase. Am J Surg; 2010 Aug;200(2):283-90
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  • [Title] Nuclear factor kappa B-dependent gene transcription in cholecystokinin- and tumor necrosis factor-alpha-stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase.
  • We investigated the relationship between the p38 MAP kinase and NF-kappaB in isolated acinar cells.
  • METHODS: Isolated rodent acinar cells were stimulated with agonists after infection with an adenovector containing a luciferase promoter driven only by NF-kappaB and an adenovector containing the dominant negative (DN) form of p38 (empty vector in controls).
  • RESULTS: Initial immunoblots confirmed that the agonist stimulated p38 activation in acinar cells was substantially attenuated by DN p38 overexpression.
  • Stimulation of native cholecystokinin (CCK)-A receptors or tumor necrosis factor-alpha (TNF-alpha) receptors promoted a significant increase in NF-kappaB-dependent gene transcription in cells infected with the empty vector, while overexpression of DN p38 significantly abrogated NF-kappaB-dependent luciferase activity.
  • CONCLUSIONS: These findings support our hypothesis that p38 is involved in the activation of proinflammatory nuclear transcription factors such as NF-kappaB in pancreatic exocrine cells.

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  • [Copyright] Published by Elsevier Inc.
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  • (PMID = 20413104.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK071731-01A2; United States / NIEHS NIH HHS / ES / R01 ES014871; United States / NIEHS NIH HHS / ES / ES-014871; United States / NIEHS NIH HHS / ES / R01 ES015981; United States / NIDDK NIH HHS / DK / DK071731-01A2; United States / NIDDK NIH HHS / DK / DK-071731; United States / NIDDK NIH HHS / DK / R01 DK071731; United States / NIEHS NIH HHS / ES / ES-015981
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 9011-97-6 / Cholecystokinin; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS182891; NLM/ PMC2910146
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75. Stark I, Mensing CH, Sander CA: [Necrolytic migratory erythema in glucagonoma syndrome]. Hautarzt; 2008 Jan;59(1):50-3
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  • [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 für 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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76. 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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77. Yang KC, Wu CC, Sumi S, Tseng CL, Wu YH, Kuo TF, Lin FH: Calcium phosphate cement chamber as an immunoisolative device for bioartificial pancreas: in vitro and preliminary in vivo study. Pancreas; 2010 May;39(4):444-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calcium phosphate cement chamber as an immunoisolative device for bioartificial pancreas: in vitro and preliminary in vivo study.
  • OBJECTIVES: This study examined a calcium phosphate cement (CPC) chamber as an immunoisolative device to facilitate the use of xenogeneic cell sources without immunosuppression for the bioartificial pancreas (BAP).
  • METHODS: Mouse insulinoma cells were encapsulated in agarose gel and then enclosed in a CPC chamber to create a BAP.
  • Bioartificial pancreas were evaluated by cell viability, live-dead cell ratio, and cytokine-mediated cytotoxicity assay and implanted into the peritoneal cavity of diabetic rats.
  • RESULTS: Insulinoma cells enclosed in the CPC chamber had normal viability, cell survival, and insulin secretion that was even cultured in media with cytokines.
  • Histological examination revealed the fibrous tissue envelopment, and immune-related cells that competed for oxygen resulting in hypoxia could be attributed to the dysfunction of BAPs.
  • An alternative implanted site should be considered to extend the functional longevity of BAPs in further study.
  • [MeSH-major] Artificial Organs. Calcium Phosphates / chemistry. Diabetes Mellitus, Experimental / metabolism. Pancreas / metabolism
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Culture Techniques / instrumentation. Cell Line, Tumor. Cell Survival / drug effects. Insulin / secretion. Insulinoma / metabolism. Insulinoma / pathology. Interleukin-1beta / pharmacology. Mice. Rats. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 20084047.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Calcium Phosphates; 0 / Insulin; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 97Z1WI3NDX / calcium phosphate
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78. Scheim DE: Cytotoxicity of unsaturated fatty acids in fresh human tumor explants: concentration thresholds and implications for clinical efficacy. Lipids Health Dis; 2009;8:54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytotoxicity of unsaturated fatty acids in fresh human tumor explants: concentration thresholds and implications for clinical efficacy.
  • BACKGROUND: Unsaturated fatty acids (UFAs) exhibit in vitro cytotoxicity against many malignant cell lines and yield decreased cancer incidence and reduced tumor growth in animal models.
  • To explore possibilities for enhanced clinical efficacy, fresh surgical explants of tumors from 22 patients with five malignancies were exposed to gamma-linolenic acid (GLA) and alpha-linolenic acid (ALA) and analyzed with an in vitro chemosensitivity testing system, the Fluorescent Cytoprint Assay (FCA).
  • A total of 282 micro-organ cultures derived from these malignant tumors were exposed to GLA and ALA at different concentrations.
  • In tests using 30-40% serum, GLA and ALA killed tumor at concentrations of 2 mM and above.
  • CONCLUSIONS: The concentration threshold of 500 microM to 2 mM exhibited for antitumor activity by GLA and ALA is much higher than that observed in most previously reported cell culture studies but consistent with physiological concentrations found to kill tumor clinically and in animals.
  • [MeSH-major] Neoplasms / pathology. alpha-Linolenic Acid / pharmacology. gamma-Linolenic Acid / pharmacology
  • [MeSH-minor] Cell Death / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Serum. Treatment Outcome

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  • (PMID = 20003514.001).
  • [ISSN] 1476-511X
  • [Journal-full-title] Lipids in health and disease
  • [ISO-abbreviation] Lipids Health Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0RBV727H71 / alpha-Linolenic Acid; 78YC2MAX4O / gamma-Linolenic Acid
  • [Other-IDs] NLM/ PMC2801488
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79. Zhu Y, Tibensky I, Schmidt J, Ryschich E, Märten A: Interferon-alpha enhances antitumor effect of chemotherapy in an orthotopic mouse model for pancreatic adenocarcinoma. J Immunother; 2008 Sep;31(7):599-606
Hazardous Substances Data Bank. FLUOROURACIL .

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  • [Title] Interferon-alpha enhances antitumor effect of chemotherapy in an orthotopic mouse model for pancreatic adenocarcinoma.
  • Data from a phase 2 trial combining chemoradiotherapy with interferon (IFN)-alpha (CapRI scheme) for adjuvant treatment of pancreatic carcinoma are very encouraging.
  • Here, we try to evaluate the effect of IFN-alpha in this combined treatment scheme.
  • Mice were inoculated with syngeneic cells in the pancreas.
  • After 5 days animals were treated with 5-fluorouracil (5-FU), cisplatin (CDDP), radiation, and IFN-alpha.
  • Tumor growth and immune responses were determined and adoptive cell transfer experiments performed.
  • The impact of IFN-alpha treatment on leukocyte-endothelium interactions was assessed by intravital microscopy.
  • Addition of IFN-alpha to chemotherapy had a significant life-prolonging effect.
  • Regimens including IFN-alpha showed a clear trend toward less metastases than monotherapy.
  • T cells and dendritic cells infiltrated tumors significantly more in 5-FU+IFN-alpha animals and these T cells secreted IFN-gamma tumor specifically.
  • Antitumor response could be transferred by injection of mononuclear cells from 5-FU+IFN-alpha-treated mice into treatment-naive animals.
  • The transferred cells homed to the tumors and proliferated there.
  • IFN-alpha significantly improves chemotherapy.
  • Although IFN-alpha acts unspecifically an additional specific immune response could be demonstrated.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Interferon-alpha / administration & dosage. Liver Neoplasms / therapy. Pancreatic Neoplasms / therapy. Peritoneal Neoplasms / therapy
  • [MeSH-minor] Adjuvants, Immunologic / administration & dosage. Animals. Cell Adhesion / drug effects. Cell Adhesion / immunology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / immunology. Cell Proliferation / drug effects. Cisplatin / administration & dosage. Combined Modality Therapy. Cytokines / drug effects. Cytokines / secretion. Fluorouracil / administration & dosage. Immunotherapy, Adoptive. Mice. Mice, Inbred C57BL. Radiotherapy. Survival Analysis. T-Lymphocytes / drug effects. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. Tumor Burden / drug effects

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  • (PMID = 18600184.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cytokines; 0 / Interferon-alpha; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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80. Lee LF, Xu B, Michie SA, Beilhack GF, Warganich T, Turley S, McDevitt HO: The role of TNF-alpha in the pathogenesis of type 1 diabetes in the nonobese diabetic mouse: analysis of dendritic cell maturation. Proc Natl Acad Sci U S A; 2005 Nov 1;102(44):15995-6000
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  • [Title] The role of TNF-alpha in the pathogenesis of type 1 diabetes in the nonobese diabetic mouse: analysis of dendritic cell maturation.
  • TNF-alpha has been linked to the development of type 1 diabetes (T1D).
  • We previously reported that neonatal treatment of nonobese diabetic (NOD) mice with TNF-alpha accelerated the onset of T1D, whereas TNF-alpha blockade in the same time period resulted in a complete absence of diabetes.
  • The mechanisms by which TNF-alpha modulates development of T1D in NOD mice remain unclear.
  • Here we tested the effects of TNF-alpha on the maturation of dendritic cells (DCs) in the NOD mouse.
  • We found that neonatal treatment with TNF-alpha caused an increase in expression of maturation markers on CD11c(+)CD11b(+) DC subpopulations, whereas treatment with anti-TNF-alpha resulted in a decrease in expression of maturation markers in the CD11c(+)CD11b(+) subset.
  • Moreover, neonatal treatment with TNF-alpha resulted in skewed development of a CD8alpha(+)CD11b(-)CD11c(+) DC subset such that TNF-alpha decreases the CD8alpha(+)CD11c(+) DC subset, increases the CD11c(+)CD11b(+) subset, and causes an increase in the expression of CD40 and CD54 on mature DCs capable of inducing immunity.
  • Anti-TNF-alpha-treated mice had an increase in the CD8alpha(+)CD11c(+) DCs.
  • Notably, adoptively transferred naïve CD4(+) T cells from BDC2.5 T cell receptor transgenic mice proliferated in the pancreatic lymph nodes in TNF-alpha-treated NOD mice but not in anti-TNF-alpha-treated mice.
  • Finally, we show that anti-TNF-alpha-treated mice showed immunological tolerance to islet cell proteins.
  • We conclude that TNF-alpha plays an important role in the initiation of T1D in the NOD mouse by regulating the maturation of DCs and, thus, the activation of islet-specific pancreatic lymph node T cells.

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  • (PMID = 16247001.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK064656; United States / NIDDK NIH HHS / DK / R01 DK051705; United States / NIDDK NIH HHS / DK / K01DK064656; United States / NIDDK NIH HHS / DK / R01DK51705
  • [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 / Antibodies; 0 / Antigens, CD; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1276103
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81. Ambrosini-Spaltro A, Potì O, De Palma M, Filotico M: Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa. Hum Pathol; 2009 May;40(5):746-9
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  • [Title] Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa.
  • Acinar cell carcinoma is an uncommon type of carcinoma of the pancreas that can exceptionally arise in ectopic pancreatic tissue.
  • Herein, we report a case of a 52-year-old man with pancreatic-type acinar cell carcinoma of the stomach and concomitant pancreatic metaplasia of the adjacent nonneoplastic gastric mucosa.
  • There was neither clinical nor radiographic evidence of a tumor in the pancreas itself.
  • Macroscopically, an ulcerated tumor, measuring 4 x 1.7 cm, was found in the distal antrum.
  • Microscopically, the biopsy and the surgical specimen revealed a neoplasm with a predominantly trabecular architecture composed of moderately atypical cells with finely dispersed chromatin and indistinct nucleoli.
  • The neoplastic cells and those of the adjacent metaplastic mucosa were both strongly immunoreactive for alpha-1-antitrypsin, consistent with pancreatic acinar cell differentiation.
  • Ectopic pancreatic-type acinar cell carcinoma is an extremely rare condition, having been previously reported only in 5 occasions, none of them in association with pancreatic acinar cell metaplasia of the gastric mucosa.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Gastric Mucosa / pathology. Pancreas / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Humans. Male. Metaplasia / pathology. Middle Aged. alpha 1-Antitrypsin / biosynthesis

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  • (PMID = 19144387.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
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82. 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
Hazardous Substances Data Bank. GLUCAGON .

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  • [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


83. Satoh A, Gukovskaya AS, Edderkaoui M, Daghighian MS, Reeve JR Jr, Shimosegawa T, Pandol SJ: Tumor necrosis factor-alpha mediates pancreatitis responses in acinar cells via protein kinase C and proline-rich tyrosine kinase 2. Gastroenterology; 2005 Aug;129(2):639-51
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  • [Title] Tumor necrosis factor-alpha mediates pancreatitis responses in acinar cells via protein kinase C and proline-rich tyrosine kinase 2.
  • BACKGROUND & AIMS: Although tumor necrosis factor alpha is implicated as an important mediator of the inflammatory response in acute pancreatitis, its role in other pathologic features of the disease remains unknown.
  • We investigated the role for tumor necrosis factor alpha in cytoskeletal responses and the underlying signaling mechanisms in pancreatic acinar cells.
  • METHODS: In isolated rat pancreatic acini and AR42J cells, we determined the effect of tumor necrosis factor alpha on the actin cytoskeleton by rhodamine-phalloidin.
  • We also studied the involvement of these signaling pathways in tumor necrosis factor-alpha-induced nuclear factor-kappaB activation and apoptosis.
  • RESULTS: Tumor necrosis factor-alpha increased the tyrosine phosphorylation of proline-rich tyrosine kinase 2 in acinar cells.
  • The broad-spectrum protein kinase C inhibitor and the Src kinase inhibitor both inhibited tumor necrosis factor-alpha-induced proline-rich tyrosine kinase 2 phosphorylation, but at different tyrosine residues.
  • Tumor necrosis factor-alpha caused disorganization of the actin cytoskeleton by a mechanism dependent on protein kinase C, Src kinases, and proline-rich tyrosine kinase 2.
  • Inhibition of protein kinase C, but not Src kinases, decreased tumor necrosis factor-alpha-induced apoptosis.
  • Furthermore, with antisense transfections, we showed that protein kinase C delta and , but not proline-rich tyrosine kinase 2, mediate tumor necrosis factor alpha-induced nuclear factor-kappaB activation.
  • CONCLUSIONS: Tumor necrosis factor-alpha activates proline-rich tyrosine kinase 2 to cause cytoskeletal disorganization and nuclear factor-kappaB to cause inflammatory response, and it triggers cell death signaling through divergent mechanisms mediated by protein kinase C.
  • The results provide insights into the mechanisms in pancreatic acinar cells that link tumor necrosis factor alpha to critical processes in acute pancreatitis.
  • [MeSH-major] Pancreas / cytology. Pancreatitis / drug therapy. Pancreatitis / enzymology. Protein Kinase C / metabolism. Protein-Tyrosine Kinases / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Acute Disease. Analysis of Variance. Animals. Apoptosis / drug effects. Apoptosis / physiology. Base Sequence. Blotting, Western. Cells, Cultured. Disease Models, Animal. Female. Focal Adhesion Kinase 2. Male. Molecular Sequence Data. Polymerase Chain Reaction / methods. Probability. Protein Kinase C-delta. Rats. Rats, Sprague-Dawley. Sensitivity and Specificity

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  • (PMID = 16083718.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIAAA NIH HHS / AA / 1 U56 AA 0114643; United States / NIDDK NIH HHS / DK / DK-59508; United States / PHS HHS / / P50-A11999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; EC 2.7.1.- / Prkcd protein, rat; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Focal Adhesion Kinase 2; EC 2.7.10.2 / Ptk2b protein, rat; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-delta
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84. 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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85. Kamohara H, Ogawa M, Ishiko T, Sakamoto K, Baba H: Leukemia inhibitory factor functions as a growth factor in pancreas carcinoma cells: Involvement of regulation of LIF and its receptor expression. Int J Oncol; 2007 Apr;30(4):977-83
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  • [Title] Leukemia inhibitory factor functions as a growth factor in pancreas carcinoma cells: Involvement of regulation of LIF and its receptor expression.
  • We have previously reported that LIF promotes cell proliferation in some human carcinoma cells through c-fos, jun-B and cyclin-E expression.
  • In the present study, we analyzed the regulation of LIF and its receptor (LIFR) expression in pancreatic carcinoma cells.
  • Seven pancreatic carcinoma cells expressed constitutively LIF and its heterodimer receptor (LIFR and gp130) mRNA in RPMI-1640 medium without FBS.
  • The amount of LIF immunoreactive protein was 132.5+/-52 pg/10(6) cells in culture supernatants without FBS.
  • Pro-inflammatory cytokines, such as TNF-alpha, IL-1beta, IL-6, IL-8, or LIF, enhanced the expression of LIF mRNA in Hs-700T and Hs-766T cells.
  • Addition of LIF significantly induced cell proliferation of Hs700T in 13 days LIF dose-dependently.
  • However, anti-LIF IgG failed to suppress cell proliferation in Hs-700T cells.
  • LIF acted as a paracrine growth factor in Hs-700T cells, which expressed low amount of LIF without stimuli.
  • Antisense LIFR oligonucleotide significantly suppressed cell growth in the presence of LIF in Hs-700T cells.
  • These results suggest that cytokine network might alter the expression and responsiveness to LIF in tumor microenvironment.
  • [MeSH-major] Carcinoma / metabolism. Leukemia Inhibitory Factor / metabolism. Pancreatic Neoplasms / metabolism. Receptors, OSM-LIF / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Cytokines / metabolism. Humans. Oligonucleotides, Antisense / pharmacology. Protein Kinase C / antagonists & inhibitors. Protein-Tyrosine Kinases / antagonists & inhibitors. RNA, Messenger / metabolism. Signal Transduction / drug effects


86. Santos AM, Jung J, Aziz N, Kissil JL, Puré E: Targeting fibroblast activation protein inhibits tumor stromagenesis and growth in mice. J Clin Invest; 2009 Dec;119(12):3613-25
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  • [Title] Targeting fibroblast activation protein inhibits tumor stromagenesis and growth in mice.
  • As the cell surface serine protease fibroblast activation protein (FAP) is selectively expressed on tumor-associated fibroblasts and pericytes in epithelial tumors, we set out to investigate the role of FAP in mouse models of epithelial-derived solid tumors.
  • In this study, we demonstrate that genetic deletion and pharmacologic inhibition of FAP inhibited tumor growth in both an endogenous mouse model of lung cancer driven by the K-rasG12D mutant and a mouse model of colon cancer, in which CT26 mouse colon cancer cells were transplanted into immune competent syngeneic mice.
  • Interestingly, growth of only the K-rasG12D-driven lung tumors was also attenuated by inhibition of the closely related protease dipeptidyl peptidase IV (DPPIV).
  • Our results indicate that FAP depletion inhibits tumor cell proliferation indirectly, increases accumulation of collagen, decreases myofibroblast content, and decreases blood vessel density in tumors.
  • These data provide proof of principle that targeting stromal cell-mediated modifications of the tumor microenvironment may be an effective approach to treating epithelial-derived solid tumors.

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  • (PMID = 19920354.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA124495; United States / NCI NIH HHS / CA / T32 CA009171; United States / NCI NIH HHS / CA / T32 CA09171
  • [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 / 1-(((3-hydroxy-1-adamantyl)amino)acetyl)-2-cyanopyrrolidine; 0 / Membrane Proteins; 0 / Protease Inhibitors; 0 / Pyrrolidines; 9007-34-5 / Collagen; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases; PJY633525U / Adamantane
  • [Other-IDs] NLM/ PMC2786791
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87. Zhu Y, Tibensky I, Schmidt J, Hackert T, Ryschich E, Jäger D, Büchler MW, Märten A: Interferon-alpha in combination with chemotherapy has potent antiangiogenic properties in an orthotopic mouse model for pancreatic adenocarcinoma. J Immunother; 2008 Jan;31(1):28-33
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  • [Title] Interferon-alpha in combination with chemotherapy has potent antiangiogenic properties in an orthotopic mouse model for pancreatic adenocarcinoma.
  • There are clinical data showing encouraging results for combining chemoradiotherapy with interferon (IFN)-alpha (CapRI scheme) for the treatment of pancreatic carcinoma.
  • Here, it was tried to evaluate the antiangiogenic effect of IFN-alpha in combination with chemotherapy.
  • Mice were inoculated with syngeneic pancreatic carcinoma cells in the pancreas.
  • After 5 days, the animals were treated with 5-fluorouracil (5-FU)+/-IFN-alpha.
  • Tumor growth, vascular endothelial growth factor (VEGF) serum levels and VEGF-R expression, real-time reverse transcription-polymerase chain reaction of mRNA coding for RGS-5, an angiogenic pericyte marker at sites of physiologic and pathologic angiogenesis and impact of IFN-alpha treatment on vessel density by CD31 stain and intravital microscopy were analyzed.
  • The addition of IFN-alpha to 5-FU-treatment decreased tumor volume, reduced serum level of VEGF, and down-regulated the expression of VEGF-receptor significantly.
  • Furthermore, the combination therapy revealed a decrease in vessel density and a down-regulation of RGS-5, which is a protein involved in angiogenic tumor vasculature.
  • IFN-alpha significantly improves the outcome of 5-FU-therapy in treating pancreatic carcinoma.
  • This is at least partly mediated by IFN-alpha antiangiogenic properties, which acts along with 5-FU on the VEGF system, vessel density, and RGS-5 expression in pericytes.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neovascularization, Pathologic / drug therapy. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Blood Vessels / drug effects. Blood Vessels / metabolism. Blood Vessels / pathology. Cell Line, Tumor. Disease Models, Animal. Fluorouracil / administration & dosage. Gene Expression / drug effects. Immunohistochemistry. Interferon-alpha / administration & dosage. Male. Mice. Mice, Inbred C57BL. RGS Proteins / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Vascular Endothelial Growth Factor / metabolism. Vascular Endothelial Growth Factor A / blood

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  • (PMID = 18157009.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Interferon-alpha; 0 / RGS Proteins; 0 / RNA, Messenger; 0 / Rgs5 protein, mouse; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; U3P01618RT / Fluorouracil
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88. Yao W, Zhu Q, Yuan Y, Qiao M, Zhang Y, Zhai Z: Thymosin alpha 1 improves severe acute pancreatitis in rats via regulation of peripheral T cell number and cytokine serum level. J Gastroenterol Hepatol; 2007 Nov;22(11):1866-71
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  • [Title] Thymosin alpha 1 improves severe acute pancreatitis in rats via regulation of peripheral T cell number and cytokine serum level.
  • AIM: The aim of this study was to investigate the effect of thymosin alpha 1 (TA1) on severe acute pancreatitis (SAP) in rats.
  • Serum amylase and lipase, interleukin (IL)-1beta, tumor necrosis factor-alpha (TNF-alpha), pancreatic wet/dry weight ratio and the percentage of CD3/CD4+/CD8+ T cells in peripheral blood mononuclear cells (PBMC) were measured.
  • Levels of serum IL-1beta, TNF-alpha and pancreatic wet/dry weight ratio were significantly reduced after TA1-treatment.
  • Application of TA1 significantly balanced CD3/CD4+/CD8+ T cells of PBMC and improved histological scores and the survival rate.
  • CONCLUSION: TA1 can reduce pancreatic inflammation by regulating differentiation of CD3/CD4+ T cells and decreasing the release of cytokines, thus attenuates pancreatic severity in SAP rats.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Interleukin-1beta / blood. Pancreas / drug effects. Pancreatitis / prevention & control. T-Lymphocytes / drug effects. Thymosin / analogs & derivatives. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Antigens, CD3 / analysis. CD4 Lymphocyte Count. CD4-CD8 Ratio. Disease Models, Animal. Lipase / blood. Lung / drug effects. Lung / pathology. Male. Organ Size / drug effects. Rats. Rats, Sprague-Dawley. Severity of Illness Index. Taurocholic Acid. Time Factors

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  • (PMID = 17914961.001).
  • [ISSN] 0815-9319
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antigens, CD3; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 0 / thymalfasin; 5E090O0G3Z / Taurocholic Acid; 61512-21-8 / Thymosin; EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases
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89. Tsao KC, Wu TL, Chang PY, Hong JH, Wu JT: Detection of carcinomas in an asymptomatic Chinese population: advantage of screening with multiple tumor markers. J Clin Lab Anal; 2006;20(2):42-6
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  • [Title] Detection of carcinomas in an asymptomatic Chinese population: advantage of screening with multiple tumor markers.
  • A total of 73,443 asymptomatic individuals were screened on a voluntary basis for cancer at Chang Gung Memorial Hospital in Taiwan using a panel of tumor markers, including alpha fetoprotein (AFP), CA 125, CA 15-3, CA 19-9, carcinoembryonic antigen (CEA), prostate specific antigen (PSA), chromogranin A (CgA), and squamous cell specific antigen (SCC).
  • A total of 210 cancers (approximately 0.3%) were detected, including cancers of the liver, lung, colon, prostate, stomach, pancreas, breast, cervix, ovary, and bladder.
  • Of the tumor markers monitored, elevated CA 19-9, CEA, and CA 125 were the most frequently detected in a variety of cancers.
  • It was surprising to find that many cancers were not detected by their dominant markers but by the elevation of tumor markers not recommended for monitoring their tumor activity.
  • Screening with multiple circulating tumor markers provides improved sensitivity for cancer detection in asymptomatic individuals before they reach the fatal advanced stage.
  • Screening with multiple tumor markers also allows cancers to be detected in the absence of their dominant markers.
  • If we had not measured the multiple tumor markers, these cancers would have gone undetected.
  • [MeSH-major] Asian Continental Ancestry Group. Biomarkers, Tumor / analysis. Carcinoma / diagnosis. Mass Screening / methods

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16538643.001).
  • [ISSN] 0887-8013
  • [Journal-full-title] Journal of clinical laboratory analysis
  • [ISO-abbreviation] J. Clin. Lab. Anal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
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90. Ito T, Omori K, Rawson J, Todorov I, Asari S, Kuroda A, Shintaku J, Itakura S, Ferreri K, Kandeel F, Mullen Y: Improvement of canine islet yield by donor pancreas infusion with a p38MAPK inhibitor. Transplantation; 2008 Jul 27;86(2):321-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improvement of canine islet yield by donor pancreas infusion with a p38MAPK inhibitor.
  • The islet isolation process, from pancreas procurement through islet collection, may activate p38MAPK leading to cytokine release and islet damage.
  • METHODS: Pancreata removed from Beagle dogs were infused with University of Wisconsin solution containing the p38IH, SB203580, and Pefabloc (n=6) or vehicle (dimethyl sulfoxide and Pefabloc) alone (n=7), through the pancreatic duct and preserved using the two-layer method.
  • RESULTS: p38IH-treated pancreata yielded significantly more islets than control pancreata (IEQ/g: 2134+/-297 vs. 1477+/-145 IEQ/g or 65,012+/-9385 vs. 45,700+/-5103 IEQ/pancreas; P<0.05).
  • Apoptotic beta-cell percentages assessed by laser scanning cytometry were lower in p38IH-treated than the controls (44%+/-9.4% vs. 61.6%+/-4.8%, P<0.05).
  • Tumor necrosis factor-alpha expression assessed by real-time reverse transcription polymerase chain reaction was significantly lower in the p38IH-treated group than controls.
  • Plasma C-peptide levels after glucagon challenge were higher in animals receiving p38IH-treated islets (n=5) versus untreated islets (n=4) (0.40+/-0.78 vs. 0.21+/-0.05 ng/mL, P<0.05).
  • CONCLUSIONS: Infusion of pancreata with University of Wisconsin solution containing p38IH through the duct before preservation suppresses cytokine release, prevents beta-cell apoptosis, and improves islet yield significantly with no adverse effect on islet function after transplantation. p38IH treatment of human pancreata may improve islet yield for use in clinical transplantation.

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  • (PMID = 18645497.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / U42 RR016607; United States / NCRR NIH HHS / RR / U42 RR 16607
  • [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 / Cytokines; 0 / Enzyme Inhibitors; 0 / Insulin; 0 / Organ Preservation Solutions; 0 / University of Wisconsin-lactobionate solution; 63CZ7GJN5I / Allopurinol; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; GAN16C9B8O / Glutathione; K72T3FS567 / Adenosine; N5O3QU595M / Raffinose
  • [Other-IDs] NLM/ NIHMS83977; NLM/ PMC3791927
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91. Inge LJ, Rajasekaran SA, Wolle D, Barwe SP, Ryazantsev S, Ewing CM, Isaacs WB, Rajasekaran AK: alpha-Catenin overrides Src-dependent activation of beta-catenin oncogenic signaling. Mol Cancer Ther; 2008 Jun;7(6):1386-97
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  • [Title] alpha-Catenin overrides Src-dependent activation of beta-catenin oncogenic signaling.
  • Loss of alpha-catenin is one of the characteristics of prostate cancer.
  • The catenins (alpha and beta) associated with E-cadherin play a critical role in the regulation of cell-cell adhesion.
  • Tyrosine phosphorylation of beta-catenin dissociates it from E-cadherin and facilitates its entry into the nucleus, where beta-catenin acts as a transcriptional activator inducing genes involved in cell proliferation.
  • Thus, beta-catenin regulates cell-cell adhesion and cell proliferation.
  • Although a wealth of information is available about beta-catenin deregulation during oncogenesis, much less is known about how or whether alpha-catenin regulates beta-catenin functions.
  • In this study, we show that alpha-catenin acts as a switch regulating the cell-cell adhesion and proliferation functions of beta-catenin.
  • In alpha-catenin-null prostate cancer cells, reexpression of alpha-catenin increased cell-cell adhesion and decreased beta-catenin transcriptional activity, cyclin D1 levels, and cell proliferation.
  • Further, Src-mediated tyrosine phosphorylation of beta-catenin is a major mechanism for decreased beta-catenin interaction with E-cadherin in alpha-catenin-null cells. alpha-Catenin attenuated the effect of Src phosphorylation by increasing beta-catenin association with E-cadherin.
  • We also show that alpha-catenin increases the sensitivity of prostate cancer cells to a Src inhibitor in suppressing cell proliferation.
  • This study reveals for the first time that alpha-catenin is a key regulator of beta-catenin transcriptional activity and that the status of alpha-catenin expression in tumor tissues might have prognostic value for Src targeted therapy.

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  • (PMID = 18566211.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK 56216; United States / NIGMS NIH HHS / GM / F31 GM068985; United States / NIDDK NIH HHS / DK / R01 DK056216-06; United States / NIDDK NIH HHS / DK / DK056216-08; United States / NIDDK NIH HHS / DK / R01 DK056216-08; United States / NIDDK NIH HHS / DK / DK056216-06; United States / NIDDK NIH HHS / DK / DK056216-07; United States / NIDDK NIH HHS / DK / R01 DK056216-07; United States / NIDDK NIH HHS / DK / R01 DK056216; United States / NIGMS NIH HHS / GM / F31-GM068985
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins; 0 / alpha Catenin; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
  • [Other-IDs] NLM/ NIHMS58917; NLM/ PMC2527861
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92. Shen SG, Zhang D, Hu HT, Li JH, Wang Z, Ma QY: Effects of alpha-adrenoreceptor antagonists on apoptosis and proliferation of pancreatic cancer cells in vitro. World J Gastroenterol; 2008 Apr 21;14(15):2358-63
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] Effects of alpha-adrenoreceptor antagonists on apoptosis and proliferation of pancreatic cancer cells in vitro.
  • AIM: To discuss the expression of alpha-adrenoreceptors in pancreatic cancer cell lines PC-2 and PC-3 and the effects of alpha1- and alpha2-adrenoreceptor antagonists, yohimbine and urapidil hydrochloride, on the cell lines in vitro.
  • METHODS: We cultured the human ductal pancreatic adenocarcinoma cell lines PC-2 and PC-3 and analyzed the mRNA expression of alpha1- and alpha2-adrenergic receptors by reverse transcription polymerase chain reaction (RT-PCR).
  • The effects of yohimbine and urapidil hydrochloride on cell proliferation were assessed by 3-(4,5-dimethylthiasol-2-yl)-2,4,-diphenyltetrazolium bromide (MTT) assay.
  • MTT assays showed that urapidil hydrochloride had no effect on PC-3 cell lines.
  • However, exposure to urapidil hydrochloride increased DNA synthesis in PC-2 cell lines as compared to the control group.
  • PC-2 cell lines were sensitive to both drugs.
  • The proliferation of the 2 cell lines was inhibited by yohimbine.
  • Cell proliferation was inhibited by yohimbine via apoptosis induction.
  • CONCLUSION: The expression of alpha1- and alpha2-adrenoreceptors is different in PC-2 and PC-3 cell lines, which might be indicative of their different functions.
  • The alpha2-adrenoceptor antagonist, yohimbine, can inhibit the proliferation of both cell lines and induce their apoptosis, suggesting that yohimbine can be used as an anticancer drug for apoptosis of PC-2 and PC-3 cells.
  • [MeSH-major] Adrenergic alpha-2 Receptor Antagonists. Adrenergic alpha-Antagonists / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Pancreatic Neoplasms / pathology. Yohimbine / pharmacology
  • [MeSH-minor] Adrenergic alpha-1 Receptor Antagonists. Cell Line, Tumor. DNA Replication / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. In Situ Nick-End Labeling. Piperazines / pharmacology. RNA, Messenger / metabolism. Receptors, Adrenergic, alpha-1 / metabolism. Receptors, Adrenergic, alpha-2 / genetics. Receptors, Adrenergic, alpha-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18416462.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-2 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / Piperazines; 0 / RNA, Messenger; 0 / Receptors, Adrenergic, alpha-1; 0 / Receptors, Adrenergic, alpha-2; 2Y49VWD90Q / Yohimbine; A78GF17HJS / urapidil
  • [Other-IDs] NLM/ PMC2705090
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93. 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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94. Garbe AI, Vermeer B, Gamrekelashvili J, von Wasielewski R, Greten FR, Westendorf AM, Buer J, Schmid RM, Manns MP, Korangy F, Greten TF: Genetically induced pancreatic adenocarcinoma is highly immunogenic and causes spontaneous tumor-specific immune responses. Cancer Res; 2006 Jan 1;66(1):508-16
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  • [Title] Genetically induced pancreatic adenocarcinoma is highly immunogenic and causes spontaneous tumor-specific immune responses.
  • Treatment options for pancreatic cancer are limited and often ineffective.
  • The aim of the present study was to analyze tumor-specific immune responses in a mouse model of pancreatic cancer, which mimics the human disease closely.
  • C57BL/6 EL-TGF-alpha x Trp53-/- mice, which develop spontaneous ductal pancreatic carcinoma, were generated.
  • EL-TGF-alpha x Trp53-/- mice developed spontaneous pancreatic tumors with pathomorphologic features close to the human disease.
  • Tumor-specific CD8+ T-cell responses and IgG responses were analyzed in EL-TGF-alpha x Trp53-/- mice during tumor development and compared with mice with s.c. growing pancreatic tumors.
  • In contrast to spontaneous pancreatic tumors, cell lines generated from these tumors were rejected after s.c. injection into wild-type mice but not in nude or RAG knockout mice.
  • Direct comparison of spontaneous and s.c. injected tumors revealed an impaired infiltration of CD8+ T cells in spontaneous pancreatic tumors, which was also evident after adoptive transfer of tumor-specific T cells.
  • Intratumoral cytokine secretion of tumor necrosis factor-alpha, IFN-gamma, IL-6, and MCP-1 was lower in spontaneous tumors as well as the number of adoptively transferred tumor-specific T cells.
  • Our data provide clear evidence for tumor-specific immune responses in a genetic mouse model for pancreatic carcinoma.
  • Comparative analysis of s.c. injected tumors and spontaneous tumors showed significant differences in tumor-specific immune responses, which will help in improving current immune-based cancer therapies against adenocarcinoma of the pancreas.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / immunology. Pancreatic Neoplasms / immunology. Transforming Growth Factor alpha / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytokines / immunology. Cytokines / secretion. Immunotherapy, Adoptive / methods. Lymphocytes, Tumor-Infiltrating / immunology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Transplantation. T-Lymphocytes / immunology

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  • (PMID = 16397267.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Transforming Growth Factor alpha; 0 / Tumor Suppressor Protein p53
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95. Ramudo L, Manso MA, Sevillano S, de Dios I: Kinetic study of TNF-alpha production and its regulatory mechanisms in acinar cells during acute pancreatitis induced by bile-pancreatic duct obstruction. J Pathol; 2005 May;206(1):9-16
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  • [Title] Kinetic study of TNF-alpha production and its regulatory mechanisms in acinar cells during acute pancreatitis induced by bile-pancreatic duct obstruction.
  • Cytokines play a critical role in acute pancreatitis (AP) but the contribution of different cell sources to cytokine production is unclear.
  • For this reason, the aim of this study was to analyse the ability of acinar cells, in comparison with leukocytes, to produce TNF-alpha at different stages of AP induced in rats by bile-pancreatic duct obstruction (BPDO) and to investigate the time course of oxidant-sensitive mechanisms involved in cytokine production.
  • The role of oxygen free radicals as messengers of the mechanisms underlying acinar cell TNF-alpha production was assessed in BPDO rats treated with N-acetylcysteine (NAC).
  • While monocytes were not able to produce TNF-alpha until 12 h after inducing AP, acinar cells triggered TNF-alpha production from 6 h after BPDO, at which time the pancreas develops maximal oxidative stress.
  • Phosphorylated p38-MAPK and activated NF-kappaB were detected in acinar cells from 6 h after BPDO.
  • NAC treatment reduced pancreatic glutathione depletion during the early stages of AP and attenuated the activation of p38-MAPK and NF-kappaB for 48 h following BPDO.
  • As a result, acinar cells in NAC-treated rats failed to produce TNF-alpha during AP.
  • In addition, NAC delayed monocyte TNF-alpha production, thereby maintaining low TNF-alpha levels in plasma during BPDO.
  • In conclusion, acinar cells contribute directly to the inflammatory response during BPDO-induced AP by producing TNF-alpha even before inflammatory cells in the peripheral blood.
  • The blockade of oxidant-mediated signal transduction pathways induced by NAC treatment prevented acinar cell TNF-alpha production.
  • [MeSH-major] Pancreas / metabolism. Pancreatitis / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Acute Disease. Animals. Blotting, Western / methods. Cell Culture Techniques. Cholestasis / complications. Cholestasis / metabolism. Flow Cytometry. Male. Models, Animal. NF-kappa B / metabolism. Pancreatic Ducts / metabolism. Rats. Rats, Wistar

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  • [Copyright] 2005 Pathological Society of Great Britain and Ireland
  • (PMID = 15761843.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha
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96. Ostermann E, Garin-Chesa P, Heider KH, Kalat M, Lamche H, Puri C, Kerjaschki D, Rettig WJ, Adolf GR: Effective immunoconjugate therapy in cancer models targeting a serine protease of tumor fibroblasts. Clin Cancer Res; 2008 Jul 15;14(14):4584-92
The Lens. Cited by Patents in .

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  • [Title] Effective immunoconjugate therapy in cancer models targeting a serine protease of tumor fibroblasts.
  • PURPOSE: Invasion and metastasis of malignant epithelial cells into normal tissues is accompanied by adaptive changes in the mesenchyme-derived supporting stroma of the target organs.
  • Altered gene expression in these nontransformed stromal cells provides potential targets for therapy.
  • The present study was undertaken to determine the antitumor effects of an antibody-conjugate against fibroblast activation protein-alpha, a cell surface protease of activated tumor fibroblasts.
  • EXPERIMENTAL DESIGN: A novel antibody-maytansinoid conjugate, monoclonal antibody (mAb) FAP5-DM1, was developed to target a shared epitope of human, mouse, and cynomolgus monkey fibroblast activation protein-alpha, enabling preclinical efficacy and tolerability assessments.
  • RESULTS: Treatment with mAb FAP5-DM1 induced long-lasting inhibition of tumor growth and complete regressions in xenograft models of lung, pancreas, and head and neck cancers with no signs of intolerability.
  • Analysis of chemically distinct conjugates, resistance models, and biomarkers implicates a unique mode of action, with mitotic arrest and apoptosis of malignant epithelial cells coupled to disruption of fibroblastic and vascular structures.
  • CONCLUSIONS: We show that mAb FAP5-DM1 combines excellent efficacy and tolerability and provides a first assessment of the mode of action of a novel drug candidate for tumor stroma targeting, thus encouraging further development toward clinical testing of this treatment paradigm.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Biomarkers, Tumor / immunology. Fibroblasts / immunology. Immunoconjugates / therapeutic use. Immunotherapy / methods. Neoplasms / therapy. Serine Endopeptidases / immunology

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  • (PMID = 18628473.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Immunoconjugates; 0 / Membrane Proteins; 14083FR882 / Maytansine; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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97. ten Kate M, Hofland LJ, van Koetsveld PM, Jeekel J, van Eijck CH: Pro-inflammatory cytokines affect pancreatic carcinoma cell. Endothelial cell interactions. JOP; 2006;7(5):454-64
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Pro-inflammatory cytokines affect pancreatic carcinoma cell. Endothelial cell interactions.
  • OBJECTIVES: The potential role of surgery-induced pro-inflammatory cytokines on the development of tumor recurrence in pancreatic cancer was investigated.
  • MAIN OUTCOME MEASURES: The adhesion of 3 human pancreatic carcinoma cell lines, PanC1, MiaPaCa and BxPC3 to monolayers of microvascular endothelial cells after pre-incubation with 0.1 or 10 ng/mL IL-1beta, TNF-alpha or IL-6 was assessed in a reproducible human in vitro assay.
  • RESULTS: Pre-incubation of microvascular endothelial cells with IL-1beta or TNF-alpha, but not IL-6, increased adhesion of all three tumor cell lines as compared to adhesion in the control group.
  • Pre-incubation of microvascular endothelial cells with IL-1beta or TNF-alpha resulted in a significant up-regulation of E-selectin, ICAM-1 and VCAM-1 expression.
  • The addition of anti-E-selectin, anti-ICAM-1 or anti-VCAM-1 monoclonal antibodies did not decrease adhesion to microvascular endothelial cells pre-incubated with IL-1beta.
  • Therefore, enhanced tumor cell binding seems to be independent of these adhesion molecules.
  • CONCLUSIONS: Pro-inflammatory cytokines derived from surgical trauma may enhance tumor cell adhesion to microvascular endothelial cells and thus bring about more successful tumor cell implantation resulting in an increased risk of metastasis formation.
  • [MeSH-major] Cytokines / immunology. Endothelial Cells / cytology. Endothelial Cells / immunology. Pancreatic Neoplasms / immunology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Cell Adhesion / drug effects. Cell Adhesion / immunology. Cell Communication / drug effects. Cell Communication / immunology. Cell Line, Tumor. E-Selectin / immunology. E-Selectin / metabolism. Humans. Immunoenzyme Techniques / standards. In Vitro Techniques. Intercellular Adhesion Molecule-1 / immunology. Intercellular Adhesion Molecule-1 / metabolism. Interleukin-1 / immunology. Interleukin-1 / pharmacology. Interleukin-6 / immunology. Interleukin-6 / pharmacology. Neoplasm Recurrence, Local / immunology. Reproducibility of Results. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / drug effects. Up-Regulation / immunology. Vascular Cell Adhesion Molecule-1 / immunology. Vascular Cell Adhesion Molecule-1 / metabolism

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  • (PMID = 16998242.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cytokines; 0 / E-Selectin; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1
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98. Spee B, Jonkers MD, Arends B, Rutteman GR, Rothuizen J, Penning LC: Specific down-regulation of XIAP with RNA interference enhances the sensitivity of canine tumor cell-lines to TRAIL and doxorubicin. Mol Cancer; 2006;5:34
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Specific down-regulation of XIAP with RNA interference enhances the sensitivity of canine tumor cell-lines to TRAIL and doxorubicin.
  • BACKGROUND: Apoptosis resistance occurs in various tumors.
  • Our aim is to evaluate whether RNA inhibition against XIAP increases the sensitivity of canine cell-lines for chemotherapeutics such as TRAIL and doxorubicin.
  • We used small interfering RNA's (siRNA) directed against XIAP in three cell-lines derived from bile-duct epithelia (BDE), mammary carcinoma (P114), and osteosarcoma (D17).
  • These cell-lines represent frequently occurring canine cancers and are highly comparable to their human counterparts.
  • The XIAP depleted cells were treated with a serial dilution of TRAIL or doxorubicin and compared to mock- and nonsense-treated controls.
  • RESULTS: All XIAP siRNA treated cell-lines showed a mRNA down-regulation over 80 percent.
  • No compensatory effect of IAP family members was seen in XIAP depleted cells.
  • The sensitivity of XIAP depleted cells for TRAIL was highest in BDE cells with an increase in the ED50 of 14-fold, compared to mock- and nonsense-treated controls.
  • The sensitivity of P114 and D17 cell-lines increased six- and five-fold, respectively.
  • Doxorubicin treatment in XIAP depleted cells increased sensitivity in BDE cells more than eight-fold, whereas P114 and D17 cell-lines showed an increase in sensitivity of three- and five-fold, respectively.
  • CONCLUSION: XIAP directed siRNA's have a strong sensitizing effect on TRAIL-reduced cell-viability and a smaller but significant effect with the DNA damaging drug doxorubicin.
  • The increase in efficacy of chemotherapeutics with XIAP depletion provides the rationale for the use of XIAP siRNA's in insensitive canine tumors.
  • [MeSH-major] Apoptosis Regulatory Proteins / pharmacology. Doxorubicin / pharmacology. Gene Expression Regulation, Neoplastic. Membrane Glycoproteins / pharmacology. RNA Interference. Tumor Necrosis Factor-alpha / pharmacology. X-Linked Inhibitor of Apoptosis Protein / genetics. X-Linked Inhibitor of Apoptosis Protein / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Dogs. Down-Regulation. Gene Expression Profiling. Homeostasis. Inhibitor of Apoptosis Proteins / classification. Inhibitor of Apoptosis Proteins / genetics. RNA, Messenger / genetics. Sensitivity and Specificity. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 16953886.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / X-Linked Inhibitor of Apoptosis Protein; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC1569868
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99. Genovese T, Mazzon E, Di Paola R, Muià C, Crisafulli C, Malleo G, Esposito E, Cuzzocrea S: Role of peroxisome proliferator-activated receptor-alpha in acute pancreatitis induced by cerulein. Immunology; 2006 Aug;118(4):559-70
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • [Title] Role of peroxisome proliferator-activated receptor-alpha in acute pancreatitis induced by cerulein.
  • The peroxisome proliferator-activated receptor-alpha (PPAR-alpha) is a member of the nuclear receptor superfamily of ligand-dependent transcription factors related to retinoid, steroid and thyroid hormone receptors.
  • The aim of the present study was to examine the effects of endogenous PPAR-alpha ligand on the development of acute pancreatitis caused by cerulein in mice.
  • Intraperitoneal injection of cerulein into PPAR-alpha wild-type (WT) mice resulted in severe, acute pancreatitis characterized by oedema, neutrophil infiltration and necrosis and by elevated serum levels of amylase and lipase.
  • Infiltration of pancreatic and lung tissue with neutrophils (measured as an increase in myeloperoxidase activity) was associated with enhanced expression of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and P-selectin.
  • Immunohistochemical examination demonstrated a marked increase in the staining (immunoreactivity) for transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF) in the pancreas of cerulein-treated PPAR-alpha wild-type (WT) mice in comparison to sham-treated mice.
  • In contrast, the degree of pancreatic inflammation and tissue injury (histological score), up-regulation/formation of ICAM-1 and P-selectin, infiltration of neutrophils, and the expression of TGF-beta and VEGF was markedly enhanced in pancreatic tissue obtained from cerulein-treated PPAR-alpha knockout (KO) mice.
  • Thus, endogenous PPAR-alpha ligands reduce the degree of pancreas injury caused by acute pancreatitis induced by cerulein administration.
  • [MeSH-major] Islets of Langerhans / metabolism. PPAR alpha / physiology. Pancreatitis / metabolism
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Biomarkers / blood. Blotting, Western / methods. Ceruletide. Intercellular Adhesion Molecule-1 / analysis. Lipase / blood. Mice. Mice, Knockout. Neutrophil Infiltration. P-Selectin / analysis. P-Selectin / metabolism. Peroxidase / metabolism. Random Allocation. Survival Rate. Transforming Growth Factor beta / analysis. Transforming Growth Factor beta / metabolism. Tumor Necrosis Factor-alpha / analysis. Tumor Necrosis Factor-alpha / metabolism. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 16764691.001).
  • [ISSN] 0019-2805
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / P-Selectin; 0 / PPAR alpha; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 126547-89-5 / Intercellular Adhesion Molecule-1; 888Y08971B / Ceruletide; EC 1.11.1.7 / Peroxidase; EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases
  • [Other-IDs] NLM/ PMC1782323
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100. Uchida H, Sasaki A, Iwaki K, Tominaga M, Yada K, Iwashita Y, Shibata K, Matsumoto T, Ohta M, Kitano S: An extramural gastrointestinal stromal tumor of the duodenum mimicking a pancreatic head tumor. J Hepatobiliary Pancreat Surg; 2005;12(4):324-7
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • [Title] An extramural gastrointestinal stromal tumor of the duodenum mimicking a pancreatic head tumor.
  • We report the case of a 53-year-old woman with a gastrointestinal stromal tumor (GIST) of the duodenum that showed only extramural growth, mimicking a pancreatic tumor.
  • Preoperatively, computed tomography (CT) and angiography revealed a hypervascular mass, 3.0 cm in diameter, in the pancreatic head.
  • Hypotonic duodenography showed compression of the second and third portions of the duodenum by the pancreatic lesion.
  • The pancreatic head tumor was diagnosed preoperatively as a nonfunctioning islet cell tumor of the pancreas, and the patient underwent pylorus-preserving pancreaticoduodenectomy.
  • A hard mass was palpated intraoperatively in the pancreatic head region, and neither peritoneal dissemination nor metastasis was detected.
  • Histologically, the tumor was composed of spindle-shaped cells with a fascicular growth pattern, and only a few mitotic features were seen.
  • Immunohistochemically, most of the tumor cells were positive for c-kit oncoprotein and CD34, but negative for alpha-smooth muscle actin and S-100 protein.
  • This is a rare case of a duodenal GIST with exclusively extramural growth mimicking a pancreatic head tumor.
  • [MeSH-major] Duodenal Neoplasms / pathology. Gastrointestinal Stromal Tumors / pathology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 16133702.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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