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

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  • [Copyright] Copyright 2005 Pathological Society of Great Britain and Ireland
  • (PMID = 15926199.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibodies, Neoplasm; 0 / SQSTM1 protein, human
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2. Gotthardt M, Béhé MP, Grass J, Bauhofer A, Rinke A, Schipper ML, Kalinowski M, Arnold R, Oyen WJ, Behr TM: Added value of gastrin receptor scintigraphy in comparison to somatostatin receptor scintigraphy in patients with carcinoids and other neuroendocrine tumours. Endocr Relat Cancer; 2006 Dec;13(4):1203-11
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  • [Title] Added value of gastrin receptor scintigraphy in comparison to somatostatin receptor scintigraphy in patients with carcinoids and other neuroendocrine tumours.
  • As gastrin-binding CCK(2) receptors are also expressed on a variety of other neuroendocrine tumours (NET), we compared GRS to somatostatin receptor scintigraphy (SRS) in patients with NET.
  • SRS and GRS were performed within 21 days in a series of 60 consecutive patients with NET.
  • Of the 60 evaluable patients, 51 had carcinoid tumours, 3 gastrinomas, 2 glucagonomas, 1 insulinoma and 3 paragangliomas.
  • The overall tumour-detection rate was 73.7% for GRS and 82.1% for SRS.
  • Based on the number of tumour sites detected and the degree of uptake, GRS performed better than SRS in 13 patients (21.7%), equivalent images were obtained in 18 cases (30.0%) and SRS performed better in 24 (40.0%) cases.
  • In six of the SRS positive patients, 18 additional sites of tumour involvement could be detected.
  • Overall, GRS detected additional tumour sites in 20% of the patients.
  • GRS should be performed in selected patients as it may provide additional information in patients with NET with equivocal or absent somatostatin uptake.
  • [MeSH-major] Carcinoid Tumor / radionuclide imaging. Neuroendocrine Tumors / radionuclide imaging. Receptor, Cholecystokinin B / metabolism. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Glucagonoma / radionuclide imaging. Humans. Indium Radioisotopes. Insulinoma / radionuclide imaging. Male. Middle Aged. Octreotide / analogs & derivatives. Paraganglioma / radionuclide imaging. Pentetic Acid / analogs & derivatives. Prognosis. Radiopharmaceuticals

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  • (PMID = 17158765.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Indium Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptor, Cholecystokinin B; 0 / Receptors, Somatostatin; 142694-57-3 / SDZ 215-811; 7A314HQM0I / Pentetic Acid; RWM8CCW8GP / Octreotide
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3. Pejcić I, Vrbić S, Filipović S, Sćekić M, Petković I, Pejcić L, Djenić N: [Significance of serum tumor markers monitoring metastases in carcinomas of unknown primary site]. Vojnosanit Pregl; 2010 Sep;67(9):723-31
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  • [Title] [Significance of serum tumor markers monitoring metastases in carcinomas of unknown primary site].
  • BACKGROUND/AIM: Unknown primary tumors represent a heterogeneous group of malignancies that are indicative of ominous prognosis.
  • Cancer of unknown primary site (CUP) is defined as the lack of any detectable primary site after full evaluation, and accounts for approximately 3-5% of all newly diagnosed patients with malignancies.
  • The aim of this report was to present the prognostic and predictive value of 8 serum tumor markers in this group of patients.
  • On histological examination, all the patients were presented with metastatic tumors whose primary site (origin) could not be detected with noninvasive diagnostic techniques.
  • In all the cases we evaluated 8 serum tumor markers: alpha-fetoproteins (AFP), chronic gonadotrophin beta submit, human (beta-HCG), neuron specific enolase (NSE), marker of malignant ovarian tumors (CA 125), prostate-specific antigene (PSA), marker of malignant brest tumor (CA 15-3), marker of malignant pancreas tumor and gastrointestinal tumor (Ca 19-9), carcinoembryonic antigen (CEA) at the time of diagnosis.
  • The patients responding to chemotherapy with complete response (CR), partial response (PR) or stable disease (SD) had the markers determined after three-month periods until the time of relapse or progression.
  • Average tumor marker values before and after the chemotherapy were significantly lower for NSE and CA 125.
  • CONCLUSION: Increased values of serum tumor markers are very often in CUP.
  • The tumors show nonspecific overexpression of tumor markers.
  • However, a routine evaluation of commonly used serum tumor markers has not been proven of any prognostic and predictive assistance.
  • [MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / blood. Carcinoma / secondary. Carcinoma, Squamous Cell / secondary. Neoplasms, Unknown Primary / pathology


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4. Duell EJ, Casella DP, Burk RD, Kelsey KT, Holly EA: Inflammation, genetic polymorphisms in proinflammatory genes TNF-A, RANTES, and CCR5, and risk of pancreatic adenocarcinoma. Cancer Epidemiol Biomarkers Prev; 2006 Apr;15(4):726-31
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  • [Title] Inflammation, genetic polymorphisms in proinflammatory genes TNF-A, RANTES, and CCR5, and risk of pancreatic adenocarcinoma.
  • Adenocarcinoma of the exocrine pancreas is the fourth leading cause of cancer-related death in men and women in the U.S.
  • Cytokines and other proinflammatory mediators have been implicated in inflammatory pancreatic diseases including pancreatitis and cancer.
  • We analyzed cytokine gene polymorphisms as risk factors for pancreatic cancer using questionnaire data obtained by in-person interviews and germ line DNA collected in a population-based case-control study of pancreatic cancer (532 cases and 1,701 controls) conducted in the San Francisco Bay Area.
  • We assessed potential interactions between these polymorphisms, proinflammatory conditions (e.g., pancreatitis, ulcer, and obesity), and smoking as risk factors for pancreatic cancer.
  • There was no overall association between pancreatic cancer risk and tumor necrosis factor-alpha (TNF-A -308G/A), regulated upon activation, normally T cell-expressed, and presumably secreted (RANTES -403G/A), and CC chemokine receptor 5 (CCR5-Delta32) polymorphisms.
  • There was a nearly 7-fold increased relative risk estimate for pancreatic cancer in individuals with a history of pancreatitis (adjusted OR, 6.9; 95% CI, 3.4-14.1).
  • Among patients with pancreatic cancer, pancreatitis was significantly associated with TNF-A -308 GA + AA (OR, 3.1; 95% CI, 1.3-7.4) and with RANTES -403 GA + AA (OR, 2.3; 95% CI, 1.0-5.4).
  • Our results lend support for the hypothesis that proinflammatory gene polymorphisms, in combination with proinflammatory conditions, may influence the development of pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / genetics. Chemokine CCL5 / genetics. Genetic Predisposition to Disease. Inflammation / genetics. Pancreatic Neoplasms / etiology. Pancreatic Neoplasms / genetics. Polymorphism, Genetic. Receptors, CCR5 / genetics. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 16614115.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA108370; United States / NCI NIH HHS / CA / CA59706; United States / NCI NIH HHS / CA / CA89726; United States / NCI NIH HHS / CA / CA988889
  • [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 / Chemokine CCL5; 0 / Receptors, CCR5; 0 / Tumor Necrosis Factor-alpha
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5. Chen X, Li SL, Wu T, Liu JD: Proteasome inhibitor ameliorates severe acute pancreatitis and associated lung injury of rats. World J Gastroenterol; 2008 May 28;14(20):3249-53
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  • A model of SAP was established by injection of 5% sodium taurocholate into the biliary-pancreatic duct of rats.
  • The changes in serum amylase, myeloperoxidase (MPO) activity of pancreatic and pulmonary tissue were measured.
  • The TNF-alpha level in pancreatic cytosolic fractions was assayed with an enzyme-linked immunosorbent assay (ELISA) kit.
  • Meanwhile, the pathological changes in both pancreatic and pulmonary tissues were also observed.
  • RESULTS: MG-132 significantly decreased serum amylase, pancreatic weight/body ratio, pancreatic TNF-alpha level, pancreatic and pulmonary MPO activity (P < 0.05).
  • Histopathological examinations revealed that pancreatic and pulmonary samples from rats pretreated with MG-132 demonstrated milder edema, cellular damage, and inflammatory activity (P < 0.05).
  • [MeSH-major] Cysteine Proteinase Inhibitors / pharmacology. Leupeptins / pharmacology. Lung / drug effects. Lung Diseases / prevention & control. Pancreas / drug effects. Pancreatitis / prevention & control. Proteasome Inhibitors
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Male. Organ Size. Peroxidase / metabolism. Proteasome Endopeptidase Complex / metabolism. Rats. Rats, Sprague-Dawley. Severity of Illness Index. Taurocholic Acid. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18506934.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cysteine Proteinase Inhibitors; 0 / Leupeptins; 0 / Proteasome Inhibitors; 0 / Tumor Necrosis Factor-alpha; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 5E090O0G3Z / Taurocholic Acid; EC 1.11.1.7 / Peroxidase; EC 3.2.1.- / Amylases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2712861
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6. 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
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  • [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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7. Rau BM, Krüger CM, Hasel C, Oliveira V, Rubie C, Beger HG, Schilling MK: Effects of immunosuppressive and immunostimulative treatment on pancreatic injury and mortality in severe acute experimental pancreatitis. Pancreas; 2006 Aug;33(2):174-83
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  • [Title] Effects of immunosuppressive and immunostimulative treatment on pancreatic injury and mortality in severe acute experimental pancreatitis.
  • Enhanced cell death by apoptosis during the postacute course was reduced in FK506-treated animals only.
  • Pancreatic interleukin (IL) 1beta messenger RNA up-regulation occurred early and was slightly suppressed in both treatment groups; tumor necrosis factor alpha (TNF-alpha) and IL-2 messenger RNA expression paralleled the onset of apoptosis and was markedly decreased in IFN-gamma- and FK506-treated rats.
  • The 2 therapeutic regimens had similar effects on intrapancreatic and systemic IL-1beta and TNF-alpha protein release; however, the profiles of both cytokines were differently influenced.
  • Whereas IFN-gamma and FK506 treatment lead to an enhanced intrapancreatic and systemic TNF-alpha protein release during the early course, IL-1beta concentrations were significantly reduced within the late intervals.
  • CONCLUSIONS: Severe acute pancreatitis is associated with early alterations of the immune response comprising overt T-cell activation and impaired monocyte/macrophage function alike.
  • Targeting either immunologic derangement improves local pancreatic damage and systemic severity.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Immunosuppressive Agents / pharmacology. Pancreas / drug effects. Pancreatitis, Acute Necrotizing / prevention & control
  • [MeSH-minor] Animals. Apoptosis. Disease Models, Animal. Gene Expression Regulation. Interferon-gamma / pharmacology. Interleukin-1beta / genetics. Interleukin-1beta / metabolism. Interleukin-2 / genetics. Interleukin-2 / metabolism. Male. Necrosis. RNA, Messenger / metabolism. Rats. Rats, Wistar. Tacrolimus / pharmacology. Taurocholic Acid. Time Factors. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16868484.001).
  • [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 / Adjuvants, Immunologic; 0 / Immunosuppressive Agents; 0 / Interleukin-1beta; 0 / Interleukin-2; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 5E090O0G3Z / Taurocholic Acid; 82115-62-6 / Interferon-gamma; WM0HAQ4WNM / Tacrolimus
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8. Qian ZY, Miao Y, Dai CC, Xu ZK, Liu XL: [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2005 Oct;27(5):572-4
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  • [Title] [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas].
  • OBJECTIVE: To investigate the feasibility and therapeutic results of multiple organ resection in patients with tumor of the body and tail of pancreas.
  • METHODS: The clinical and pathological data were analysed in 16 consecutive patients with neoplasm of the body and tail of pancreas from 1999 to 2004 retrospectively.
  • RESULTS: Multiple organ resection was performed in 6 cases of primary pancreatic adenocarcinoma of the body and tail (3 cases of pancreatic cancer, 2 cases of malignant glucagonoma, and 1 case of well-differentiated pancreatic stromal sarcoma) and 10 cases of extrapancreatic malignancy (4 cases of gastric cancer, 2 cases of gastric leiomyosarcoma, 1 case of duodenal cancer, and 3 cases of colon cancer of hepatic flexure).
  • Patients with primary pancreatic cancer or pancreatic stromal sarcoma died within 1 year.
  • Two patients with malignant glucagonoma died 51 and 39 months later.
  • [MeSH-major] Adenocarcinoma / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16274034.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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9. Liao SY, Lerman MI, Stanbridge EJ: Expression of transmembrane carbonic anhydrases, CAIX and CAXII, in human development. BMC Dev Biol; 2009 Mar 16;9:22
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  • BACKGROUND: Transmembrane CAIX and CAXII are members of the alpha carbonic anhydrase (CA) family.
  • Expression of CAIX and CAXII proteins in tumor tissues is primarily induced by hypoxia and this is particularly true for CAIX, which is regulated by the transcription factor, hypoxia inducible factor-1 (HIF-1).
  • Their distributions in normal adult human tissues are restricted to highly specialized cells that are not always hypoxic.
  • RESULTS: The co-localization of CAIX and HIF-1alpha was limited to certain cell types in embryonic and early fetal tissues.
  • Those cells comprised the primitive mesenchyma or involved chondrogenesis and skin development.
  • Transient CAIX expression was limited to immature tissues of mesodermal origin and the skin and ependymal cells.
  • The only tissues that persistently expressed CAIX protein were coelomic epithelium (mesothelium) and its remnants, the epithelium of the stomach and biliary tree, glands and crypt cells of duodenum and small intestine, and the cells located at those sites previously identified as harboring adult stem cells in, for example, the skin and large intestine.
  • CAXII expression is restricted to cells involved in secretion and water absorption such as parietal cells of the stomach, acinar cells of the salivary glands and pancreas, epithelium of the large intestine, and renal tubules.
  • 3) CAIX and CAXII expression is closely related to cell origin and secretory activity involving proton transport, respectively.
  • The intriguing finding of rare CAIX-expressing cells in those sites corresponding to stem cell niches requires further investigation.

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  • (PMID = 19291313.001).
  • [ISSN] 1471-213X
  • [Journal-full-title] BMC developmental biology
  • [ISO-abbreviation] BMC Dev. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-56000; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2666674
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10. 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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11. 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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12. Rizvi IA, Robinson K, McFadden DW, Riggs DR, Jackson BJ, Vona-Davis L: Peptide YY reverses TNF-alpha induced transcription factor binding of interferon regulatory factor-1 and p53 in pancreatic acinar cells. J Surg Res; 2006 Nov;136(1):25-30
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  • [Title] Peptide YY reverses TNF-alpha induced transcription factor binding of interferon regulatory factor-1 and p53 in pancreatic acinar cells.
  • Transcription factors interferon regulatory factor-1 (IRF-1) and the tumor suppressor gene p53 collaborate to enhance p21 related cell cycle regulation during pathological disease progression.
  • However, little is known about their role in the pancreas after cytokine challenge.
  • Our laboratory has previously shown that TNF-alpha induces the binding of many transcription factors, including NF-kappa B, and treatment with the gut hormone, Peptide YY (PYY), ameliorates the effects.
  • We hypothesized that TNF-alpha would induce IRF-1 and p53 protein binding in pancreatic acinar cells and that PYY would attenuate the effect.
  • MATERIALS AND METHODS: Rat pancreatic acinar AR42J cells were treated with rat recombinant TNF-alpha (200 ng/ml).
  • To verify that our model was inducing pancreatitis, alpha-amylase activity was measured in the cell culture supernatant by fluorescence spectroscopy.
  • PYY [3-36] was added at 500 pM 30 min post-TNF treatment; cells were harvested at 2 h for extraction of nuclear protein.
  • RESULTS: Amylase enzyme activity was significantly (P < 0.05) elevated in the TNF-alpha-treated cells by 2 h.
  • Induction by TNF-alpha increased IRF-1 protein binding 3.5-fold, while binding levels of p53 protein increased six-fold.
  • The addition of PYY to TNF-treated cells reduced IRF-1 and p53 binding to control levels.
  • CONCLUSIONS: We have shown for the first time that short-term exposure to TNF-alpha induces the binding activity of transcription factors IRF-1 and p53 in rat pancreatic acinar cells, and that addition of PYY reduces it.
  • [MeSH-major] Interferon Regulatory Factor-1 / metabolism. Pancreas, Exocrine / metabolism. Peptide YY / metabolism. Tumor Necrosis Factor-alpha / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Acute Disease. Amylases / metabolism. Animals. Cell Line. Oligonucleotide Array Sequence Analysis. Pancreatitis / metabolism. Protein Binding / drug effects. Rats. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16978650.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Regulatory Factor-1; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 106388-42-5 / Peptide YY; EC 3.2.1.- / Amylases
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13. Aerts JM, Ottenhoff R, Powlson AS, Grefhorst A, van Eijk M, Dubbelhuis PF, Aten J, Kuipers F, Serlie MJ, Wennekes T, Sethi JK, O'Rahilly S, Overkleeft HS: Pharmacological inhibition of glucosylceramide synthase enhances insulin sensitivity. Diabetes; 2007 May;56(5):1341-9
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  • In cultured 3T3-L1 adipocytes, the iminosugar derivative N-(5'-adamantane-1'-yl-methoxy)-pentyl-1-deoxynojirimycin (AMP-DNM) counteracted tumor necrosis factor-alpha-induced abnormalities in glycosphingolipid concentrations and concomitantly reversed abnormalities in insulin signal transduction.
  • [MeSH-minor] 3T3 Cells. Animals. Ceramides / metabolism. Glucose Intolerance / blood. Glucosylceramides / metabolism. Glycosphingolipids / metabolism. Humans. Liver / drug effects. Liver / physiology. Mice. Mice, Inbred C57BL. Mice, Obese. Pancreas / drug effects. Pancreas / physiology. Signal Transduction

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  • (PMID = 17287460.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / JF16994; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ceramides; 0 / Enzyme Inhibitors; 0 / Glucosylceramides; 0 / Glycosphingolipids; 0 / Insulin; 0 / N-(5-adamantane-1-yl-methoxy-pentyl)deoxynojirimycin; 19130-96-2 / 1-Deoxynojirimycin; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase; PJY633525U / Adamantane
  • [Other-IDs] NLM/ EMS61739; NLM/ PMC4298701
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14. Chong MM, Metcalf D, Jamieson E, Alexander WS, Kay TW: Suppressor of cytokine signaling-1 in T cells and macrophages is critical for preventing lethal inflammation. Blood; 2005 Sep 1;106(5):1668-75
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  • [Title] Suppressor of cytokine signaling-1 in T cells and macrophages is critical for preventing lethal inflammation.
  • Here, cre/loxP deletion of Socs1 was used to investigate the contribution of specific cells/tissues to inflammatory disease.
  • Mice with SOCS-1 deficiency in myeloid and lymphoid cells, but not lymphoid alone, became ill at 50 to 250 days of age.
  • These mice developed splenomegaly and T-cell/macrophage infiltration of many organs, including liver, lung, pancreas, and muscle.
  • There were also abnormally high levels of the proinflammatory cytokines interferon gamma (IFN-gamma), tumor necrosis factor (TNF), and interleukin-12 (IL-12), and activated T cells circulating in these mice.
  • Socs1(null) T cells were found to be hypersensitive to multiple cytokines, including IL-1, IL-2, and IL-12, resulting in IFN-gamma production without requiring T-cell receptor (TCR) ligation.
  • A dysregulated cytokine network between T cells and macrophages is thus associated with this inflammatory disease.
  • These findings indicate that SOCS-1 is critical in both T cells and macrophages for preventing uncontrolled inflammation.
  • [MeSH-minor] Animals. Cell Lineage / drug effects. Cell Lineage / immunology. Dose-Response Relationship, Drug. Interferon-gamma / pharmacology. Lipopolysaccharides / pharmacology. Mice. Mice, Transgenic. Myeloid Progenitor Cells / drug effects. Myeloid Progenitor Cells / immunology. Suppressor of Cytokine Signaling Proteins. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 15899915.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carrier Proteins; 0 / Lipopolysaccharides; 0 / Repressor Proteins; 0 / Socs1 protein, mouse; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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15. de Herder WW: Biochemistry of neuroendocrine tumours. Best Pract Res Clin Endocrinol Metab; 2007 Mar;21(1):33-41
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  • [Title] Biochemistry of neuroendocrine tumours.
  • Several circulating or urinary tumour markers can be used for the diagnosis and follow-up of functioning and clinically non-functioning neuroendocrine tumours of the pancreatic islet cells and intestinal tract.
  • Among the specific tumour markers are serotonin and its metabolites--e.g.
  • 5-hydroxyindoleacetic acid (5-HIAA)--in carcinoid tumours and the carcinoid syndrome, insulin and its precursors or breakdown products in insulinoma, and gastrin in gastrinoma.
  • Plasma vasointestinal polypeptide (VIP) determinations have been used in the diagnosis of VIPoma, plasma glucagon for glucagonoma, and serum somatostatin for somatostatinoma.
  • Among the tumour-non-specific markers are: chromogranins, neuron-specific enolase (NSE), alpha-subunits of the glycoprotein hormones, catecholamines, pancreatic polypeptide (PP), ghrelin and adrenomedullin.
  • [MeSH-major] Biomarkers, Tumor / analysis. Neuroendocrine Tumors / diagnosis
  • [MeSH-minor] Biomarkers / analysis. Carcinoid Tumor / diagnosis. Gastrinoma / diagnosis. Gastrins / analysis. Humans. Insulin / analysis. Insulin / metabolism. Insulinoma / diagnosis. Malignant Carcinoid Syndrome / diagnosis. Pancreatic Neoplasms / diagnosis. Serotonin / analysis. Serotonin / metabolism

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  • (PMID = 17382264.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Gastrins; 0 / Insulin; 333DO1RDJY / Serotonin
  • [Number-of-references] 49
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16. Zhang XP, Lin Q, Zhou YF: Progress of study on the relationship between mediators of inflammation and apoptosis in acute pancreatitis. Dig Dis Sci; 2007 May;52(5):1199-205
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  • As an important pathological feature of acute pancreatitis, apoptosis may occur in multiple organs and relate directly to the progression of disease.
  • We summarize here the roles of the main inflammatory mediators (e.g., NO, TNF-alpha, TGF-beta1, IL-10, NF-kappaB) during the pathologic process of acute pancreatitis.
  • [MeSH-minor] Acute Disease. Animals. Humans. Interleukin-10 / metabolism. NF-kappa B / metabolism. Nitric Oxide / metabolism. Transforming Growth Factor beta1 / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17372825.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Inflammation Mediators; 0 / NF-kappa B; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 74
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17. Chaw L, Krop TM, Hood AF: What is your diagnosis? Necrolytic migratory erythema associated with a glucagonoma. Cutis; 2008 Jan;81(1):25, 30-2
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  • [Title] What is your diagnosis? Necrolytic migratory erythema associated with a glucagonoma.
  • [MeSH-major] Erythema / etiology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / pathology. Skin / pathology. Skin Diseases / etiology
  • [MeSH-minor] Female. Glucagon / blood. Humans. Middle Aged

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  • (PMID = 18306843.001).
  • [ISSN] 0011-4162
  • [Journal-full-title] Cutis
  • [ISO-abbreviation] Cutis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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18. Long C, Yin B, Lu Q, Zhou X, Hu J, Yang Y, Yu F, Yuan Y: Promoter hypermethylation of the RUNX3 gene in esophageal squamous cell carcinoma. Cancer Invest; 2007 Dec;25(8):685-90
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  • [Title] Promoter hypermethylation of the RUNX3 gene in esophageal squamous cell carcinoma.
  • Alteration in transforming growth factor-beta (TGF-beta) signaling pathway is one of the main causes of esophageal squamous cell carcinoma (ESCC).
  • Hypermethylation of RUNX3 promoter was frequently found in gastrointestinal cancers, including those of stomach, liver, colon and pancreas.
  • The aim of this study was to determine whether promoter methylation of the RUNX3 gene correlates with ESCC tumor progression.Accordingly, we first determined RUNX3 mRNA expression and methylation status of its promoter region in 42 primary tumors with ESCC and Eca-109, an ESCC cell line.
  • Loss of RUNX3 mRNA expression was detected by RT-PCR in 23 out of 42 (54.8%) ESCC specimens and Eca-109 cells.
  • The Promoter hypermethylation was detected by Methylation Specific Polymerase Chain Reaction (MS-PCR) in 27 out of 42 (64.3%) ESCC specimen and Eca-109 cells.
  • Importantly, we found positive correlations, not only between the promoter hypermethylation and tumor clinical pathologic stages (P = 0.003), but also between the loss of RUNX3 mRNA expression and the tumor progression (P = 0.016).
  • Finally, we observed that the loss of RUNX3 mRNA expression is statistically correlated with the promoter hypermethylation in these tumors (P < 0.001).
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Core Binding Factor Alpha 3 Subunit / genetics. DNA Methylation. Esophageal Neoplasms / genetics. Promoter Regions, Genetic
  • [MeSH-minor] Aged. Azacitidine / pharmacology. Cell Line, Tumor. Female. Humans. Male. Middle Aged. RNA, Messenger / analysis. Signal Transduction. Transforming Growth Factor beta / physiology

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  • (PMID = 18058463.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit; 0 / RNA, Messenger; 0 / Runx3 protein, human; 0 / Transforming Growth Factor beta; M801H13NRU / Azacitidine
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19. Cheung SS, Metzger DL, Wang X, Huang J, Tai J, Tingle AJ, Ou D: Tumor necrosis factor-related apoptosis-inducing ligand and CD56 expression in patients with type 1 diabetes mellitus. Pancreas; 2005 Mar;30(2):105-14
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  • [Title] Tumor necrosis factor-related apoptosis-inducing ligand and CD56 expression in patients with type 1 diabetes mellitus.
  • OBJECTIVES: Our previous report showed that beta-cell antigen-specific CD56+ T-cells and cytokine TRAIL mediate destruction of human pancreatic [beta] cells in vitro.
  • To determine whether CD56 and TRAIL are present during islet cell destruction at the onset of clinical symptoms of type 1 diabetes mellitus (T1D), we studied cell marker and cytokine expression in the pancreatic islets of 2 children who died at presentation of acute-onset T1D and in T-cell lines derived from a group of children with new-onset T1D.
  • METHODS: TRAIL, CD56, and other T-cell markers and cytokine expression were studied using immunohistochemistry on pancreatic sections from 2 children with acute-onset T1D.
  • TRAIL and CD56 expression was analyzed by flow cytometry in the antigen-activated T-cell lines derived from 29 children with new-onset T1D.
  • RESULTS: TRAIL+, CD56+, CD45RO+, and CD3+ cells were present in the islets of acute-onset T1D patients, while none were present in the normal islets.
  • T-cell lines from new-onset T1D expressed TRAIL and CD56 in response to stimulation with beta-cell antigens GAD, IA-2 and insulin beta chain.
  • CONCLUSION: The presence of TRAIL and CD56 markers is part of the T-cell response repertoire in beta-cell destruction.
  • [MeSH-major] Antigens, CD56 / metabolism. Apoptosis / immunology. Apoptosis Regulatory Proteins / metabolism. Biomarkers. Diabetes Mellitus, Type 1 / immunology. Diabetes Mellitus, Type 1 / metabolism. Membrane Glycoproteins / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adolescent. Adult. Child. Female. Humans. Immunohistochemistry. Immunophenotyping. Insulin-Secreting Cells / immunology. Insulin-Secreting Cells / metabolism. Insulin-Secreting Cells / pathology. Interferon-gamma / metabolism. Male. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / pathology. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 15714132.001).
  • [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 / Antigens, CD56; 0 / Apoptosis Regulatory Proteins; 0 / Biomarkers; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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20. Miettinen M, Lasota J: Gastrointestinal stromal tumors: pathology and prognosis at different sites. Semin Diagn Pathol; 2006 May;23(2):70-83
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  • [Title] Gastrointestinal stromal tumors: pathology and prognosis at different sites.
  • Gastrointestinal (GI) stromal tumors (GISTs) are the most common mesenchymal tumors specific to the GI tract, generally defined as KIT (CD117)-positive tumors with a characteristic set of histologic features.
  • These tumors, derived from Cajal cells or their precursors, most commonly occur at the age >50 years in the stomach (60%), jejunum and ileum (30%), duodenum (4-5%), rectum (4%), colon and appendix (1-2%), and esophagus (<1%), and rarely as apparent primary extragastrointestinal tumors in the vicinity of stomach or intestines.
  • Their overall incidence has been estimated as 10 to 20 per million, including incidental minimal tumors.
  • GISTs contain a spectrum from minute indolent tumors to sarcomas at all sites of occurrence.
  • Their gross patterns are diverse, including nodular, cystic, and diverticular tumors.
  • External involvement of pancreas and liver can simulate primary tumor in these organs.
  • In general, gastric tumors have a more favorable prognosis than the intestinal ones with similar parameters.
  • Gastric GISTs can be divided into histologic subgroups including 4 spindle cell and 4 epithelioid variants.
  • Immunohistochemical demonstration of KIT, CD34, or protein kinase theta positivity helps to properly identify these tumors.
  • [MeSH-major] Biomarkers, Tumor / analysis. Gastrointestinal Stromal Tumors / pathology. Gastrointestinal Tract / pathology. Neurofibromatosis 1 / complications
  • [MeSH-minor] Adolescent. Animals. Child. Humans. Immunohistochemistry. Muscle Cells / metabolism. Neurons / metabolism. Prognosis. Receptor, Platelet-Derived Growth Factor alpha / metabolism

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  • (PMID = 17193820.001).
  • [ISSN] 0740-2570
  • [Journal-full-title] Seminars in diagnostic pathology
  • [ISO-abbreviation] Semin Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 91
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21. Shen HC, Ylaya K, Pechhold K, Wilson A, Adem A, Hewitt SM, Libutti SK: Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice. Endocrinology; 2010 Aug;151(8):4024-30
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  • [Title] Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice.
  • The pancreatic alpha- and beta-cells are critical components in regulating blood glucose homeostasis via secretion of glucagon and insulin, respectively.
  • Both cell types are typically localized in the islets of Langerhans.
  • The lack of suitable cell lines to study alpha- and beta-cells interactions have led us to develop an alpha-cell-specific Cre-expressing transgenic line utilizing a glucagon promoter sequence, the Glu-Cre transgenic mouse.
  • Here, we demonstrate that the Glu-Cre could specifically and efficiently excise floxed target genes in adult islet alpha-cells.
  • We further showed that deletion of the tumor suppressor gene, multiple endocrine neoplasia type 1 (Men1), in alpha-cells led to tumorigenesis.
  • However, to our surprise, the lack of Men1 in alpha-cells did not result in glucagonomas but rather beta-cell insulinomas.
  • Because deletion of the Men1 alleles was only present in alpha-cells, our data suggested that cross communication between alpha- and beta-cells contributes to tumorigenesis in the absence of Men1.
  • Together, we believed that the new model systems described here will allow future studies to decipher cellular interactions between islet alpha- and beta-cells in a physiological context.

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  • (PMID = 20555035.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Men1 protein, mouse; 0 / Proto-Oncogene Proteins; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ PMC2940531
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22. Yu G, Tang B, Yu PW, Peng ZH, Qian F, Sun G: Systemic and peritoneal inflammatory response after laparoscopic-assisted gastrectomy and the effect of inflammatory cytokines on adhesion of gastric cancer cells to peritoneal mesothelial cells. Surg Endosc; 2010 Nov;24(11):2860-70
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  • [Title] Systemic and peritoneal inflammatory response after laparoscopic-assisted gastrectomy and the effect of inflammatory cytokines on adhesion of gastric cancer cells to peritoneal mesothelial cells.
  • We designed this trial to investigate the effects of the inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) on the interaction between gastric cancer cells and mesothelial cells, and to evaluate differences in both the peritoneal and systemic cytokine (IL-1β and TNF-α) concentrations after laparoscopic and conventional surgical approaches, thus offering another possible advantage of laparoscopic procedures for treatment of gastric cancer.
  • EXPERIMENTAL DESIGN: A reproducible human in vitro assay was developed to study adhesion of SGC-7901 and MKN-45 human gastric cancer cells to monolayers of primary cultured human peritoneal mesothelial cells (HPMCs).
  • Tumor cell adhesion to a mesothelial monolayer was assessed after preincubation of the monolayer with IL-1β and TNF-α using flow cytometry.
  • RESULTS: Preincubation of the mesothelial monolayer with IL-1β and TNF-α resulted in enhanced tumor cell adhesion of SGC-7901 and MKN-45 cells.
  • Mesothelial cells showed significant enhancement of expression of ICAM-1, VCAM-1, and CD44 after stimulation with IL-1β and TNF-α.
  • Meanwhile their counterparts (LFA-1, VLA-4, and CD44) were identified in gastric cancer cells.
  • CONCLUSIONS: The presented results prove that IL-1β and TNF-α are significant stimulating factors in gastric cancer cell adhesion in vitro and may therefore partly account for local tumor recurrence and peritoneal metastasis in vivo.
  • [MeSH-major] Cell Adhesion Molecules / metabolism. Gastrectomy. Inflammation Mediators / pharmacology. Interleukin-1beta / pharmacology. Laparoscopy. Peritoneum / physiopathology. Stomach Neoplasms / physiopathology. Stomach Neoplasms / surgery. Tumor Necrosis Factor-alpha / pharmacology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Ascitic Fluid / chemistry. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Proliferation. Cell Survival. Epithelial Cells / physiology. Humans. Peritoneal Neoplasms / secondary. Tumor Cells, Cultured

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  • (PMID = 20419322.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Inflammation Mediators; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha
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23. Zou GM, Maitra A: Small-molecule inhibitor of the AP endonuclease 1/REF-1 E3330 inhibits pancreatic cancer cell growth and migration. Mol Cancer Ther; 2008 Jul;7(7):2012-21
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  • [Title] Small-molecule inhibitor of the AP endonuclease 1/REF-1 E3330 inhibits pancreatic cancer cell growth and migration.
  • APE1 is overexpressed in several human cancers, and disruption of APE1 function has detrimental effects on cancer cell viability.
  • In the present study, we used E3330, a small-molecule inhibitor of APE1 redox domain function, to interrogate the functional relevance of sustained redox function in pancreatic cancer.
  • We show that E3330 significantly reduces the growth of human pancreatic cancer cells in vitro.
  • This phenomenon was further confirmed by a small interfering RNA experiment to knockdown APE1 expression in pancreatic cancer cells.
  • E3330 exposure promotes endogenous reactive oxygen species formation in pancreatic cancer cells, and the resulting oxidative stress is associated with higher levels of oxidized, and hence inactive, SHP-2, an essential protein tyrosine phosphatase that promotes cancer cell proliferation in its active state.
  • Finally, E3330 treatment inhibits pancreatic cancer cell migration as assessed by in vitro chemokine assays.
  • E3330 shows anticancer properties at multiple functional levels in pancreatic cancer, such as inhibition of cancer cell growth and migration.
  • Inhibition of the APE1 redox function through pharmacologic means has the potential to become a promising therapeutic strategy in this disease.
  • [MeSH-major] Benzoquinones / pharmacology. Cell Movement / drug effects. DNA-(Apurinic or Apyrimidinic Site) Lyase / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology. Propionates / pharmacology
  • [MeSH-minor] Antigens, CD44 / metabolism. Cell Hypoxia / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Chemokine CXCL12 / metabolism. DNA, Neoplasm / metabolism. Enzyme Activation / drug effects. Epithelial Cells / drug effects. Epithelial Cells / pathology. G1 Phase / drug effects. G2 Phase / drug effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Models, Biological. Oxidation-Reduction / drug effects. Pancreas / pathology. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism. Reactive Oxygen Species / metabolism

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  • (PMID = 18645011.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Benzoquinones; 0 / Chemokine CXCL12; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Propionates; 0 / Reactive Oxygen Species; 136164-66-4 / E 3330; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase
  • [Other-IDs] NLM/ NIHMS436971; NLM/ PMC3569736
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24. Eastham LL, Mills CN, Niles RM: PPARalpha/gamma expression and activity in mouse and human melanocytes and melanoma cells. Pharm Res; 2008 Jun;25(6):1327-33
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  • [Title] PPARalpha/gamma expression and activity in mouse and human melanocytes and melanoma cells.
  • PURPOSE: We examined the expression of PPARs and the effects of PPARalpha and PPARgamma agonists on growth of mouse and human melanocytes and melanoma cells.
  • METHODS: PPARalpha,beta, and PPARgamma mRNA qualitative expression in melan-a mouse melanocytes, B16 mouse melanoma, human melanocytes, and A375 and SK-mel28 human melanoma cells was determined by RT-PCR, while quantitative PPARalpha mRNA levels were determined by QuantiGene assay.
  • The effect of natural and synthetic PPAR ligands on cell growth was determined by either hemocytometer counting or crystal violet assay.
  • RESULTS: Both mouse and human melanoma cells produced more PPARalpha and PPARgamma protein compared to melanocytes.
  • PPARalpha mRNA levels were elevated in human melanoma cells, but not in mouse melanoma cells relative to melanocytes.
  • Silencing of PPARalpha in human melanoma cells did not alter cell proliferation or morphology.
  • PPARgamma-selective agonists inhibited the growth of both mouse and human melanoma cells, while PPARalpha-selective agonists had limited effects.
  • [MeSH-major] Melanocytes / metabolism. Melanoma / metabolism. PPAR alpha / physiology. PPAR gamma / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. RNA, Messenger / analysis. Transcriptional Activation

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  • (PMID = 18172578.001).
  • [ISSN] 0724-8741
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59530; United States / NCI NIH HHS / CA / CA59539/S; United States / NCRR NIH HHS / RR / P20 RR20180
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / PPAR alpha; 0 / PPAR gamma; 0 / RNA, Messenger
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25. Yang F, Shi P, Xi X, Yi S, Li H, Sun Q, Sun M: Recombinant adenoviruses expressing TRAIL demonstrate antitumor effects on non-small cell lung cancer (NSCLC). Med Oncol; 2006;23(2):191-204
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  • [Title] Recombinant adenoviruses expressing TRAIL demonstrate antitumor effects on non-small cell lung cancer (NSCLC).
  • INTRODUCTION: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in a variety of malignant cells, but not in normal cells.
  • This preferential toxicity to the abnormal cells renders TRAIL potentially a very powerful therapeutic weapon against cancer.
  • However, a requirement for large quantities of TRAIL to suppress tumor growth in vivo is one of the major factors that has hindered it from being widely applied clinically.
  • To overcome this, we constructed a replication-deficient adenovirus that carries a human full-length TRAIL gene (Ad-TRAIL) and tested its efficacy against a lung cancer model system in comparison to that of the recombinant soluble TRAIL protein.
  • METHODS: To investigate the antitumor activity and therapeutic value of the Ad-TRAIL on the non-small cell lung cancer (NSCLC), four NSCLC cell lines, namely, YTMLC, GLC, A549, and H460 cells, were used.
  • Cell viability was analyzed by proliferation assay, and DNA ladder and cell-cycle analysis were used to identify apoptosis.
  • To further evaluate the effect of Ad-TRAIL in vivo, YTMLC cells were inoculated to the subcutis of nude mice.
  • The Ad-TRAIL was subsequently administered into the established tumors.
  • Tumor growth and the TRAIL toxicity were evaluated after treatment.
  • RESULTS: YTMLC cells infected with Ad-TRAIL showed decreased cell viability and a higher percentage of apoptosis.
  • Similar, Ad-TRAIL treatment also significantly suppressed tumor growth in vivo.
  • [MeSH-major] Adenoviridae. Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. Carcinoma, Non-Small-Cell Lung / therapy. Genetic Therapy. Lung Neoplasms / therapy. Membrane Glycoproteins / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / therapy. Neoplasms, Experimental / ultrastructure. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 16720919.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha
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26. Stoeltzing O, Liu W, Fan F, Wagner C, Stengel K, Somcio RJ, Reinmuth N, Parikh AA, Hicklin DJ, Ellis LM: Regulation of cyclooxygenase-2 (COX-2) expression in human pancreatic carcinoma cells by the insulin-like growth factor-I receptor (IGF-IR) system. Cancer Lett; 2007 Dec 18;258(2):291-300
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  • [Title] Regulation of cyclooxygenase-2 (COX-2) expression in human pancreatic carcinoma cells by the insulin-like growth factor-I receptor (IGF-IR) system.
  • Both the insulin-like growth factor-I receptor (IGF-IR) and cyclooxygenase-2 (COX-2) are frequently overexpressed in pancreatic cancer.
  • Pancreatic cancer cells (L3.6pl) were stably transfected with a dominant-negative receptor (IGF-IR DN) construct or empty vector (pcDNA).
  • Cells were stimulated with IGF-I to determine activated signaling intermediates and induction of COX-2.
  • In addition, IGF-IR DN cells showed a marked decrease in constitutive COX-2 and a blunted response to IGF-I.
  • Similarly, treatment with an anti-IGF-IR antibody effectively inhibited IGF-IR and MAPK/Erk activation and decreased COX-2 in parental cells.
  • In conclusion, activation of IGF-IR mediates COX-2 expression in human pancreatic cancer cells.

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  • (PMID = 17950526.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA009599-15; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA16672; United States / PHS HHS / / T-32 09599; United States / NCI NIH HHS / CA / T32 CA009599-15; United States / NCI NIH HHS / CA / T32 CA009599
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Enzyme Inhibitors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / IRS1 protein, human; 0 / Insulin Receptor Substrate Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ NIHMS35362; NLM/ PMC2147684
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27. 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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28. Nishiuchi T, Imachi H, Murao K, Fujiwara M, Muraoka T, Kikuchi F, Nishiuchi Y, Kushida Y, Haba R, Ishida T: Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1). Endocrine; 2009 Aug;36(1):20-4
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  • [Title] Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1).
  • Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by tumors of the parathyroid glands, the anterior pituitary, and the endocrine pancreas.
  • He was admitted to our hospital because of recurrent hypoglycemia and a growth of pancreatic tumors.
  • He subsequently underwent surgery for the pancreatic tumors.
  • The majority of these tumor cells were immunohistochemically positive for insulin and negative for glucagon.
  • A few nodules showed immunohistochemical staining positivity for glucagon but they were negative for insulin.
  • Although it is uncommon for patients with MEN1 to exhibit insulinoma and glucagonoma, this case suggests the need for careful analysis of pancreatic tumors in patients with MEN1.
  • [MeSH-major] Glucagonoma / pathology. Insulinoma / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / pathology


29. 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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30. Peracaula R, Tabarés G, López-Ferrer A, Brossmer R, de Bolós C, de Llorens R: Role of sialyltransferases involved in the biosynthesis of Lewis antigens in human pancreatic tumour cells. Glycoconj J; 2005 Mar;22(3):135-44
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  • [Title] Role of sialyltransferases involved in the biosynthesis of Lewis antigens in human pancreatic tumour cells.
  • The sialylated carbohydrate antigens, sialyl-Lewisx and sialyl-Lewisa, are expressed in pancreatic tumour cells and are related to their metastatic potential.
  • While the action of the fucosyltransferases involved in the synthesis of these antigens has already been investigated, no studies have been carried out on the activity and expression of the alpha 2,3-sialyltransferases in pancreatic tumour cells.
  • We describe the sialyltransferase (ST) activity, mRNA expression, and analysis of the cell carbohydrate structures in four human pancreatic adenocarcinoma cell lines of a wide range of neoplastic differentiation stages and in normal human pancreatic tissues.
  • Total ST activity measured on asialofetuin, employing a CMP fluorescent sialic acid, varied among the pancreatic cell lines and could be correlated to the expression of their cell surface antigens.
  • However, in some of the pancreatic cell lines, no relationship could be established with their ST3Gal III and IV mRNA expression.
  • Human pancreatic tissues also showed ST expression and activity.
  • In conclusion, ST activity levels in pancreatic cells could be correlated to their expression of sialylated epitopes, which indicates their involvement in the formation of the sialyl-Lewis antigens, in addition to fucosyltransferase activities.
  • [MeSH-major] Adenocarcinoma / enzymology. Antigens, Tumor-Associated, Carbohydrate / metabolism. Lewis Blood-Group System / biosynthesis. Sialyltransferases / metabolism
  • [MeSH-minor] Enzyme-Linked Immunosorbent Assay. Fucosyltransferases / metabolism. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Pancreas / enzymology. Pancreatic Neoplasms / enzymology. RNA, Messenger / metabolism. Tumor Cells, Cultured

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  • (PMID = 16133834.001).
  • [ISSN] 0282-0080
  • [Journal-full-title] Glycoconjugate journal
  • [ISO-abbreviation] Glycoconj. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Lewis Blood-Group System; 0 / RNA, Messenger; EC 2.4.1.- / Fucosyltransferases; EC 2.4.99.- / Sialyltransferases; EC 2.4.99.4 / beta-galactoside alpha-2,3-sialyltransferase
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31. Cuzzocrea S, Malleo G, Genovese T, Mazzon E, Esposito E, Muià C, Abdelrahman M, Di Paola R, Thiemermann C: Effects of glycogen synthase kinase-3beta inhibition on the development of cerulein-induced acute pancreatitis in mice. Crit Care Med; 2007 Dec;35(12):2811-21
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  • TDZD-8 significantly reduced the degree of pancreas injury, amylase, and lipase serum levels (p < .01); nuclear factor-kappaB activation (p < .01); the production of tumor necrosis factor-alpha and interleukin-1beta (p < .01); the expression of adhesion molecules and neutrophil accumulation (p < .01); the formation of oxygen and nitrogen-derived radicals (p < .01); the degree of lipid peroxidation (p < .01); the expression of transforming growth factor-beta and vascular endothelial growth factor (p < .01); and-ultimately-the mortality rate (p < .01).
  • [MeSH-minor] Acute Disease. Animals. Cell Adhesion Molecules / drug effects. Ceruletide. Cytokines / drug effects. Male. Mice. Mice, Inbred Strains. NF-kappa B / drug effects. Neutrophil Activation / drug effects. Oxidative Stress / drug effects. Prospective Studies. Random Allocation. Survival Analysis

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  • [CommentIn] Crit Care Med. 2007 Dec;35(12):2874-5 [18043215.001]
  • (PMID = 18074481.001).
  • [ISSN] 0090-3493
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione; 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / Thiadiazoles; 888Y08971B / Ceruletide; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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32. Takahashi H, Funahashi H, Sawai H, Matsuo Y, Yamamoto M, Okada Y, Takeyama H, Manabe T: Synthetic serine protease inhibitor, gabexate mesilate, prevents nuclear factor-kappaB activation and increases TNF-alpha-mediated apoptosis in human pancreatic cancer cells. Dig Dis Sci; 2007 Oct;52(10):2646-52
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  • [Title] Synthetic serine protease inhibitor, gabexate mesilate, prevents nuclear factor-kappaB activation and increases TNF-alpha-mediated apoptosis in human pancreatic cancer cells.
  • Gabexate mesilate (GM), a synthetic serine protease inhibitor, suppresses nuclear factor-kappaB (NF-kappaB) activity in human monocytes or human umbilical vein endothelial cells (HUVECs).
  • In this study we examine whether GM also suppresses NF-kappaB activation and induces apoptosis in human pancreatic cancer cell lines.
  • The addition of tumor necrosis factor alpha (TNF-alpha) did not change the rates of growth of BxPC-3 and MIA PaCa-2.
  • However, in the presence of GM and TNF-alpha, proliferation decreased in a dose-dependent manner.
  • GM- and TNF-alpha-treated cells exhibited morphologic changes indicative of apoptosis, including chromatin condensation and nuclear fragmentation.
  • The NF-kappaB activity of both cell lines was increased by the addition of TNF-alpha, while TNF-alpha-induced NF-kappaB activity was suppressed by prestimulation with GM in a dose-dependent manner.
  • Caspase 3 and 7 activity was significantly increased by TNF-alpha with GM stimulation.
  • Furthermore, GM also suppressed the invasive potential of both cell lines.
  • These results indicate that GM inhibits TNF-alpha-induced NF-kappaB activation and enhances apoptosis in human pancreatic cancer cell lines.
  • [MeSH-major] Apoptosis / drug effects. Gabexate / pharmacology. NF-kappa B / drug effects. Pancreatic Neoplasms / drug therapy. Serine Proteinase Inhibitors / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Humans

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  • (PMID = 17357832.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Serine Proteinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 4V7M9137X9 / Gabexate
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33. Granata R, Settanni F, Gallo D, Trovato L, Biancone L, Cantaluppi V, Nano R, Annunziata M, Campiglia P, Arnoletti E, Ghè C, Volante M, Papotti M, Muccioli G, Ghigo E: Obestatin promotes survival of pancreatic beta-cells and human islets and induces expression of genes involved in the regulation of beta-cell mass and function. Diabetes; 2008 Apr;57(4):967-79
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  • [Title] Obestatin promotes survival of pancreatic beta-cells and human islets and induces expression of genes involved in the regulation of beta-cell mass and function.
  • We investigated obestatin effect on survival of beta-cells and human pancreatic islets and the underlying signaling pathways.
  • RESEARCH DESIGN AND METHODS: beta-Cells and human islets were used to assess obestatin effect on cell proliferation, survival, apoptosis, intracellular signaling, and gene expression.
  • RESULTS: Obestatin showed specific binding on HIT-T15 and INS-1E beta-cells, bound to glucagon-like peptide-1 receptor (GLP-1R), and recognized ghrelin binding sites.
  • Obestatin exerted proliferative, survival, and antiapoptotic effects under serum-deprived conditions and interferon-gamma/tumor necrosis factor-alpha/interleukin-1 beta treatment, particularly at pharmacological concentrations.
  • Ghrelin receptor antagonist [D-Lys(3)]-growth hormone releasing peptide-6 and anti-ghrelin antibody prevented obestatin-induced survival in beta-cells and human islets. beta-Cells and islet cells released obestatin, and addition of anti-obestatin antibody reduced their viability.
  • Obestatin increased beta-cell cAMP and activated extracellular signal-related kinase 1/2 (ERK1/2) and phosphatidylinositol 3-kinase (PI 3-kinase)/Akt; its antiapoptotic effect was blocked by inhibition of adenylyl cyclase/cAMP/protein kinase A (PKA), PI 3-kinase/Akt, and ERK1/2 signaling.
  • The GLP-1R antagonist exendin-(9-39) reduced obestatin effect on beta-cell survival.
  • In human islets, obestatin, whose immunoreactivity colocalized with that of ghrelin, promoted cell survival and blocked cytokine-induced apoptosis through cAMP increase and involvement of adenylyl cyclase/cAMP/PKA signaling.
  • 2) stimulated insulin secretion and gene expression; and 3) upregulated GLP-1R, IRS-2, pancreatic and duodenal homeobox-1, and glucokinase mRNA.
  • CONCLUSIONS: These results indicate that obestatin promotes beta-cell and human islet cell survival and stimulates the expression of main regulatory beta-cell genes, identifying a new role for this peptide within the endocrine pancreas.
  • [MeSH-major] Cell Survival / drug effects. Gene Expression Regulation / drug effects. Insulin-Secreting Cells / cytology. Islets of Langerhans / cytology. Peptide Hormones / pharmacology
  • [MeSH-minor] Caspase 3 / metabolism. Cell Culture Techniques. Cell Division / drug effects. Cell Membrane / drug effects. Cell Membrane / physiology. Cyclic AMP / metabolism. Ghrelin / secretion. Glucagon-Like Peptide 1 / secretion. Humans. Insulin Receptor Substrate Proteins. Intracellular Signaling Peptides and Proteins / drug effects. Intracellular Signaling Peptides and Proteins / metabolism. Phosphoproteins / drug effects. Phosphoproteins / metabolism


34. He J, Haskins K: Pathogenicity of T helper 2 T-cell clones from T-cell receptor transgenic non-obese diabetic mice is determined by tumour necrosis factor-alpha. Immunology; 2008 Jan;123(1):108-17
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  • [Title] Pathogenicity of T helper 2 T-cell clones from T-cell receptor transgenic non-obese diabetic mice is determined by tumour necrosis factor-alpha.
  • Although T cells producing Th2 cytokines are generally thought to counter a Th1 response, there have been reports of Th2 T-cell clones with pathogenic activity, including one previously reported by us in which the Th2 T-cell clone was derived from a T-cell receptor transgenic (TCR-Tg) mouse bearing pathogenic TCR.
  • In this study, our goal was to determine whether Th2 T-cell clones derived from a TCR-Tg in which the autoantigen was absent would be pathogenic and if so, to investigate possible mechanisms by which the Th2 T-cell clone could promote disease.
  • We found that a Th2 T-cell clone derived from the 6.9 TCR-Tg/non-obese diabetic (NOD).C6 mouse in which 6.9 T cells do not encounter autoantigen, produced Th2 cytokines but not interferon-gamma.
  • This Th2 T-cell clone, like the previous one we had isolated from the 2.5 TCR-Tg/NOD mouse, also turned out to be pathogenic.
  • Intracellular staining revealed that these Th2 T-cell clones produce low levels of tumour necrosis factor-alpha (TNF-alpha) in vitro, and after adoptive transfer, they migrate to the pancreas where they produce TNF-alpha as well as Th2 cytokines (interleukin (IL)-4, IL-10).
  • Induction of disease was prevented by administration of soluble TNF-alpha receptor to recipient mice, suggesting that the diabetogenicity of these Th2 T-cell clones is caused by their low level production of TNF-alpha.

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  • (PMID = 17983440.001).
  • [ISSN] 1365-2567
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK050561; United States / NIDDK NIH HHS / DK / R56 DK050561; United States / NIDDK NIH HHS / DK / R01DK50561
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Cytokines; 0 / Icos protein, mouse; 0 / Inducible T-Cell Co-Stimulator Protein; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Tumor Necrosis Factor; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide
  • [Other-IDs] NLM/ PMC2433281
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35. Chamson-Reig A, Arany EJ, Summers K, Hill DJ: A low protein diet in early life delays the onset of diabetes in the non-obese diabetic mouse. J Endocrinol; 2009 May;201(2):231-9
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  • Dietary insult in early life can affect the development and future function of the endocrine pancreas.
  • Serum insulin and pancreatic insulin content were reduced in LP-fed NOD offspring at 8 weeks, as were serum interferon gamma and pancreatic tumor necrosis factor alpha, while the number of pancreatic islets demonstrating peri-insulitis, and the degree of invasiveness were reduced.
  • To determine if LP caused early morphometric changes in the pancreas, we measured mean islet area at days 3 and 21.
  • Mean islet size did not differ with diet, but by 8 weeks of age LP-fed NOD females exhibited a significantly reduced islet number and mean islet area, and a lower fractional area of pancreas occupied by both alpha- and beta-cells than control-fed mice.
  • The mechanism is likely to involve both altered beta-cell morphology and function and changes in cytotoxic cytokines.

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  • (PMID = 19228796.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Insulin
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41. Cheshire H, Stather P, Vorster J: Acquired acrodermatitis enteropathica due to zinc deficiency in a patient with pre-existing Darier's disease. J Dermatol Case Rep; 2009 Nov 28;3(3):41-3
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  • [Title] Acquired acrodermatitis enteropathica due to zinc deficiency in a patient with pre-existing Darier's disease.
  • Typically these patches start near the body's orifices before migrating to other sites, however in this patient the presentation was atypical thus delaying the diagnosis.
  • OBSERVATIONS: We report a case of an atypical presentation of acrodermatitis enteropathica (AE) due to acquired zinc deficiency in a 65 year old female patient with a previous diagnosis of histologically confirmed Darier's disease.
  • Acrodermatitis enteropathica typically presents in infants, either due to an autosomal recessive genetic disorder, or after the cessation of breast feeding.
  • In adults acquired zinc deficiency can be caused by glucagonoma syndrome, poor nutritional state, intestinal malabsorption, nephrotic syndrome and after major trauma (i.e. burns or significant surgery).
  • In our patient low zinc levels confirmed hypozincaemia and the diagnosis of acrodermatitis enteropathica.
  • CONCLUSION: We believe this to be an unusual presentation of acrodermatitis enteropathica due to a probable dietary zinc deficiency in a lady with pre-existing Darier's disease which may possibly have influenced the uncharacteristic clinical presentation.

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  • (PMID = 21886729.001).
  • [ISSN] 1898-7249
  • [Journal-full-title] Journal of dermatological case reports
  • [ISO-abbreviation] J Dermatol Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Other-IDs] NLM/ PMC3157796
  • [Keywords] NOTNLM ; Darier's disease / acrodermatitis enteropathica / hair loss / mucous membranes / zinc
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42. Lewis RB, Lattin GE Jr, Paal E: Pancreatic endocrine tumors: radiologic-clinicopathologic correlation. Radiographics; 2010 Oct;30(6):1445-64
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  • [Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
  • Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.
  • They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and glucagonoma are the most common functioning PETs.
  • Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.
  • At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.
  • Cystic change, calcification, and necrosis are common in large tumors, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller tumors.
  • Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such tumors have a poor prognosis.
  • Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

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  • [Copyright] © RSNA, 2010.
  • (PMID = 21071369.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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43. Shi Y, Sahu RP, Srivastava SK: Triphala inhibits both in vitro and in vivo xenograft growth of pancreatic tumor cells by inducing apoptosis. BMC Cancer; 2008;8:294
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  • [Title] Triphala inhibits both in vitro and in vivo xenograft growth of pancreatic tumor cells by inducing apoptosis.
  • This study elucidates the molecular mechanism of Triphala against human pancreatic cancer in the cellular and in vivo model.
  • METHODS: Growth-inhibitory effects of Triphala were evaluated in Capan-2, BxPC-3 and HPDE-6 cells by Sulphoradamine-B assay.
  • Apoptosis was determined by cell death assay and western blotting.
  • Tumors were analyzed by immunohistochemistry and western blotting.
  • RESULTS: Exposure of Capan-2 cells to the aqueous extract of Triphala for 24 h resulted in the significant decrease in the survival of cells in a dose-dependent manner with an IC50 of about 50 microg/ml.
  • Triphala-mediated reduced cell survival correlated with induction of apoptosis, which was associated with reactive oxygen species (ROS) generation.
  • Triphala-induced apoptosis was linked with phosphorylation of p53 at Ser-15 and ERK at Thr-202/Tyr-204 in Capan-2 cells.
  • Above mentioned effects were significantly blocked when the cells were pretreated with an antioxidant N-acetylcysteine (NAC), suggesting the involvement of ROS generation.
  • Pretreatment of cells with pifithrin-alpha or U0126, specific inhibitors of p53 or MEK-1/2, significantly attenuated Triphala-induced apoptosis.
  • Similarly, Triphala induced apoptosis in another pancreatic cancer cell line BxPC-3 by activating ERK.
  • On the other hand, Triphala failed to induce apoptosis or activate ERK or p53 in normal human pancreatic ductal epithelial (HPDE-6) cells.
  • Further, oral administration of 50 mg/kg or 100 mg/kg Triphala in PBS, 5 days/week significantly suppressed the growth of Capan-2 pancreatic tumor-xenograft.
  • Reduced tumor-growth in Triphala fed mice was due to increased apoptosis in the tumors cells, which was associated with increased activation of p53 and ERK.
  • CONCLUSION: Our preclinical studies demonstrate that Triphala is effective in inhibiting the growth of human pancreatic cancer cells in both cellular and in vivo model.
  • Our data also suggests that the growth inhibitory effects of Triphala is mediated by the activation of ERK and p53 and shows potential for the treatment and/or prevention of human pancreatic cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Pancreatic Neoplasms / pathology. Plant Extracts / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. DNA Damage. Enzyme Activation. Enzyme-Linked Immunosorbent Assay. Extracellular Signal-Regulated MAP Kinases / genetics. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Immunohistochemistry. Mice. Neoplasm Transplantation. Pancreas / metabolism. Pancreas / pathology. Reactive Oxygen Species / metabolism. Transplantation, Heterologous. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18847491.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106953
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Plant Extracts; 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; 0 / triphala; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ PMC2576337
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44. Esposito I, Penzel R, Chaib-Harrireche M, Barcena U, Bergmann F, Riedl S, Kayed H, Giese N, Kleeff J, Friess H, Schirmacher P: Tenascin C and annexin II expression in the process of pancreatic carcinogenesis. J Pathol; 2006 Apr;208(5):673-85
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  • [Title] Tenascin C and annexin II expression in the process of pancreatic carcinogenesis.
  • Cell surface annexin II is a high-affinity receptor for large TNC splice variants.
  • The aim of this study was to analyse whether TNC and annexin II play a role in the development of pancreatic ductal adenocarcinoma (PDAC).
  • PDAC is characterized by a rich ECM populated by pancreatic stellate cells, which play a crucial role in pancreatic desmoplasia.
  • The mRNA and protein levels of TNC and of annexin II were analysed in pancreatic tissues by DNA array, quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) and immunohistochemistry.
  • TNC and annexin II mRNA levels were significantly higher in pancreatic cancer tissues than in the normal pancreas.
  • TNC expression was detected with increased frequency in the progression from PanIN-1 lesions to PDAC, and a parallel switch from cytoplasmic to cell surface expression of annexin II was observed.
  • Large TNC transcripts were found in pancreatic cancer and in chronic pancreatitis, but not in the normal pancreas.
  • TNC expression was demonstrated in pancreatic stellate cells, where it could be induced by tumour necrosis factor alpha (TNFalpha), transforming growth factor beta1 (TGF-beta1) and by cancer cell supernatants supplemented with TGF-beta1.
  • In conclusion, the expression of TNC and cell surface annexin II increases in the progression from low-grade PanIN lesions to pancreatic cancer.
  • Pancreatic stellate cells are identified as a source of TNC in pancreatic tissues, possibly under the influence of soluble factors released by the tumour cells.
  • [MeSH-major] Adenocarcinoma / metabolism. Annexin A2 / metabolism. Cell Transformation, Neoplastic / metabolism. Pancreatic Neoplasms / metabolism. Tenascin / metabolism
  • [MeSH-minor] Blotting, Western. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunoenzyme Techniques. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Pancreatitis, Chronic / metabolism. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Transforming Growth Factor beta / pharmacology. Transforming Growth Factor beta1. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16450333.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A2; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TGFB1 protein, human; 0 / Tenascin; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha
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45. Sanlioglu AD, Griffith TS, Omer A, Dirice E, Sari R, Altunbas HA, Balci MK, Sanlioglu S: Molecular mechanisms of death ligand-mediated immune modulation: a gene therapy model to prolong islet survival in type 1 diabetes. J Cell Biochem; 2008 Jun 1;104(3):710-20
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  • [Title] Molecular mechanisms of death ligand-mediated immune modulation: a gene therapy model to prolong islet survival in type 1 diabetes.
  • Type 1 diabetes results from the T cell-mediated destruction of pancreatic beta cells.
  • Islet transplantation has recently become a potential therapeutic approach for patients with type 1 diabetes.
  • However, islet-graft failure appears to be a challenging issue to overcome.
  • Thus, complementary gene therapy strategies are needed to improve the islet-graft survival following transplantation.
  • Immune modulation through gene therapy represents a novel way of attacking cytotoxic T cells targeting pancreatic islets.
  • The over-expression of TNF or FasL in pancreatic islets exacerbates the onset of type 1 diabetes generating lymphocyte infiltrates responsible for the inflammation.
  • Conversely, the lack of TRAIL expression results in higher degree of islet inflammation in the pancreas.
  • These results suggested that contrary to what was observed with TNF or FasL, adenovirus mediated TRAIL gene delivery into pancreatic islets is expected to be therapeutically beneficial in the setting of experimental models of type 1 diabetes.
  • [MeSH-minor] Adenoviridae / genetics. Adenoviridae / metabolism. Animals. Fas Ligand Protein / metabolism. Gene Transfer Techniques. Humans. Islets of Langerhans / cytology. Rats. T-Lymphocytes, Cytotoxic / metabolism. Treatment Outcome. Tumor Necrosis Factor-alpha / metabolism


46. Kerem M, Bedirli A, Pasaoglu H, Unsal C, Yilmaz TU, Ofluoglu E, Sahin TT: Role of ghrelin and leptin in predicting the severity of acute pancreatitis. Dig Dis Sci; 2007 Apr;52(4):950-5
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  • Ghrelin and leptin are the hormones that influence endocrine and exocrine functions of the pancreas and regulate feeding behaviors and energy metabolism.
  • After blood withdrawal, the pancreas was totally excised.
  • The levels of blood sugar, lipase, serum tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), ghrelin, and leptin were investigated and histopathologic examination was performed.
  • The levels of TNF-alpha and IL-1beta in the AEP and ANP groups reached the peak level at 24 hr and then decreased to a level close to that of the control group at 48 hr.
  • While TNF-alpha and IL-1beta can be used as a prognostic factor in the first 24 hr, ghrelin and leptin can be used subsequently.
  • [MeSH-major] Leptin / blood. Pancreatitis / diagnosis. Peptide Hormones / blood
  • [MeSH-minor] Acute Disease. Animals. Biomarkers / blood. Blood Glucose / analysis. Ghrelin. Interleukin-1beta / blood. Lipase / blood. Male. Pancreas / pathology. Pancreatitis, Acute Necrotizing / diagnosis. Prognosis. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 17333355.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Blood Glucose; 0 / Ghrelin; 0 / Interleukin-1beta; 0 / Leptin; 0 / Peptide Hormones; 0 / Tumor Necrosis Factor-alpha; EC 3.1.1.3 / Lipase
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47. Stehr SN, Heller AR: Omega-3 fatty acid effects on biochemical indices following cancer surgery. Clin Chim Acta; 2006 Nov;373(1-2):1-8
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  • Mechanisms accounting for these anti-tumor effects are reduced levels of PGE(2) and inducible NO synthase as well as an increased lipid peroxidation, or translation inhibition with subsequent cell cycle arrest.
  • Further, omega-3 eicosapentaenoic acid is capable of down-regulating the production and effect of a number of mediators of cachexia, such as IL-1, IL-6, TNF-alpha and proteolysis-inducing factor.
  • In patients undergoing tumor resection surgery we observed improvement of liver and pancreas biochemical indices when omega-3 fatty acids were administered.

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  • (PMID = 16796997.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Fatty Acids, Omega-3
  • [Number-of-references] 66
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48. Hoffmann AC, Mori R, Vallbohmer D, Brabender J, Klein E, Drebber U, Baldus SE, Cooc J, Azuma M, Metzger R, Hoelscher AH, Danenberg KD, Prenzel KL, Danenberg PV: High expression of HIF1a is a predictor of clinical outcome in patients with pancreatic ductal adenocarcinomas and correlated to PDGFA, VEGF, and bFGF. Neoplasia; 2008 Jul;10(7):674-9
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  • [Title] High expression of HIF1a is a predictor of clinical outcome in patients with pancreatic ductal adenocarcinomas and correlated to PDGFA, VEGF, and bFGF.
  • PURPOSE: Pancreatic cancer still has one of the worst prognoses in gastrointestinal cancers with a 5-year survival rate of 5%, making it necessary to find markers or gene sets that would further classify patients into different risk categories and thus allow more individually adapted multimodality treatment regimens.
  • EXPERIMENTAL DESIGN: Formalin-fixed paraffin-embedded tissue samples were obtained from 41 patients with pancreatic adenocarcinoma (age, 65; range, 34-85 years).
  • Tumor size, P = .04, and high HIF1a mRNA expression (cutoff, 75th percentile) had a significant impact on survival, P = .009 (overall model fit, P = .02).
  • High HIF1a expression had a sensitivity of 87.1% and a specificity of 55.6% for the diagnosis short (<6 months) versus long (6-60 months) survival.
  • CONCLUSIONS: Measuring PDGFA, bFGF, and HIF1a expression may contribute to a better understanding of the prognosis of patients with pancreatic cancer and may even play a crucial role for the distribution of patients to multimodal therapeutic regimens.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / diagnosis. Fibroblast Growth Factor 2 / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Pancreatic Neoplasms / diagnosis. Platelet-Derived Growth Factor / genetics. Vascular Endothelial Growth Factors / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Prognosis. Survival Analysis. Up-Regulation

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  • (PMID = 18592007.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Platelet-Derived Growth Factor; 0 / Vascular Endothelial Growth Factors; 0 / platelet-derived growth factor A; 103107-01-3 / Fibroblast Growth Factor 2
  • [Other-IDs] NLM/ PMC2435004
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49. 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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50. Ma RY, Tam TS, Suen AP, Yeung PM, Tsang SW, Chung SK, Thomas MK, Leung PS, Yao KM: Secreted PDZD2 exerts concentration-dependent effects on the proliferation of INS-1E cells. Int J Biochem Cell Biol; 2006;38(5-6):1015-22
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  • [Title] Secreted PDZD2 exerts concentration-dependent effects on the proliferation of INS-1E cells.
  • PDZD2 (PDZ domain containing 2) is a multi-PDZ protein expressed in pancreas and many other tissues.
  • To understand the possible functional role of PDZD2 in pancreas, we investigated the cellular distribution of PDZD2 in adult pancreas using an antiserum that recognizes both the full-length and secreted forms of PDZD2.
  • Immunohistochemical analysis revealed a strong expression of PDZD2 in pancreatic islet beta cells but not alpha cells.
  • Consistent with the beta-cell-enriched expression of PDZD2, immunoblot analysis indicated expression of both full-length PDZD2 and sPDZD2 in the insulinoma cell line INS-1E.
  • A recombinant sPDZD2 protein was synthesized for study of its functional effect on INS-1E cells.
  • In culture media with limiting serum, co-incubation with sPDZD2 stimulated the proliferation of INS-1E cells.
  • As a potential mitogen of beta-like cells, sPDZD2 may be useful for the optimization of beta-cell growth and differentiation in vitro.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adult. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Insulin-Secreting Cells / metabolism. Mitogens / pharmacology. Neoplasm Proteins. Pancreas / metabolism

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  • (PMID = 16413998.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Intracellular Signaling Peptides and Proteins; 0 / Mitogens; 0 / Neoplasm Proteins; 0 / PDZD2 protein, human
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51. Ralhan R, Desouza LV, Matta A, Tripathi SC, Ghanny S, Datta Gupta S, Bahadur S, Siu KW: Discovery and verification of head-and-neck cancer biomarkers by differential protein expression analysis using iTRAQ labeling, multidimensional liquid chromatography, and tandem mass spectrometry. Mol Cell Proteomics; 2008 06;7(6):1162-73
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  • Multidimensional LC-MS/MS has been used for the analysis of biological samples labeled with isobaric mass tags for relative and absolute quantitation (iTRAQ) to identify proteins that are differentially expressed in human head-and-neck squamous cell carcinomas (HNSCCs) in relation to non-cancerous head-and-neck tissues (controls) for cancer biomarker discovery.
  • Some of the proteins include stratifin (14-3-3sigma); YWHAZ (14-3-3zeta); three calcium-binding proteins of the S100 family, S100-A2, S100-A7 (psoriasin), and S100-A11 (calgizarrin); prothymosin alpha (PTHA); L-lactate dehydrogenase A chain; glutathione S-transferase Pi; APC-binding protein EB1; and fascin.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromatography, Liquid / methods. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Head and Neck Neoplasms / metabolism. Proteomics / methods. Tandem Mass Spectrometry / methods


52. Dourakis SP, Alexopoulou A, Georgousi KK, Delladetsima JK, Tolis G, Archimandritis AJ: Glucagonoma syndrome: survival 21 years with concurrent liver metastases. Am J Med Sci; 2007 Sep;334(3):225-7
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  • [Title] Glucagonoma syndrome: survival 21 years with concurrent liver metastases.
  • A patient who survived for 21 years since initial discovery of glucagonoma with concurrent liver metastases is described.
  • Psychiatric symptoms, weight loss, necrolytic migratory erythema, diarrhea, and diabetes mellitus developed gradually after diagnosis of the tumor.
  • The longevity of this patient may be related to the slow tumor growth expressed histologically by ischemic necrosis of the malignant cells and in imaging by extensive tumor calcifications, a very rare finding in this type of the tumor.
  • [MeSH-major] Glucagonoma / pathology. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology


53. Chow JY, Ban M, Wu HL, Nguyen F, Huang M, Chung H, Dong H, Carethers JM: TGF-beta downregulates PTEN via activation of NF-kappaB in pancreatic cancer cells. Am J Physiol Gastrointest Liver Physiol; 2010 Feb;298(2):G275-82
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  • [Title] TGF-beta downregulates PTEN via activation of NF-kappaB in pancreatic cancer cells.
  • TGF-beta utilizes receptor-activated SMAD signaling to mediate growth suppression; however, non-SMAD signaling that modulates the TGF-beta response in epithelial cells become apparent when the SMAD signaling is abrogated, a common occurrence in pancreatic cancers.
  • Here, we examined whether TGF-beta utilized NF-kappaB to downregulate PTEN, a gene that is rarely mutated in pancreatic cancers.
  • SMAD4-null BxPc3 and CAPAN-1 pancreatic cancer cells were treated with TGF-beta (10 ng/ml) and lysed, and cellular proteins were analyzed by Western blots using p-IkappaB, p65, and PTEN antibodies.
  • Dominant negative p-IkappaB-alpha-M (NF-kappaB superrepressor) was used to block activation of NF-kappaB.
  • Cell motility was assessed by Boyden chamber migration assay.
  • TGF-beta induced IkappaB-alpha phosphorylation followed by NF-kappaB p65 subunit nuclear translocation and increased NF-kappaB activity.
  • IkappaB-alpha-M blocked TGF-beta-induced NF-kappaB activity, reversed downregulated PTEN promoter activity and PTEN expression, and prevented augmentation of cell motility induced by TGF-beta.
  • Thus TGF-beta suppresses PTEN in pancreatic cancer cells through NF-kappaB activation and enhances cell motility and invasiveness in a SMAD4-independent manner that can be counteracted when TGF-beta-SMAD signaling is restored.
  • The TGF-beta/NF-kappaB/PTEN cascade may be a critical pathway for pancreatic cancer cells to proliferate and metastasize.

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  • (PMID = 19940030.001).
  • [ISSN] 1522-1547
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK067287; United States / NIDDK NIH HHS / DK / R01 DK067287-02; United States / NIDDK NIH HHS / DK / DK-067287; United States / NIDDK NIH HHS / DK / R24 DK080506; United States / NIDDK NIH HHS / DK / DK-073090; United States / NIDDK NIH HHS / DK / DK067287-02; United States / NIDDK NIH HHS / DK / R24 DK080506-01; United States / NIDDK NIH HHS / DK / DK-080506
  • [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 / I-kappa B Proteins; 0 / SMAD2 protein, human; 0 / SMAD3 protein, human; 0 / SMAD4 protein, human; 0 / Smad2 Protein; 0 / Smad3 Protein; 0 / Smad4 Protein; 0 / Transcription Factor RelA; 0 / Transforming Growth Factor beta; 139874-52-5 / NF-kappaB inhibitor alpha; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC3774494
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54. 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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55. Yubero S, Ramudo L, Manso MA, De Dios I: Targeting peripheral immune response reduces the severity of necrotizing acute pancreatitis. Crit Care Med; 2009 Jan;37(1):240-5
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  • INTERVENTIONS: Retrograde infusion of 3.5% of sodium taurocholate into pancreatic-biliary duct was used to induce AP in rats.
  • MEASUREMENTS AND MAIN RESULTS: Dx and NAC treatments reduced the severity of AP in terms of amylasemia, pancreatic edema, and pancreatic and liver necrosis.
  • Dx, administered before or after AP, and NAC reduced the leukocytosis induced by AP and blocked the ability of circulating monocytes to produce tumor necrosis factor-alpha and monocyte chemoattractant protein-1; however none of them significantly reduced the overexpression of intercellular cell adhesion molecule-1 found in monocytes 6 hrs after inducing AP.
  • Leukocyte infiltration in the pancreas was attenuated in Dx-pretreated rats and significantly reduced 6 hrs after inducing AP in rats treated with NAC.
  • CONCLUSIONS: Our data demonstrated that treatments targeting the peripheral immune response reduced the severity of sodium taurocholate -induced AP attenuating pancreatic and liver injury, but they were not effective for limiting the spread of the inflammatory damage to the lung.

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  • (PMID = 19050604.001).
  • [ISSN] 1530-0293
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 7S5I7G3JQL / Dexamethasone; WYQ7N0BPYC / Acetylcysteine
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56. Gibo J, Ito T, Kawabe K, Hisano T, Inoue M, Fujimori N, Oono T, Arita Y, Nawata H: Camostat mesilate attenuates pancreatic fibrosis via inhibition of monocytes and pancreatic stellate cells activity. Lab Invest; 2005 Jan;85(1):75-89
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  • [Title] Camostat mesilate attenuates pancreatic fibrosis via inhibition of monocytes and pancreatic stellate cells activity.
  • Our aim was to evaluate the therapeutic efficacy of CM in the experimental pancreatic fibrosis model induced by dibutyltin dichloride (DBTC), and we also determined the effect of CM on isolated monocytes and panceatic stellate cells (PSCs).
  • Thereafter, the effect of CM on monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) production from monocytes was examined.
  • In vivo, the oral administration of CM inhibited inflammation, cytokines expression and fibrosis in the pancreas.
  • The in vitro study revealed that CM inhibited both MCP-1 and TNF-alpha production from monocytes, and proliferation and MCP-1 production from PSCs.
  • These results suggest that CM attenuated DBTC-induced rat pancreatic fibrosis via inhibition of monocytes and PSCs activity.
  • [MeSH-major] Fibrosis / drug therapy. Gabexate / analogs & derivatives. Gabexate / therapeutic use. Monocytes / pathology. Pancreas / pathology. Pancreatitis / drug therapy. Protease Inhibitors / therapeutic use
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Chemokine CCL2 / genetics. Chemokine CCL2 / metabolism. Disease Models, Animal. Dose-Response Relationship, Drug. Male. Organotin Compounds / toxicity. Procollagen / genetics. Procollagen / metabolism. RNA, Messenger / metabolism. Rats. Rats, Inbred Lew. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 15531908.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccl2 protein, rat; 0 / Chemokine CCL2; 0 / Organotin Compounds; 0 / Procollagen; 0 / Protease Inhibitors; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0FD207WKDU / camostat; 4V7M9137X9 / Gabexate; J4AQN88R8P / dibutyldichlorotin
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57. Miao Q, Sun Y, Wei T, Zhao X, Zhao K, Yan L, Zhang X, Shu H, Yang F: Chymotrypsin B cached in rat liver lysosomes and involved in apoptotic regulation through a mitochondrial pathway. J Biol Chem; 2008 Mar 28;283(13):8218-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although it was long recognized as a digestive protease exclusively secreted by the exocrine pancreas, our data support that it also expresses and intracellularly resides in rat liver lysosomes.
  • Translocation of lysosomal chymotrypsin B into cytosol was triggered by apoptotic stimuli such as tumor necrosis factor-alpha, and intracellular delivery of chymotrypsin B protein induced apoptotic cell death with a potency comparable with cathepsin B, suggestive of a lysosomal-mitochondrial pathway to apoptosis regulated by chymotrypsin B following its release.
  • Noteworthily, either knockdown of chymotrypsin B expression by RNA interference or pretreatment with chymotrypsin B inhibitor N-p-tosyl-L-phenylalanine chloromethyl ketone significantly reduced tumor necrosis factor-alpha-induce apoptosis.
  • These results demonstrate for the first time that chymotrypsin B is not only restricted to the pancreas but can function intracellularly as a pro-apoptotic protease.
  • [MeSH-minor] Animals. Cell Line. Gene Expression Regulation, Enzymologic. Hepatocytes / enzymology. RNA, Messenger / genetics. Rats. Rats, Sprague-Dawley

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  • (PMID = 18211899.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.4.21.1 / Chymotrypsin; EC 3.4.21.1 / chymotrypsin B
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58. Gin VC, Zacharias M: Glucagonoma: anaesthetic management. Anaesth Intensive Care; 2009 Mar;37(2):329-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma: anaesthetic management.
  • [MeSH-major] Anesthesia, General / methods. Glucagonoma / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Blood Glucose / analysis. Female. Glucagon / blood. Humans. Middle Aged

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  • (PMID = 19400510.001).
  • [ISSN] 0310-057X
  • [Journal-full-title] Anaesthesia and intensive care
  • [ISO-abbreviation] Anaesth Intensive Care
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Blood Glucose; 9007-92-5 / Glucagon
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59. Büyükberber M, Savaş MC, Bağci C, Koruk M, Gülşen MT, Tutar E, Bilgiç T, Deveci R, Küçük C: The beneficial effect of propolis on cerulein-induced experimental acute pancreatitis in rats. Turk J Gastroenterol; 2009 Jun;20(2):122-8
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  • Serum amylase and lipase levels, white blood cell count and serum tumor necrosis factor-alpha levels were measured and pancreatic tissue was evaluated histologically.
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Disease Models, Animal. Edema. Lipase / blood. Male. Pancreas / drug effects. Pancreas / pathology. Rats. Rats, Wistar. Treatment Outcome

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  • (PMID = 19530045.001).
  • [ISSN] 2148-5607
  • [Journal-full-title] The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
  • [ISO-abbreviation] Turk J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Gastrointestinal Agents; 888Y08971B / Ceruletide; 9009-62-5 / Propolis; EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases
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60. Baker AF, Koh MY, Williams RR, James B, Wang H, Tate WR, Gallegos A, Von Hoff DD, Han H, Powis G: Identification of thioredoxin-interacting protein 1 as a hypoxia-inducible factor 1alpha-induced gene in pancreatic cancer. Pancreas; 2008 Mar;36(2):178-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of thioredoxin-interacting protein 1 as a hypoxia-inducible factor 1alpha-induced gene in pancreatic cancer.
  • OBJECTIVE: To investigate the expression of thioredoxin-interacting protein (TXNIP) during hypoxia and its dependency on hypoxia-inducible factor 1alpha (HIF-1alpha) in pancreatic cancer cell lines.
  • METHODS: MiaPaCa-2 pancreatic cancer cells were transiently transfected with siRNA to HIF-1alpha and TXNIP protein measured after growth in normoxia or hypoxia.
  • In addition, HIF-1alpha dependency was assessed by transiently transfecting MiaPaCa-2 pancreatic cancer cells with HIF-1alpha with a mutated oxygen degradation domain resulting in stable HIF-1alpha expression in normoxic conditions.
  • Panc-1 pancreatic cancer cells with low endogenous TXNIP expression were stably transfected with TXNIP, and cell survival and response to platinum cancer agents were tested.
  • Quantitative immunohistochemistry was utilized to measure the expression of TXNIP and thioredoxin 1 in human pancreatic cancer tissues.
  • RESULTS: Thioredoxin-interacting protein was induced during hypoxia in pancreatic cancer cells in a HIF-1alpha-dependent manner.
  • Overexpression of TXNIP in the Panc-1 cells resulted in a higher basal apoptosis and increased sensitivity to cisplatin and oxaliplatin.
  • A negative correlation was observed between TXNIP and thioredoxin 1 expression in human pancreatic cancer tissues.
  • CONCLUSIONS: Thioredoxin-interacting protein, a putative tumor suppressor gene, is induced in response to hypoxia in a HIF-1alpha-dependent manner in pancreatic cancer cells, resulting in increased apoptosis and increased sensitivity to platinum anticancer therapy.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Carrier Proteins / metabolism. Gene Expression Regulation, Neoplastic. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Apoptosis. Cell Hypoxia. Cell Line, Tumor. Cell Survival / drug effects. Cisplatin / pharmacology. Cisplatin / therapeutic use. Humans. Immunohistochemistry. Mutation. Organoplatinum Compounds / pharmacology. Organoplatinum Compounds / therapeutic use. RNA Interference. RNA, Small Interfering / metabolism. Thioredoxins / metabolism. Tissue Array Analysis. Transfection. Up-Regulation

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  • (PMID = 18376310.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA077204; United States / NCI NIH HHS / CA / CA109552; United States / NCI NIH HHS / CA / CA90821
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Organoplatinum Compounds; 0 / RNA, Small Interfering; 0 / TXN protein, human; 0 / TXNIP protein, human; 04ZR38536J / oxaliplatin; 52500-60-4 / Thioredoxins; Q20Q21Q62J / Cisplatin
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61. Sbarra V, Ristorcelli E, Petit-Thévenin JL, Teissedre PL, Lombardo D, Vérine A: In vitro polyphenol effects on activity, expression and secretion of pancreatic bile salt-dependent lipase. Biochim Biophys Acta; 2005 Sep 5;1736(1):67-76
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  • [Title] In vitro polyphenol effects on activity, expression and secretion of pancreatic bile salt-dependent lipase.
  • In the present in vitro studies, we have evaluated and compared the effects of resveratrol, an active compound of red wine, and of a whole red wine polyphenolic extract (RWE) on the pancreatic bile salt-dependent lipase (BSDL).
  • Resveratrol and RWE also impaired the secretion of BSDL by the rat pancreatic AR4-2J cells used as secreting model.
  • This effect is reversed by the removal of resveratrol or RWE from the cell culture medium.
  • Further, resveratrol (but not RWE) affects the transcription of the gene encoding BSDL and dramatically diminishes the quantity of the enzyme that is expressed and secreted by AR4-2J cells.
  • [MeSH-major] Flavonoids / physiology. Pancreas / enzymology. Sterol Esterase / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Phenols. Polyphenols. RNA, Messenger / metabolism. Rats. Stilbenes / pharmacology. Wine. alpha-Amylases / secretion

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  • (PMID = 16099206.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 0 / RNA, Messenger; 0 / Stilbenes; EC 3.1.1.- / bile salt-stimulated lipase; EC 3.1.1.13 / Sterol Esterase; EC 3.2.1.1 / alpha-Amylases; Q369O8926L / resveratrol
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62. Li YY, Li XJ, Lv S, Li K, Li YN, Gao ZR, Feng JY, Chen CJ, Schaefer C: Ascitic fluid and serum from rats with acute pancreatitis injure rat pancreatic tissues and alter the expression of heat shock protein 60. Cell Stress Chaperones; 2010 Sep;15(5):583-91
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  • [Title] Ascitic fluid and serum from rats with acute pancreatitis injure rat pancreatic tissues and alter the expression of heat shock protein 60.
  • After onset, extrapancreatic stimuli can induce the expression of cytokines in pancreatic acinar cells, thereby amplifying this inflammatory loop.
  • To further determine the role and mechanism of irritating agents in the pathogenesis of AP, rat pancreatic tissues were stimulated with ascitic fluid (APa) and serum (APs) from rats with AP or with lipopolysaccharide (LPS).
  • Rat pancreas was removed and meticulously snipped to fragments.
  • During this period, the tissue viability as well as amylase and TNF-alpha levels in the supernatant and the HSP60 expression in the pancreatic tissue before and after stimulation by APa, APs, and LPS were assayed time-dependently.
  • At different time-points during the culture, the viability and the amylase activity in the pancreatic tissue remained largely stable.
  • After stimulation with APa, APs, or LPS for 1 h, the pancreatic tissues showed some damage, and this was followed by a sharp decrease in the viability accompanied by increased levels of amylase and TNF-alpha in the culture medium 2 or 4 h after stimulation (p < 0.05).
  • APa, APs, or LPS induce injuries on isolated pancreatic tissues, accompanied by an altered HSP60 expression pattern in a time-dependent manner.
  • [MeSH-major] Ascitic Fluid / chemistry. Chaperonin 60 / metabolism. Pancreas / metabolism. Pancreatitis / blood. Pancreatitis / metabolism. Serum / chemistry
  • [MeSH-minor] Amylases / metabolism. Animals. Immunohistochemistry. In Vitro Techniques. Lipopolysaccharides / pharmacology. RNA, Messenger. Rats. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20146106.001).
  • [ISSN] 1466-1268
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chaperonin 60; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.2.1.- / Amylases
  • [Other-IDs] NLM/ PMC3006631
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63. 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


64. Izumi K, Ishikawa K, Tojigamori M, Matsui Y, Shiraishi N, Kitano S: Liver metastasis and ICAM-1 mRNA expression in the liver after carbon dioxide pneumoperitoneum in a murine model. Surg Endosc; 2005 Aug;19(8):1049-54
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  • Little is known about intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-(alpha) mRNA expression in the liver after CO2 pneumoperitoneum.
  • METHODS: Forty-five male BALB/c mice were randomly divided into three groups after intra-splenic tumor cell (colon 26) inoculation and the following procedures were performed: CO2 pneumoperitoneum (n = 15), open laparotomy (n = 15), and anesthesia alone (n = 15).
  • On day 7 after each procedure, the livers were excised and the number and diameter of the tumor nodules and the cancer index score were determined.
  • After each procedure, the livers were excised on days 0, 1, 3, and ICAM-1 and TNF-alpha mRNA expression were examined by real-time RT-PCR using SYBR Green I.
  • RESULTS: The number of tumor nodules and the cancer index score were larger in the CO2 pneumoperitoneum group than in the control group (p < 0.05).
  • The mean diameter of the tumor nodules was not different among the three groups.
  • The expression of ICAM-1 in the CO2 pneumoperitoneum group was higher than that in the other groups on day 1 (p < 0.05), and the TNF-alpha mRNA was higher than that in the control group on day 1 (p < 0.05).
  • [MeSH-minor] Animals. Disease Models, Animal. Male. Mice. Mice, Inbred BALB C

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  • (PMID = 15976944.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / RNA, Messenger; 126547-89-5 / Intercellular Adhesion Molecule-1; 142M471B3J / Carbon Dioxide
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65. 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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66. Prout TM, Taylor AJ: Case of the season: glucagonoma syndrome. Semin Roentgenol; 2005 Jan;40(1):4-7
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  • [Title] Case of the season: glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / radiography. Pancreatic Neoplasms / radiography
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged. Syndrome. Tomography, X-Ray Computed


67. Bai J, Sui J, Demirjian A, Vollmer CM Jr, Marasco W, Callery MP: Predominant Bcl-XL knockdown disables antiapoptotic mechanisms: tumor necrosis factor-related apoptosis-inducing ligand-based triple chemotherapy overcomes chemoresistance in pancreatic cancer cells in vitro. Cancer Res; 2005 Mar 15;65(6):2344-52
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  • [Title] Predominant Bcl-XL knockdown disables antiapoptotic mechanisms: tumor necrosis factor-related apoptosis-inducing ligand-based triple chemotherapy overcomes chemoresistance in pancreatic cancer cells in vitro.
  • Pancreatic cancer is lethal because of its invasiveness, rapid progression, and profound resistance to chemotherapy and radiation therapy.
  • To identify the molecular mechanisms underlying this, we have examined the expression and potency of three major death receptors: tumor necrosis factor receptor (TNF-R), TNF-related apoptosis-inducing ligand receptor (TRAIL-R), and Fas in mediating cytotoxicity in four invasive pancreatic cancer cell lines.
  • We have analyzed the expression of major antiapoptotic factors, cell cycle regulators and death receptor decoys (DcR) in comparison with normal pancreas tissues and five other human malignant tumor cell lines.
  • We have found that different pancreatic cancer cell lines coexpress high-level TRAIL-R, Fas, and TNF-R1 but are strongly resistant to apoptosis triggered by the death receptors.
  • DcR2 and DcR3 overexpression may partly contribute to the resistance of pancreatic cancer cells to TRAIL-R- and Fas-mediated cytotoxicity.
  • Bcl-XL and Bcl-2 are predominantly overexpressed in pancreatic cancer cell lines, respectively.
  • Bcl-XL is also predominantly overexpressed in prostate, colorectal, and intestinal cancer cells.
  • The knockdown of the predominant Bcl-XL overexpression significantly reduces the viability of pancreatic cancer cells to TNFalpha- and TRAIL-mediated apoptosis by sublethal-dose single and combined antitumor drugs, including geldanamycin, PS-341, Trichostatin A, and doxorubicine.
  • Bcl-XL plays a vital role in pancreatic cancer chemoresistance.
  • Geldanamycin, PS-341, and TRAIL triple combination may be a novel therapeutic strategy for pancreatic cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / physiology. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins c-bcl-2 / deficiency. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Apoptosis Regulatory Proteins. Benzoquinones. Boronic Acids / administration & dosage. Boronic Acids / pharmacology. Bortezomib. Cell Line, Tumor. Doxorubicin / administration & dosage. Doxorubicin / pharmacology. Drug Synergism. Gene Expression Regulation, Neoplastic. Gene Silencing. HSP90 Heat-Shock Proteins / metabolism. Humans. Hydroxamic Acids / administration & dosage. Hydroxamic Acids / pharmacology. Lactams, Macrocyclic. Membrane Glycoproteins. Pyrazines / administration & dosage. Pyrazines / pharmacology. Quinones / administration & dosage. Quinones / pharmacology. TNF-Related Apoptosis-Inducing Ligand. bcl-X Protein


68. Marogy G, De Man M, Verslype C: Necrolytic migratory erythaema and glucagonoma syndrome. Acta Clin Belg; 2009 Jan-Feb;64(1):70-1
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  • [Title] Necrolytic migratory erythaema and glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Glucagonoma / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Female. Humans. Middle Aged. Syndrome


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


70. Lin YY, Viterbo D, Mueller CM, Stanek AE, Smith-Norowitz T, Drew H, Wadgaonkar R, Zenilman ME, Bluth MH: Small-interference RNA gene knockdown of pancreatitis-associated proteins in rat acute pancreatitis. Pancreas; 2008 May;36(4):402-10
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  • METHODS: Pancreatitis-associated protein-specific siRNA was administered to AR42J cell cultures or rats induced with pancreatitis.
  • After 24 hours, cells and pancreata were harvested and assessed for PAP (PAP 1, PAP 2, PAP 3) gene expression and pancreatitis severity.
  • RESULTS: In vitro, PAP protein, and mRNA levels were reduced (PAP 1, 76%; PAP 2, 8%; PAP 3, 24%) in cells treated with PAP siRNA.
  • Serum amylase and lipase levels decreased (> or =50%) after administration of siRNA; interleukin (IL) 1beta, IL-4, and IL-6 increased, whereas C-reactive protein and tumor necrosis factor-alpha decreased when compared with vehicle control.

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  • (PMID = 18437087.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK054511-05; United States / NIDDK NIH HHS / DK / R01 DK054511-05
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / pancreatitis-associated protein; 5E090O0G3Z / Taurocholic Acid
  • [Other-IDs] NLM/ NIHMS109845; NLM/ PMC3151650
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71. 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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72. Neutzner M, Lopez T, Feng X, Bergmann-Leitner ES, Leitner WW, Udey MC: MFG-E8/lactadherin promotes tumor growth in an angiogenesis-dependent transgenic mouse model of multistage carcinogenesis. Cancer Res; 2007 Jul 15;67(14):6777-85
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  • [Title] MFG-E8/lactadherin promotes tumor growth in an angiogenesis-dependent transgenic mouse model of multistage carcinogenesis.
  • The relevance of angiogenesis in tumor biology and as a therapeutic target is well established.
  • MFG-E8 (also termed lactadherin) and developmental endothelial locus 1 (Del1) constitute a two-gene family of alpha(v)beta(3)/beta(5) ligands that regulate angiogenesis.
  • After detecting MFG-E8 mRNA in murine tumor cell lines, we sought to determine if MFG-E8 influenced tumorigenesis in Rip1-Tag2 transgenic mice, a cancer model in which angiogenesis is critical.
  • MFG-E8 mRNA and protein were increased in angiogenic islets and tumors in Rip1-Tag2 mice compared with normal pancreas.
  • Frequencies of angiogenic islets and tumor burdens were decreased in MFG-E8-deficient Rip1-Tag2 mice compared with those in control Rip1-Tag2 mice.
  • Invasive carcinomas were modestly underrepresented in MFG-E8-deficient mice, but tumor frequencies and survivals were comparable in these two strains.
  • Absence of MFG-E8 also led to decreases in tumor vascular permeability without obvious changes in vascular morphology.
  • Decreased proliferation was noted in angiogenic islets and increases in apoptotic cells were detected in islets and tumors.
  • Compensatory increases in mRNA encoding proangiogenic proteins, including FGF2, in angiogenic islets, and Del1, in angiogenic islets and tumors, were also detected in MFG-E8-deficient mice.
  • [MeSH-major] Antigens, Surface / genetics. Antigens, Surface / physiology. Cell Transformation, Neoplastic. Milk Proteins / genetics. Neovascularization, Pathologic
  • [MeSH-minor] Animals. Apoptosis. Cell Proliferation. Female. Fibroblast Growth Factor 2 / metabolism. GTPase-Activating Proteins / physiology. Male. Mice. Mice, Knockout. Mice, Transgenic. Pancreas / metabolism. RNA, Messenger / metabolism

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  • (PMID = 17638889.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / GTPase-Activating Proteins; 0 / Mfge8 protein, mouse; 0 / Milk Proteins; 0 / RNA, Messenger; 0 / Ralbp1 protein, mouse; 103107-01-3 / Fibroblast Growth Factor 2
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73. Hu HT, Ma QY, Zhang D, Shen SG, Han L, Ma YD, Li RF, Xie KP: HIF-1alpha links beta-adrenoceptor agonists and pancreatic cancer cells under normoxic condition. Acta Pharmacol Sin; 2010 Jan;31(1):102-10
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  • [Title] HIF-1alpha links beta-adrenoceptor agonists and pancreatic cancer cells under normoxic condition.
  • AIM: To examine whether beta-adrenoceptor (beta-AR) agonists can induce hypoxia-inducible factor (HIF)-1alpha accumulation which then up-regulate the expression of its target genes in pancreatic cancer cells at normoxia, and to further elucidate the mechanism involved.
  • METHODS: Pulse-chase assay, RT-PCR, and Western blot were employed to detect the effects of beta-AR agonists and antagonists, siRNA as well as several inhibitors of signal transduction pathways on MIA PaCa2 and BxPC-3 pancreatic cancer cells.
  • RESULTS: Treatment of pancreatic cancer cell lines with beta-AR agonists led to accumulation of HIF-1alpha and then up-regulated expression of its target genes independently of oxygen levels.
  • Our data suggest a novel mechanism in pancreatic cancer cells that links beta-AR and HIF-1alpha signaling under normoxic conditions, with implications for the control of glucose transport, angiogenesis and metastasis.
  • [MeSH-major] Adrenergic beta-Agonists / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / drug effects. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adrenergic beta-1 Receptor Agonists. Adrenergic beta-2 Receptor Agonists. Blotting, Western. Cell Line, Tumor. Cyclic AMP-Dependent Protein Kinases / metabolism. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. Receptor, Epidermal Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Up-Regulation / drug effects

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  • (PMID = 20037603.001).
  • [ISSN] 1745-7254
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic beta-1 Receptor Agonists; 0 / Adrenergic beta-2 Receptor Agonists; 0 / Adrenergic beta-Agonists; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Small Interfering; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ PMC4002695
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74. Wei D, Li J, Shen M, Jia W, Chen N, Chen T, Su D, Tian H, Zheng S, Dai Y, Zhao A: Cellular production of n-3 PUFAs and reduction of n-6-to-n-3 ratios in the pancreatic beta-cells and islets enhance insulin secretion and confer protection against cytokine-induced cell death. Diabetes; 2010 Feb;59(2):471-8
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  • [Title] Cellular production of n-3 PUFAs and reduction of n-6-to-n-3 ratios in the pancreatic beta-cells and islets enhance insulin secretion and confer protection against cytokine-induced cell death.
  • OBJECTIVE: To evaluate the direct impact of n-3 polyunsaturated fatty acids (n-3 PUFAs) on the functions and viability of pancreatic beta-cells.
  • RESEARCH DESIGN AND METHODS: We developed an mfat-1 transgenic mouse model in which endogenous production of n-3 PUFAs was achieved through overexpressing a C. elegans n-3 fatty acid desaturase gene, mfat-1.
  • The islets and INS-1 cells expressing mfat-1 were analyzed for insulin secretion and viability in response to cytokine treatment.
  • Insulin secretion stimulated by glucose, amino acids, and glucagon-like peptide-1 (GLP-1) was significantly elevated in the transgenic islets.
  • When challenged with tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and gamma-interferon (IFN-gamma), the transgenic islets completely resisted cytokine-induced cell death.
  • Adenoviral transduction of mfat-1 gene in wild-type islets and in INS-1 cells led to acute changes in the cellular levels of n-3- and n-6 PUFAs and recapitulated the results in the transgenic islets.
  • We further found that cytokine-induced activation of NF-kappaB and extracellular signal-related kinase 1/2 (ERK(1/2)) was significantly attenuated and that the expression of pancreatic duodenal hemeobox-1 (PDX-1), glucokinase, and insulin-1 was increased as a result of n-3 PUFA production.
  • CONCLUSIONS: Stable cellular production of n-3 PUFAs via mfat-1 can enhance insulin secretion and confers strong resistance to cytokine-induced beta-cell destruction.

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  • (PMID = 19933995.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK064383; United States / NIDDK NIH HHS / DK / 1R01DK064383-01
  • [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 / Caenorhabditis elegans Proteins; 0 / Cytokines; 0 / DNA Primers; 0 / DNA Probes; 0 / DNA, Complementary; 0 / Fatty Acids, Omega-3; 0 / Fatty Acids, Omega-6; 0 / Insulin; 0 / NF-kappa B; 0 / fat-1 protein, C elegans; 0RH81L854J / Glutamine; EC 1.14.19.- / Fatty Acid Desaturases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; GMW67QNF9C / Leucine
  • [Other-IDs] NLM/ PMC2809969
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75. 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
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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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76. Joo KR, Shin HP, Cha JM, Nam S, Huh Y: Effect of Korean red ginseng on superoxide dismutase inhibitor-induced pancreatitis in rats: a histopathologic and immunohistochemical study. Pancreas; 2009 Aug;38(6):661-6
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  • At week 7, all rats were killed, and pancreatic tissues were analyzed.
  • Tissues from the non-KRG-treated pancreatitis group exhibited marked pancreatic damage including changes in histological architecture, acinar cell necrosis and degeneration, and cytoplasmic vacuolization.
  • However, tissues from the KRG-treated pancreatitis group exhibited no cellular damage and had normal histological pancreatic architecture.
  • Immunohistochemical examination revealed that the expressions of nuclear factor kappaB, tumor necrosis factor alpha, inducible nitric oxide synthase, and the oxidant stress markers, malondialdehyde and 4-hydroxynonenal, were significantly decreased in the KRG-treated pancreatitis group as compared with the non-KRG-treated pancreatitis group.
  • [MeSH-minor] Animals. Antioxidants / pharmacology. Ditiocarb / toxicity. Enzyme Inhibitors / toxicity. Korea. Male. NF-kappa B / metabolism. Nitric Oxide Synthase Type II / metabolism. Oxidative Stress / drug effects. Peroxidase / metabolism. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19531970.001).
  • [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 / Antioxidants; 0 / Drugs, Chinese Herbal; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 99Z2744345 / Ditiocarb; EC 1.11.1.7 / Peroxidase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, rat; EC 1.15.1.1 / Superoxide Dismutase
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77. Zhang XP, Zhang L, Yang P, Zhang RP, Cheng QH: Protective effects of baicalin and octreotide on multiple organ injury in severe acute pancreatitis. Dig Dis Sci; 2008 Feb;53(2):581-91
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  • PURPOSE: To discuss the application value of Baicalin which is a new drug by comparing the protecting effects of Baicalin and Octreotide on multiple organs (pancreas, liver, kidney, and lung) in Severe acute pancreatitis (SAP).
  • METHODS: The improved Aho method was adopted to prepare SAP rat models via retrograde injection of 3.5% sodium taurocholate to the pancreatic duct.
  • (2) observation of the pathological changes of multiple organ samples fixed according to the relevant requirements after HE staining; and (3) serum content of amylase, NO, malonaldehyde (MDA), and tumor necrosis factor alpha (TNF-alpha). RESULTS:.
  • The gross pathological changes showed a similarity between the Octreotide and Baicalin treatment groups in terms of the pathological changes of pancreatic tissue.
  • in this regard there was no marked difference between the Baicalin and Octreotide treatment groups at different time points (P > 0.05). (5) The serum MDA contents of the Baicalin treatment group were significantly lower than those of the model group (P < 0.01), while in the Octreotide treatment group it was significantly less than the model group at 6 and 12 h (P < 0.05), and in the Baicalin treatment group was significantly less than in the Octreotide treatment group at 12 h (P < 0.05). (6) There was no marked difference among the model group, Baicalin treatment group and Octreotide treatment group in terms of serum TNF-alpha content at 3 h and 12 h (P > 0.05).
  • [MeSH-minor] Amylases / blood. Animals. Injections, Intravenous. Kidney / pathology. Liver / pathology. Lung / pathology. Male. Malondialdehyde / blood. Nitric Oxide. Pancreas / pathology. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17549629.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Flavonoids; 0 / Gastrointestinal Agents; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; 347Q89U4M5 / baicalin; 4Y8F71G49Q / Malondialdehyde; EC 3.2.1.- / Amylases; RWM8CCW8GP / Octreotide
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78. Cappello P, Tomaino B, Chiarle R, Ceruti P, Novarino A, Castagnoli C, Migliorini P, Perconti G, Giallongo A, Milella M, Monsurrò V, Barbi S, Scarpa A, Nisticò P, Giovarelli M, Novelli F: An integrated humoral and cellular response is elicited in pancreatic cancer by alpha-enolase, a novel pancreatic ductal adenocarcinoma-associated antigen. Int J Cancer; 2009 Aug 1;125(3):639-48
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  • [Title] An integrated humoral and cellular response is elicited in pancreatic cancer by alpha-enolase, a novel pancreatic ductal adenocarcinoma-associated antigen.
  • Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease with a very poor 5-year survival rate. alpha-Enolase is a glycolytic enzyme that also acts as a surface plasminogen receptor.
  • We find that it is overexpressed in PDAC and present on the cell surface of PDAC cell lines.
  • The clinical correlation of its expression with tumor status has been reported for lung and hepatocellular carcinoma.
  • We have previously demonstrated that sera from PDAC patients contain IgG autoantibodies to alpha-enolase.
  • The present work was intended to assess the ability of alpha-enolase to induce antigen-specific T cell responses.
  • We show that alpha-enolase-pulsed dendritic cells (DC) specifically stimulate healthy autologous T cells to proliferate, secrete IFN-gamma and lyse PDAC cells but not normal cells.
  • In vivo, alpha-enolase-specific T cells inhibited the growth of PDAC cells in immunodeficient mice.
  • In 8 out of 12 PDAC patients with circulating IgG to alpha-enolase, the existence of alpha-enolase-specific T cells was also demonstrated.
  • Taken as a whole, these results indicate that alpha-enolase elicits a PDAC-specific, integrated humoral and cellular response.
  • It is thus a promising and clinically relevant molecular target candidate for immunotherapeutic approaches as new adjuvants to conventional treatments in pancreatic cancer.
  • [MeSH-major] Antibodies, Neoplasm / immunology. Antigens, Neoplasm / immunology. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / immunology. Cell Proliferation. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / immunology. Phosphopyruvate Hydratase / metabolism. T-Lymphocytes
  • [MeSH-minor] Animals. Antibody Formation. Blotting, Western. Cell Line, Tumor. Dendritic Cells / immunology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunity, Cellular. Immunoglobulin G / blood. Immunohistochemistry. Interferon-gamma / secretion. Keratinocytes / immunology. Mice. Pancreas / enzymology. Pancreas / immunology. Skin / cytology. T-Lymphocytes, Cytotoxic / immunology. Up-Regulation

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  • (PMID = 19425054.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Immunoglobulin G; 82115-62-6 / Interferon-gamma; EC 4.2.1.11 / Phosphopyruvate Hydratase
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79. Zamora V, Cabanne A, Salanova R, Bestani C, Domenichini E, Marmissolle F, Giacomi N, O'Connor J, Méndez G, Roca E, Buenos Aires and La Plata Argentina Argentum Working Group: Immunohistochemical expression of somatostatin receptors in digestive endocrine tumours. Dig Liver Dis; 2010 Mar;42(3):220-5
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  • The somatostatin receptors types 1-5 expression in a series including 100 gastro-entero-pancreatic endocrine tumours were analysed.
  • METHODS: From a prospectively built database of patients with gastro-entero-pancreatic endocrine tumours referred from three institutions, 100 cases with clinical and pathological data were selected.
  • Somatostatin receptors expression by immunohistochemistry with somatostatin receptor types 1-5 antibodies in tissue paraffin sections were studied and correlated with the histological diagnosis according to the WHO classification, location and functional status.
  • RESULTS: Of the 100 cases, 67 were gastrointestinal tumours, 25 pancreatic and 8 liver metastasis of unknown origin.
  • Thirty-one of them were functioning tumours: 2 insulinomas, 5 gastrinomas, 1 glucagonoma and 23 carcinoids.
  • Somatostatin receptors expression was less frequent in pancreatic than in gastrointestinal tumours.
  • CONCLUSIONS: Immunohistochemistry revealed that somatostatin receptors were highly expressed in both primary and metastatic gastro-entero-pancreatic endocrine tumours with heterogeneous staining distribution.
  • It proved to be a reliable technique even in small tumour samples.

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  • [Copyright] 2009 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
  • [CommentIn] Dig Liver Dis. 2010 Mar;42(3):173-4 [20117969.001]
  • (PMID = 19819769.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Somatostatin
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80. 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
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  • [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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81. Zhou C, Dhall D, Nissen NN, Chen CR, Yu R: Homozygous P86S mutation of the human glucagon receptor is associated with hyperglucagonemia, alpha cell hyperplasia, and islet cell tumor. Pancreas; 2009 Nov;38(8):941-6
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  • [Title] Homozygous P86S mutation of the human glucagon receptor is associated with hyperglucagonemia, alpha cell hyperplasia, and islet cell tumor.
  • OBJECTIVE: The goal of the study was to investigate the genetic and molecular basis of a novel syndrome of marked hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.
  • METHODS: The glucagon receptor (GCGR) gene and the glucagon gene were sequenced in a patient with hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.
  • RESULTS: The glucagon gene sequence was normal, but the GCGR sequencing uncovered a homozygous missense mutation, c.256C>T, p.P86S in the extracellular domain of GCGR.
  • When expressed in human embryonic kidney 293 cells, GCGR P86S localized to the plasma membrane but bound 96% less radiolabeled glucagon than WT GCGR.
  • The median effective concentration of glucagon-induced cyclic adenosine monophosphate production was 24 nmol/L for GCGR P86S but 2.4 nmol/L for WT GCGR.
  • The patient's alpha cells also express glucagonlike peptide 1 and pancreatic polypeptide.
  • CONCLUSIONS: We hereby report the first homozygous missense mutation in the human GCGR, which is associated with alpha cell hyperplasia and hyperglucagonemia.
  • This mutation lowers the receptor's affinity to glucagon and decreases cyclic adenosine monophosphate production with physiological concentrations of glucagon.
  • Thus, the P86S mutation in GCGR likely causes alpha cell hyperplasia and hyperglucagonemia.

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  • (PMID = 19657311.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK071870-04; United States / NIDDK NIH HHS / DK / K08 DK071870; United States / NIDDK NIH HHS / DK / DK071870; United States / NIDDK NIH HHS / DK / K08 DK071870-04
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Glucagon; 147336-22-9 / Green Fluorescent Proteins; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ NIHMS139678; NLM/ PMC2767399
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82. Krause W: Skin diseases in consequence of endocrine alterations. Aging Male; 2006 Jun;9(2):81-95
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  • There, knowledge of skin alterations is important not only for dermatologists, but also for endocrinologists and other physicians, because a clinical diagnosis of the underlying disease is often possible.
  • These include acanthosis nigricans, diseases due to alterations of androgen metabolism, carcinoid syndrome, diseases due to alterations of corticosteroid metabolism, diseases in association with diabetes mellitus, diseases due to alterations of estrogen metabolism, genetic syndromes including dermatological and endocrine symptoms, the glucagonoma syndrome, diseases due to dysfunctions of growth hormone secretion, diseases in association with Merkel cells of the skin, diseases due to dysfunctions of the thyroid gland, diseases to alteration of vitamin D metabolism, and vitiligo and disorders of pigmentation.
  • [MeSH-minor] Androgens / deficiency. Androgens / secretion. Estrogens / deficiency. Estrogens / secretion. Glucagonoma / etiology. Malignant Carcinoid Syndrome / etiology. Thyroid Hormones / deficiency. Thyroid Hormones / secretion. Vitamin D / secretion. Vitiligo / etiology