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81. Ostermann E, Garin-Chesa P, Heider KH, Kalat M, Lamche H, Puri C, Kerjaschki D, Rettig WJ, Adolf GR: Effective immunoconjugate therapy in cancer models targeting a serine protease of tumor fibroblasts. Clin Cancer Res; 2008 Jul 15;14(14):4584-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effective immunoconjugate therapy in cancer models targeting a serine protease of tumor fibroblasts.
  • PURPOSE: Invasion and metastasis of malignant epithelial cells into normal tissues is accompanied by adaptive changes in the mesenchyme-derived supporting stroma of the target organs.
  • Altered gene expression in these nontransformed stromal cells provides potential targets for therapy.
  • The present study was undertaken to determine the antitumor effects of an antibody-conjugate against fibroblast activation protein-alpha, a cell surface protease of activated tumor fibroblasts.
  • EXPERIMENTAL DESIGN: A novel antibody-maytansinoid conjugate, monoclonal antibody (mAb) FAP5-DM1, was developed to target a shared epitope of human, mouse, and cynomolgus monkey fibroblast activation protein-alpha, enabling preclinical efficacy and tolerability assessments.
  • RESULTS: Treatment with mAb FAP5-DM1 induced long-lasting inhibition of tumor growth and complete regressions in xenograft models of lung, pancreas, and head and neck cancers with no signs of intolerability.
  • Analysis of chemically distinct conjugates, resistance models, and biomarkers implicates a unique mode of action, with mitotic arrest and apoptosis of malignant epithelial cells coupled to disruption of fibroblastic and vascular structures.
  • CONCLUSIONS: We show that mAb FAP5-DM1 combines excellent efficacy and tolerability and provides a first assessment of the mode of action of a novel drug candidate for tumor stroma targeting, thus encouraging further development toward clinical testing of this treatment paradigm.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Biomarkers, Tumor / immunology. Fibroblasts / immunology. Immunoconjugates / therapeutic use. Immunotherapy / methods. Neoplasms / therapy. Serine Endopeptidases / immunology

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  • (PMID = 18628473.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Immunoconjugates; 0 / Membrane Proteins; 14083FR882 / Maytansine; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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82. 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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83. 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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8
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4. 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


85. 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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86. Armanet M, Wojtusciszyn A, Morel P, Parnaud G, Rousselle P, Sinigaglia C, Berney T, Bosco D: Regulated laminin-332 expression in human islets of Langerhans. FASEB J; 2009 Dec;23(12):4046-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Laminin-332 (LN-332) is a basement membrane component known to exert a beneficial effect on rat pancreatic beta cells in vitro.
  • By immunofluorescence on pancreas sections, we observed that labeling was confined to endocrine cells in islets.
  • Confocal microscopy analysis on isolated islet cells revealed that labeling was granular but did not colocalize with hormone secretory granules.
  • No effect was observed with tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma.
  • These results show that LN-332, known to have some beneficial effect on beta cells in vitro, is produced and secreted by endocrine islet cells and is up-regulated by stressing conditions such as culture and IL-1beta-exposure.
  • [MeSH-major] Cell Adhesion Molecules / genetics. Cell Adhesion Molecules / metabolism. Gene Expression Regulation / physiology. Islets of Langerhans / metabolism
  • [MeSH-minor] Cells, Cultured. Cytokines / pharmacology. Glucagon / pharmacology. Humans. Insulin / pharmacology. Phosphatidylinositol 3-Kinases / metabolism. Protein Subunits. Signal Transduction

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  • (PMID = 19667121.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / Insulin; 0 / Protein Subunits; 0 / kalinin; 9007-92-5 / Glucagon; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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87. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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88. Wan X, Shen N, Mendoza A, Khanna C, Helman LJ: CCI-779 inhibits rhabdomyosarcoma xenograft growth by an antiangiogenic mechanism linked to the targeting of mTOR/Hif-1alpha/VEGF signaling. Neoplasia; 2006 May;8(5):394-401
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  • Angiogenesis is one of the critical steps in tumor growth and metastasis.
  • The goal of this study was to evaluate whether the antitumor activity of CCI-779 is related to antiangiogenic effects in vivo in tumors of mice bearing human rhabdomyosarcoma (RMS) xenografts.
  • Based on these data, an intermittent treatment schedule (every 3 days for 30 days) was chosen and displayed a significant suppression of both tumor growth and mTOR signaling.

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  • (PMID = 16790088.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [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 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1592447
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89. 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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90. 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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91. Krause W: Skin diseases in consequence of endocrine alterations. Aging Male; 2006 Jun;9(2):81-95
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  • There, knowledge of skin alterations is important not only for dermatologists, but also for endocrinologists and other physicians, because a clinical diagnosis of the underlying disease is often possible.
  • These include acanthosis nigricans, diseases due to alterations of androgen metabolism, carcinoid syndrome, diseases due to alterations of corticosteroid metabolism, diseases in association with diabetes mellitus, diseases due to alterations of estrogen metabolism, genetic syndromes including dermatological and endocrine symptoms, the glucagonoma syndrome, diseases due to dysfunctions of growth hormone secretion, diseases in association with Merkel cells of the skin, diseases due to dysfunctions of the thyroid gland, diseases to alteration of vitamin D metabolism, and vitiligo and disorders of pigmentation.
  • [MeSH-minor] Androgens / deficiency. Androgens / secretion. Estrogens / deficiency. Estrogens / secretion. Glucagonoma / etiology. Malignant Carcinoid Syndrome / etiology. Thyroid Hormones / deficiency. Thyroid Hormones / secretion. Vitamin D / secretion. Vitiligo / etiology

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  • (PMID = 16916743.001).
  • [ISSN] 1368-5538
  • [Journal-full-title] The aging male : the official journal of the International Society for the Study of the Aging Male
  • [ISO-abbreviation] Aging Male
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Thyroid Hormones; 1406-16-2 / Vitamin D
  • [Number-of-references] 71
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92. Davies K, Conlon KC: Neuroendocrine tumors of the pancreas. Curr Gastroenterol Rep; 2009 Apr;11(2):119-27
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  • [Title] Neuroendocrine tumors of the pancreas.
  • Pancreatic endocrine tumors are rare neoplasms accounting for less than 5% of pancreatic malignancies.
  • They are broadly classified into either functioning tumors (insulinomas, gastrinomas, glucagonomas, VIPomas, and somatostatinomas) or nonfunctioning tumors.
  • The diagnosis of these tumors is difficult and requires a careful history and examination combined with laboratory tests and radiologic imaging.
  • Signs and symptoms are usually related to hormone hypersecretion in the case of functioning tumors and to tumor size or metastases with nonfunctioning tumors.
  • Surgical resection remains the treatment of choice even in the face of metastatic disease.
  • Further development of novel diagnostic and treatment modalities offers potential to greatly improve quality of life and prolong disease-free survival for patients with pancreatic endocrine tumors.
  • [MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms
  • [MeSH-minor] Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Catheter Ablation. Chemoembolization, Therapeutic / methods. Evidence-Based Medicine. Gastrins / secretion. Glucagon / secretion. Humans. Insulin / secretion. Quality of Life. Somatostatin / secretion. Survival Analysis. Treatment Outcome

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  • (PMID = 19281699.001).
  • [ISSN] 1534-312X
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins; 0 / Insulin; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon
  • [Number-of-references] 44
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93. Hong J, Abudula R, Chen J, Jeppesen PB, Dyrskog SE, Xiao J, Colombo M, Hermansen K: The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro. Metabolism; 2005 Oct;54(10):1329-36
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  • [Title] The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro.
  • The influence of fatty acids on beta cell function has been well established whereas little is known about the role of fatty acids on alpha cell function.
  • The aim of our study was to investigate the short-term effects of chain length, spatial configuration, and degree of unsaturation of fatty acids on glucagon secretion from isolated mouse islets and alpha tumor cell 1 clone 6 cells (alpha TC1-6 cells).
  • Glucagon release was measured with different saturated and unsaturated fatty acids as well as cis and trans isomers of fatty acids at low and high glucose.
  • Palmitate (0.1-0.5 mmol/L) immediately stimulated glucagon release in a dose-dependent manner from both isolated islets and alpha TC 1-6 cells.
  • The longer chain length of saturated fatty acids, the higher glucagon responses were obtained.
  • The average fold increase in glucagon to saturated fatty acids (0.3 mmol/L) compared to control was octanoate 1.5, laurate 2.0, myristate 2.9, palmitate 5.4, and stearate 6.2, respectively.
  • Saturated fatty acids were more effective than unsaturated fatty acids in stimulating glucagon secretion.
  • Fatty acids immediately stimulate glucagon secretion from isolated mouse islets pancreatic alpha cells.
  • [MeSH-major] Fatty Acids / pharmacology. Glucagon / secretion

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  • (PMID = 16154432.001).
  • [ISSN] 0026-0495
  • [Journal-full-title] Metabolism: clinical and experimental
  • [ISO-abbreviation] Metab. Clin. Exp.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids; 0 / Insulin; 9007-92-5 / Glucagon
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94. 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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95. 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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96. 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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97. Igaz P: MEN1 clinical background. Adv Exp Med Biol; 2009;668:1-15
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  • Multiple endocrine neoplasia Type 1 (MEN1) is a rare hereditary tumor syndrome predisposing to tumor development in several endocrine organs.
  • Its major manifestations include hyperparathyroidism, tumors of endocrine pancreas and pituitary.
  • Beside these three, several other endocrine (adrenocortical, foregut carcinoid) and nonendocrine (lipoma, angiofibroma, collagenoma, ependymoma, meningioma) tumors have been described to be associated with this syndrome.
  • Both familial and sporadic forms of the disease are known.
  • The diagnosis of MEN1 can be established if two of the three major manifestations are found in the same patient, whereas the diagnosis of familial MEN1 requires one MEN1 patient and a first degree relative with at least one MEN1 manifestation.
  • Both benign (parathyroid, anterior pituitary) and malignant (gastrinoma, glucagonoma) lesions may develop in MEN1 patients.
  • Regular surveillance of MEN1 gene mutation carriers is necessary to reveal disease manifestations.
  • Several diagnostic modalities can be used to screen for and to examine MEN1-related tumors.
  • The therapy of MEN1-associated tumors requires specific approach in some cases, as multiple tumors and recurrence is frequently observed.
  • [MeSH-minor] Adult. Child. Child, Preschool. Diagnosis, Differential. Genetic Predisposition to Disease. Genetic Testing. Humans. Middle Aged. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2a / pathology. Multiple Endocrine Neoplasia Type 2a / physiopathology. Mutation. Young Adult

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  • (PMID = 20175448.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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98. Li YH, Huang ZW, Xue P, Guo J, He FQ, You Z, Wang ZR: [Effects of Chaiqin Chengqi Decoction on activation of nuclear factor-kappaB in pancreas of rats with acute necrotizing pancreatitis]. Zhong Xi Yi Jie He Xue Bao; 2008 Feb;6(2):180-4
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  • [Title] [Effects of Chaiqin Chengqi Decoction on activation of nuclear factor-kappaB in pancreas of rats with acute necrotizing pancreatitis].
  • Blood sample was collected from abdominal vein for examination and the pancreatic tissue samples were taken for making pathology section 6 hours later.
  • The pancreatic tissue (HE staining) was observed by light microscope.
  • The content of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) was detected with the method of enzyme-linked immunosorbent assay, and the activation of nuclear factor-kappaB (NF-kappaB) in pancreas was detected by immunohistochemical method.
  • RESULTS: Compared with the SO group, there was dramatic increase in the white blood cell (WBC) counts and AMY level in the ANP group (P<0.05, P<0.01).
  • The integral optical density of NF-kappaB p65 positive cells of pancreas in CQCQD-treated group was lower than that in the ANP group (P<0.05).
  • CONCLUSION: CQCQD can reduce the content of serum TNF-alpha and IL-6, depress the activation of NF-kappaB, and lessen the pancreatic lesions.
  • [MeSH-major] Drugs, Chinese Herbal / therapeutic use. NF-kappa B / metabolism. Pancreas / metabolism. Pancreatitis, Acute Necrotizing / drug therapy. Phytotherapy
  • [MeSH-minor] Animals. Female. Interleukin-6 / blood. Male. Random Allocation. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 18241655.001).
  • [ISSN] 1672-1977
  • [Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
  • [ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Chai Qin Cheng Qi decoction; 0 / Drugs, Chinese Herbal; 0 / Interleukin-6; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha
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99. Shen HC, Adem A, Ylaya K, Wilson A, He M, Lorang D, Hewitt SM, Pechhold K, Harlan DM, Lubensky IA, Schmidt LS, Linehan WM, Libutti SK: Deciphering von Hippel-Lindau (VHL/Vhl)-associated pancreatic manifestations by inactivating Vhl in specific pancreatic cell populations. PLoS One; 2009;4(4):e4897
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  • [Title] Deciphering von Hippel-Lindau (VHL/Vhl)-associated pancreatic manifestations by inactivating Vhl in specific pancreatic cell populations.
  • The von Hippel-Lindau (VHL) syndrome is a pleomorphic familial disease characterized by the development of highly vascularized tumors, such as hemangioblastomas of the central nervous system, pheochromocytomas, renal cell carcinomas, cysts and neuroendocrine tumors of the pancreas.
  • Up to 75% of VHL patients are affected by VHL-associated pancreatic lesions; however, very few reports in the published literature have described the cellular origins and biological roles of VHL in the pancreas.
  • Since homozygous loss of Vhl in mice resulted in embryonic lethality, this study aimed to characterize the functional significance of VHL in the pancreas by conditionally inactivating Vhl utilizing the Cre/LoxP system.
  • Specifically, Vhl was inactivated in different pancreatic cell populations distinguished by their roles during embryonic organ development and their endocrine lineage commitment.
  • With Cre recombinase expression directed by a glucagon promoter in alpha-cells or an insulin promoter in beta-cells, we showed that deletion of Vhl is dispensable for normal functions of the endocrine pancreas.
  • In addition, deficiency of VHL protein (pVHL) in terminally differentiated alpha-cells or beta-cells is insufficient to induce pancreatic neuroendocrine tumorigenesis.
  • Most significantly, we presented the first mouse model of VHL-associated pancreatic disease in mice lacking pVHL utilizing Pdx1-Cre transgenic mice to inactivate Vhl in pancreatic progenitor cells.
  • The highly vascularized microcystic adenomas and hyperplastic islets that developed in Pdx1-Cre;Vhl f/f homozygous mice exhibited clinical features similar to VHL patients.
  • Establishment of three different, cell-specific Vhl knockouts in the pancreas have allowed us to provide evidence suggesting that VHL is functionally important for postnatal ductal and exocrine pancreas, and that VHL-associated pancreatic lesions are likely to originate from progenitor cells, not mature endocrine cells.
  • The novel model systems reported here will provide the basis for further functional and genetic studies to define molecular mechanisms involved in VHL-associated pancreatic diseases.

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  • (PMID = 19340311.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / PHS HHS / / HHSN 261200800001E; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Other-IDs] NLM/ PMC2660574
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100. Maksan SM, Schmidt E, Ryschich E, Harms W, Schmidt J: Enhancement of leukocyte adhesion after percutaneous irradiation in rats with hepatocellular carcinoma. World J Gastroenterol; 2005 Apr 7;11(13):1991-4
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  • RESULTS: LEI was significantly reduced in tumor tissue.
  • However, irradiation of liver sinusoids and tumor tissue with 6 Gy led to a significant activation of leukocyte adhesion in the tumor with a marked increase of the proinflammatory cytokine TNF-alpha.
  • CONCLUSION: The findings indicate that the immunological tumor-endothelial barrier can be overcome by external irradiation.
  • [MeSH-major] Carcinoma, Hepatocellular / radiotherapy. Cell Adhesion / radiation effects. Leukocytes / radiation effects. Liver Neoplasms, Experimental / radiotherapy. Radiotherapy / methods
  • [MeSH-minor] Animals. Cell Movement / immunology. Cell Movement / radiation effects. Disease Models, Animal. Male. Rats. Rats, Inbred ACI

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  • (PMID = 15800992.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC4305723
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