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6. Maher JC, Savaraj N, Priebe W, Liu H, Lampidis TJ: Differential sensitivity to 2-deoxy-D-glucose between two pancreatic cell lines correlates with GLUT-1 expression. Pancreas; 2005 Mar;30(2):e34-9
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  • [Title] Differential sensitivity to 2-deoxy-D-glucose between two pancreatic cell lines correlates with GLUT-1 expression.
  • OBJECTIVES: To determine whether the differential growth inhibition of pancreatic tumor cells to the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) correlates with uptake, expression of GLUT-1 transporter, and levels of hypoxic-inducible factor-1alpha.
  • METHODS: Growth inhibition assays with 2-DG, lactic acid analysis, Western blots of GLUT-1, and hypoxic-inducible factor-1alpha were correlated with each other and with uptake and accumulation of radio-labeled 2-DG in 2 pancreatic cell lines.
  • RESULTS: Under normal oxygen tension, we find that the pancreatic cell line MIA PaCa2 (1420) is 7 times more sensitive to 2-DG and equally sensitive to oxamate, as compared with Panc-1 (1469).
  • Lactate levels in both cell types are similarly low, indicating that mitochondria are functioning normally in these cells and that they are not solely dependent on glycolysis for survival under an aerobic microenvironment.
  • Since oxamate does not use glucose transporters for entry into the cell, the equal sensitivity to this drug suggests that the selective growth inhibition of 2-DG in these 2 cell types might be reflective of differential expression of glucose transporters.
  • Indeed, we find that GLUT-1 is more highly expressed in 1420 and that this cell line accumulates 2-DG twice as much as 1469.
  • Additionally, hypoxic-inducible factor, which is known to upregulate the expression of GLUT-1, is found at equally low levels in both cell types.
  • CONCLUSION: Overall, our results suggest that certain pancreatic tumors may be inherently sensitive to 2-DG, even under normal oxygen tension, due to greater intracellular accumulation of this inhibitor.
  • Moreover, if 2-DG shows clinical efficacy, it may be possible to predict which pancreatic tumors would be sensitive to this agent based on their GLUT-1 expression profile and their increased uptake of 2-fluoro-deoxy-D-glucose currently used to image tumors via PET scanning.
  • [MeSH-major] Antimetabolites / pharmacokinetics. Deoxyglucose / pharmacokinetics. Excitatory Amino Acid Transporter 2 / metabolism. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Line, Tumor. Drug Resistance, Neoplasm. Glycolysis / drug effects. Glycolysis / physiology. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Lactic Acid / metabolism. Mitochondria / metabolism

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  • (PMID = 15714127.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA37109
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites; 0 / Biomarkers, Tumor; 0 / Excitatory Amino Acid Transporter 2; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 33X04XA5AT / Lactic Acid; 9G2MP84A8W / Deoxyglucose
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7. Uchida Y, Freitas MC, Zhao D, Busuttil RW, Kupiec-Weglinski JW: The protective function of neutrophil elastase inhibitor in liver ischemia/reperfusion injury. Transplantation; 2010 May 15;89(9):1050-6
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  • The expression of proinflammatory cytokines (tumor necrosis factor-alpha and interleukin-6), chemokines (CXCL-1, CXCL-2, and CXCL-10), and toll-like receptor 4 was significantly reduced in the treatment group, along with diminished apoptosis through caspase-3 pathway.
  • Moreover, in vitro studies confirmed downregulation of proinflammatory cytokine and chemokine programs in mouse macrophage cell cultures, along with depression of innate toll-like receptor 4 signaling.
  • CONCLUSION.: Sivelestat-mediated NE inhibition may represent an effective therapeutic option in liver transplantation and other inflammation disease states.

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  • (PMID = 20160675.001).
  • [ISSN] 1534-6080
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI023847; United States / NIAID NIH HHS / AI / R21 AI023847; United States / NIAID NIH HHS / AI / AI42223; United States / NIAID NIH HHS / AI / AI23847; United States / NIAID NIH HHS / AI / R01 AI042223; United States / NIAID NIH HHS / AI / R56 AI023847; United States / NIDDK NIH HHS / DK / R01 DK062357
  • [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 CXCL1; 0 / Cxcl1 protein, mouse; 0 / DNA Primers; 0 / Interleukin-6; 0 / Proteinase Inhibitory Proteins, Secretory; 0 / Sulfonamides; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA; DWI62G0P59 / sivelestat; EC 1.11.1.7 / Peroxidase; EC 3.4.21.37 / Leukocyte Elastase; TE7660XO1C / Glycine
  • [Other-IDs] NLM/ NIHMS198937; NLM/ PMC3627371
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8. Li YY, Lu S, Li K, Feng JY, Li YN, Gao ZR, Chen CJ: Down-regulation of HSP60 expression by RNAi increases lipopolysaccharide- and cerulein-induced damages on isolated rat pancreatic tissues. Cell Stress Chaperones; 2010 Nov;15(6):965-75
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  • [Title] Down-regulation of HSP60 expression by RNAi increases lipopolysaccharide- and cerulein-induced damages on isolated rat pancreatic tissues.
  • The objective of this study was to investigate the function of heat shock protein 60 (HSP60) on pancreatic tissues by applying HSP60 small interfering RNA (siRNA) to reduce HSP60 expression.
  • Rat pancreas was isolated and pancreatic tissue snips were prepared, cultured, and stimulated with low and high concentrations of cerulein (10(-11) and 10(-5) mol/L) or lipopolysaccharide (LPS, 10 and 20 μg/mL).
  • Before the stimulation and 1 and 4 h after the stimulation, the viability and the level of trypsinogen activation peptide (TAP) in the tissue fragments were determined and the levels of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) in the culture supernatants were measured.
  • The pancreatic tissues in the control (mock-interfering) group showed a decreased viability to varying degrees after being stimulated with cerulein or LPS, and the levels of TAP, TNF-α, and IL-6 increased significantly (p < 0.05) in the tissues and/or in the culture supernatant.
  • The results indicated that both cerulein and LPS can induce injuries on isolated pancreatic tissues, but the induction effects are dependent on the duration of the stimulation and on the concentrations of the toxicants.
  • HSP60 siRNA reduces HSP60 expression and worsens the cerulein- or LPS-induced injuries on isolated pancreatic tissues, suggesting that HSP60 has a protective effect on pancreatic tissues against these toxicants.
  • [MeSH-major] Ceruletide / toxicity. Chaperonin 60 / metabolism. Lipopolysaccharides / toxicity. Pancreas / metabolism
  • [MeSH-minor] Animals. Cells, Cultured. Down-Regulation. Interleukin-6 / metabolism. Oligopeptides / metabolism. RNA Interference. RNA, Small Interfering / metabolism. Rats. Rats, Sprague-Dawley. Time Factors. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20574674.001).
  • [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 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Oligopeptides; 0 / RNA, Small Interfering; 0 / Tumor Necrosis Factor-alpha; 0 / trypsinogen activation peptide; 888Y08971B / Ceruletide
  • [Other-IDs] NLM/ PMC3024061
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9. Xu L, Kwon YJ, Frolova N, Steg AD, Yuan K, Johnson MR, Grizzle WE, Desmond RA, Frost AR: Gli1 promotes cell survival and is predictive of a poor outcome in ERalpha-negative breast cancer. Breast Cancer Res Treat; 2010 Aug;123(1):59-71
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  • [Title] Gli1 promotes cell survival and is predictive of a poor outcome in ERalpha-negative breast cancer.
  • Gli1 is a transcription factor and oncogene with documented roles in the progression of several cancer types, including cancers of the skin and pancreas.
  • In order to investigate the functional impact of Gli1 in breast cancer, expression of Gli1 and its contribution to cell growth was assessed in breast cancer cell lines.
  • In these cancers, the association of Gli1 with expression of estrogen receptor alpha (ERalpha) and progesterone receptor (PR), ErbB2, p53, the rate of proliferation, and clinicopathologic parameters and outcome was assessed.
  • Expression of Gli1 and ERalpha mRNA was strongly correlated in ERalpha-positive cell lines (r = 0.999).
  • Treatment with estrogen increased expression of Gli1 in 2 of 3 ERalpha-positive cell lines; this increase was prevented by treatment with the ERalpha-specific antagonist MPP.
  • Silencing of Gli1 by shRNA markedly reduced the survival of two ERalpha-negative cell lines, but caused only a modest reduction in ERalpha-positive cell lines.
  • However, nuclear localization of Gli1 was predictive of a poorer cancer-specific survival in ERalpha-negative, including triple negative, cancers (P = 0.005), but not ERalpha-positive cancers.

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  • (PMID = 19902354.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA130057-02; United States / NCI NIH HHS / CA / R03 CA130057; United States / NCI NIH HHS / CA / R03 CA130057-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Gli protein; 0 / Oncogene Proteins; 0 / Trans-Activators; 4TI98Z838E / Estradiol
  • [Other-IDs] NLM/ NIHMS172145; NLM/ PMC2888711
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10. Zhang ZW, Zhang QY, Zhou MT, Liu NX, Chen TK, Zhu YF, Wu L: Antioxidant inhibits HMGB1 expression and reduces pancreas injury in rats with severe acute pancreatitis. Dig Dis Sci; 2010 Sep;55(9):2529-36
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  • [Title] Antioxidant inhibits HMGB1 expression and reduces pancreas injury in rats with severe acute pancreatitis.
  • OBJECTIVE: To investigate the effect of treatment with antioxidant pyrrolidine dithiocarbamate on pancreas injury in rats with severe acute pancreatitis and its possible mechanism.
  • The pancreas histopathologies were observed and serum amylase levels were tested.
  • Meanwhile, the nuclear factor-kappaB activation, tumor necrosis factor-alpha levels and high-mobility group box protein-1 expression levels in pancreatic tissue were studied.
  • RESULTS: Animals receiving pyrrolidine dithiocarbamate had significantly improved pancreas histopathology and lower serum amylase levels (p<0.05).
  • In the severe acute pancreatitis group, pancreas tumor necrosis factor-alpha levels reached a peak at 6 h after operation and afterwards rapidly declined to normal levels.
  • However, high-mobility group box protein-1 levels in pancreatic tissue increased remarkably at the 12th hour, reached a peak at 24 h, and maintained up to 48 h post-severe acute pancreatitis.
  • Compared to the severe acute pancreatitis group, the pancreas nuclear factor-kappaB activity, tumor necrosis factor-alpha, high-mobility group box protein-1 levels in the pyrrolidine dithiocarbamate-treated group all remarkably decreased (p<0.05).
  • Pyrrolidine dithiocarbamate might inhibit the activation of nuclear factor-kappaB to blockade tumor necrosis factor-alpha, thereby indirectly suppressing the high-mobility group box protein-1 and reducing pancreatic tissue damage in rats with severe acute pancreatitis.
  • [MeSH-major] Antioxidants / pharmacology. HMGB1 Protein / metabolism. Pancreas / drug effects. Pancreatitis / drug therapy. Pyrrolidines / pharmacology. Thiocarbamates / pharmacology
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Disease Models, Animal. Down-Regulation. Male. NF-kappa B / metabolism. Rats. Rats, Sprague-Dawley. Severity of Illness Index. Time Factors. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19997973.001).
  • [ISSN] 1573-2568
  • [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 / Antioxidants; 0 / HMGB1 Protein; 0 / Hbp1 protein, rat; 0 / NF-kappa B; 0 / Pyrrolidines; 0 / Thiocarbamates; 0 / Tumor Necrosis Factor-alpha; 25769-03-3 / pyrrolidine dithiocarbamic acid; EC 3.2.1.- / Amylases
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11. Selva DM, Hogeveen KN, Innis SM, Hammond GL: Monosaccharide-induced lipogenesis regulates the human hepatic sex hormone-binding globulin gene. J Clin Invest; 2007 Dec;117(12):3979-87
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  • In overweight children and adults, low plasma SHBG levels are a biomarker of the metabolic syndrome and its associated pathologies.
  • Here, we showed in transgenic mice and HepG2 hepatoblastoma cells that monosaccharides (glucose and fructose) reduce human SHBG production by hepatocytes.
  • The dose-dependent reduction of HNF-4alpha levels in HepG2 cells after treatment with glucose or fructose occurred in concert with parallel increases in cellular palmitate levels and could be mimicked by treatment with palmitoyl-CoA.
  • Moreover, inhibition of lipogenesis prevented monosaccharide-induced downregulation of HNF-4alpha and reduced SHBG expression in HepG2 cells.
  • This provides a biological explanation for why SHBG is a sensitive biomarker of the metabolic syndrome and the metabolic disturbances associated with increased fructose consumption.
  • [MeSH-minor] Adult. Animals. Biomarkers / blood. Cell Line, Tumor. Chickens / genetics. Child. Child, Preschool. Gene Expression Regulation / drug effects. Gene Expression Regulation / genetics. Gonadal Steroid Hormones / blood. Hepatocyte Nuclear Factor 1-alpha / genetics. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Metabolic Syndrome X / blood. Metabolic Syndrome X / genetics. Metabolic Syndrome X / pathology. Mice. Mice, Transgenic. Overweight / blood. Overweight / genetics. Overweight / pathology

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  • (PMID = 17992261.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Gonadal Steroid Hormones; 0 / HNF1A protein, human; 0 / HNF4A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Hepatocyte Nuclear Factor 4; 0 / Hnf1a protein, mouse; 0 / Sex Hormone-Binding Globulin; 0 / Sweetening Agents; 30237-26-4 / Fructose; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2066187
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12. Kayed H, Jiang X, Keleg S, Jesnowski R, Giese T, Berger MR, Esposito I, Löhr M, Friess H, Kleeff J: Regulation and functional role of the Runt-related transcription factor-2 in pancreatic cancer. Br J Cancer; 2007 Oct 22;97(8):1106-15
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  • [Title] Regulation and functional role of the Runt-related transcription factor-2 in pancreatic cancer.
  • In the present study, the localisation of the Runt-related transcription factor-2 (Runx2), its transcriptional activity, as well as its regulation of expression was analysed in human pancreatic ductal adenocarcinoma (PDAC).
  • Runt-related transcription factor-2 expression was silenced using specific siRNA oligonucleotides in pancreatic cancer cells (Panc-1) and immortalised pancreatic stellate cells (IPSCs).
  • There was a 6.1-fold increase in median Runx2 mRNA levels in PDAC tissues compared to normal pancreatic tissues (P<0.0001).
  • Runt-related transcription factor-2 was localised in pancreatic cancer cells, tubular complexes, and PanIN lesions of PDAC tissues as well as in tumour-associated fibroblasts/stellate cells.
  • Coculture of IPSCs and Panc-1 cells, as well as treatment with TGF-beta1 and BMP2, led to increased Runx2 expression in Panc-1 cells.
  • Runt-related transcription factor-2 overexpression was associated with decreased MMP1 release as well as decreased growth and invasion of Panc-1 cells.
  • In addition, Runx2 has the potential to regulate the transcription of extracellular matrix modulators such as SPARC and MMP1, thereby influencing the tumour microenvironment.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Core Binding Factor Alpha 1 Subunit / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Gene Expression. Humans. Immunohistochemistry. Matrix Metalloproteinase 1 / biosynthesis. RNA, Messenger / analysis. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 17876328.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 1 Subunit; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / RUNX2 protein, human; EC 3.4.24.7 / Matrix Metalloproteinase 1
  • [Other-IDs] NLM/ PMC2360444
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13. Sandoval J, Pereda J, Rodriguez JL, Escobar J, Hidalgo J, Joosten LA, Franco L, Sastre J, López-Rodas G: Ordered transcriptional factor recruitment and epigenetic regulation of tnf-alpha in necrotizing acute pancreatitis. Cell Mol Life Sci; 2010 May;67(10):1687-97
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  • [Title] Ordered transcriptional factor recruitment and epigenetic regulation of tnf-alpha in necrotizing acute pancreatitis.
  • Tauhe expression of the critical initiator cytokine TNF-alpha was strongly upregulated in vivo in acute necrotic pancreatitis (AP) in rodents and in vitro in TNF-alpha activated acinar AR42J cells.
  • Upregulation of tnf-alpha, inos, icam-1 and il-6 occurred both in TNF-alpha receptor 1 and 2 knock-out mice, but not in TNF-alpha knock-out mice, in cerulein-induced acute pancreatitis.
  • Activation of tnf-alpha gene was also accompanied by an ordered increased level of histone H3K9, H3K14 and H3K18-acetylation and H3K4 methylation, as well as H4K5 acetylation.
  • A better knowledge of the molecular mechanisms that control tnf-alpha gene regulation will provide deeper understanding of the initiation and development of the inflammatory processes occurring in acute pancreatitis triggered by TNF-alpha cytokine.
  • [MeSH-major] Epigenesis, Genetic. Pancreatitis, Acute Necrotizing / genetics. Transcription Factors / metabolism. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Animals. Cell Line. Chromatin Immunoprecipitation. Histones / metabolism. Inflammation Mediators / metabolism. Mice. Mice, Inbred C57BL. Mice, Knockout. Promoter Regions, Genetic / genetics. Protein Processing, Post-Translational. Rats. Receptors, Tumor Necrosis Factor, Type I / deficiency. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / deficiency. Receptors, Tumor Necrosis Factor, Type II / metabolism. Taurocholic Acid. Up-Regulation / genetics

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  • (PMID = 20130956.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Histones; 0 / Inflammation Mediators; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 5E090O0G3Z / Taurocholic Acid
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4. 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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15. 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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16. 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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17. Long YM, Chen K, Liu XJ, Xie WR, Wang H: Cell-permeable Tat-NBD peptide attenuates rat pancreatitis and acinus cell inflammation response. World J Gastroenterol; 2009 Feb 7;15(5):561-9
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  • [Title] Cell-permeable Tat-NBD peptide attenuates rat pancreatitis and acinus cell inflammation response.
  • AIM: To investigate the effects of Tat-NEMO-binding domain (NBD) peptide on taurocholate-induced pancreatitis and lipopolysaccharide (LPS)-stimulated AR42J acinus cells inflammatory response in rats.
  • The pancreatic histopathology was analyzed by hematoxylin staining.
  • LPS was added to the culture medium to stimulate the AR42J cells.
  • For pretreatment, cells were incubated with different peptides for 2 h before LPS stimulation.
  • Expression of IL-1beta and TNF-alpha mRNA was analyzed using a semi-quantitative reverse-transcript polymerase chain reaction (RT-PCR) method.
  • IL-1beta and TNF-alpha protein in culture medium were detected by enzyme linked immunosorbent assay (ELISA).
  • NF-kappaB DNA-binding in pancreas was examined by electrophoretic mobility shift assays.
  • LPS (10 mg/L) resulted in an increase of IL-1beta mRNA, IL-1beta protein, TNF-alpha mRNA and TNF-alpha protein, whereas significantly inhibitory effects were observed when cells were incubated with Tat-NBD (WT).
  • [MeSH-minor] Amino Acid Sequence. Amino Acid Substitution. Animals. Cell Line. Interleukin-1beta / genetics. NF-kappa B / physiology. Peptide Fragments / genetics. Peptide Fragments / therapeutic use. RNA, Messenger / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Taurocholic Acid / toxicity. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 19195057.001).
  • [ISSN] 2219-2840
  • [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 / Gene Products, tat; 0 / Interleukin-1beta; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Peptides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 5E090O0G3Z / Taurocholic Acid
  • [Other-IDs] NLM/ PMC2653342
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18. El-Rayes BF, Ali S, Philip PA, Sarkar FH: Protein kinase C: a target for therapy in pancreatic cancer. Pancreas; 2008 May;36(4):346-52
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  • [Title] Protein kinase C: a target for therapy in pancreatic cancer.
  • OBJECTIVES: Protein kinase C (PKC) is involved in tumor growth and apoptosis and hence represents a potential target for cancer therapy.
  • This study investigated the expression of PKC in pancreatic tumor tissue in comparison to adjacent normal tissue and determined the modulation of PKC by bryostatin-1 (BRYO) on pancreatic cancer cell lines.
  • METHODS: Pancreatic tissue was obtained from 18 patients who had a resection (14 with ductal adenocarcinoma and 4 with adenoma and high-grade dysplasia).
  • HPAC cells were treated with gemcitabine and BRYO and in sequential and concomitant combination.
  • To evaluate cell viability, apoptosis, and electrophoretic mobility shift assay, 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, enzyme-linked immunosorbent assay, and nuclear factor kappaB (NF-kappaB) assays were used.
  • RESULTS: As compared with the adjacent normal tissue, PKC-alpha, PKC-beta1, and PKC-delta were higher in the tumor; PKC-epsilon was higher in the normal tissue.
  • Pretreatment with gemcitabine followed by BRYO resulted in decreased cell viability, increased apoptosis, and inhibited NF-kappaB than either agent alone or BRYO followed by gemcitabine.
  • CONCLUSION: Protein kinase C is overexpressed and activated in pancreatic cancer as compared with normal tissue.
  • Inhibition of PKC could sensitize pancreatic cancer cell lines to the effects of gemcitabine.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Isoenzymes / antagonists & inhibitors. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / enzymology. Protein Kinase C / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Adenoma / drug therapy. Adenoma / enzymology. Adenoma / pathology. Bryostatins / administration & dosage. Cell Survival / drug effects. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Humans. Protein Kinase Inhibitors / therapeutic use. Reference Values

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  • (PMID = 18437080.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bryostatins; 0 / Isoenzymes; 0 / Protein Kinase Inhibitors; 0W860991D6 / Deoxycytidine; 37O2X55Y9E / bryostatin 1; B76N6SBZ8R / gemcitabine; EC 2.7.11.13 / Protein Kinase C
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19. 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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20. Grimsholm O, Rantapää-Dahlqvist S, Dalén T, Forsgren S: BDNF in RA: downregulated in plasma following anti-TNF treatment but no correlation with inflammatory parameters. Clin Rheumatol; 2008 Oct;27(10):1289-97
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  • Furthermore, the effects of anti-tumour necrosis factor (anti-TNF; infliximab) treatment on BDNF levels in the plasma of RA patients were analysed.
  • Cells in the synovium showed immunoreactivity for BDNF and BDNF-, p75- and TrkB-receptor immunoreactions were seen in nerve fibres of nerve fascicles and in association with sensory corpuscles.
  • The levels of BDNF in synovial tissue were not correlated with the number of inflammatory cells observed microscopically or with levels of TNFalpha.
  • Nor did the BDNF levels in synovial fluid correlate with erythrocyte sedimentation rate (ESR) or white blood cell counts.
  • However, the levels of BDNF in plasma of patients treated with anti-TNF did not correlate with the changes in ESR or a disease activity score.
  • Instead it is likely that sources other than inflammatory cells, including nerve structures, are important sources of BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to effects on circulating and various local cells and/or BDNF-containing neurons.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Arthritis, Rheumatoid / blood. Arthritis, Rheumatoid / drug therapy. Brain-Derived Neurotrophic Factor / blood. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 18484150.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Brain-Derived Neurotrophic Factor; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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21. Zhai Y, Qiao B, Shen XD, Gao F, Busuttil RW, Cheng G, Platt JL, Volk HD, Kupiec-Weglinski JW: Evidence for the pivotal role of endogenous toll-like receptor 4 ligands in liver ischemia and reperfusion injury. Transplantation; 2008 Apr 15;85(7):1016-22
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  • Furthermore, we demonstrated that liver perfusates, generated by isolated liver perfusion system, contained LPS-independent, heat-sensitive protein molecules that activated macrophages to produce tumor necrosis factor (TNF)-alpha through TLR4 but not TLR2 pathway.

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  • (PMID = 18408583.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI023847; United States / NIAID NIH HHS / AI / AI42223; United States / NIAID NIH HHS / AI / AI23847; United States / NIAID NIH HHS / AI / R01 AI042223; United States / NIDDK NIH HHS / DK / R01 DK062357; United States / NIAID NIH HHS / AI / AI53733
  • [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 / Lipopolysaccharides; 0 / Toll-Like Receptor 4
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22. Yang KC, Wu CC, Sumi S, Tseng CL, Wu YH, Kuo TF, Lin FH: Calcium phosphate cement chamber as an immunoisolative device for bioartificial pancreas: in vitro and preliminary in vivo study. Pancreas; 2010 May;39(4):444-51
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  • [Title] Calcium phosphate cement chamber as an immunoisolative device for bioartificial pancreas: in vitro and preliminary in vivo study.
  • OBJECTIVES: This study examined a calcium phosphate cement (CPC) chamber as an immunoisolative device to facilitate the use of xenogeneic cell sources without immunosuppression for the bioartificial pancreas (BAP).
  • METHODS: Mouse insulinoma cells were encapsulated in agarose gel and then enclosed in a CPC chamber to create a BAP.
  • Bioartificial pancreas were evaluated by cell viability, live-dead cell ratio, and cytokine-mediated cytotoxicity assay and implanted into the peritoneal cavity of diabetic rats.
  • RESULTS: Insulinoma cells enclosed in the CPC chamber had normal viability, cell survival, and insulin secretion that was even cultured in media with cytokines.
  • Histological examination revealed the fibrous tissue envelopment, and immune-related cells that competed for oxygen resulting in hypoxia could be attributed to the dysfunction of BAPs.
  • An alternative implanted site should be considered to extend the functional longevity of BAPs in further study.
  • [MeSH-major] Artificial Organs. Calcium Phosphates / chemistry. Diabetes Mellitus, Experimental / metabolism. Pancreas / metabolism
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Culture Techniques / instrumentation. Cell Line, Tumor. Cell Survival / drug effects. Insulin / secretion. Insulinoma / metabolism. Insulinoma / pathology. Interleukin-1beta / pharmacology. Mice. Rats. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 20084047.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Calcium Phosphates; 0 / Insulin; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 97Z1WI3NDX / calcium phosphate
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23. 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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24. Steiner AA, Romanovsky AA: Leptin: at the crossroads of energy balance and systemic inflammation. Prog Lipid Res; 2007 Mar;46(2):89-107
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  • In leptin-irresponsive mutants, the hypothermia of systemic inflammation is exaggerated, presumably due to the enhanced production and cryogenic action of tumor necrosis factor (TNF)-alpha.
  • The enhanced production of TNF-alpha and IL-1beta may be due, at least in part, to insufficient activation of the anti-inflammatory hypothalamo-pituitary-adrenal axis by immune stimuli in the absence of leptin signaling.

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  • (PMID = 17275915.001).
  • [ISSN] 0163-7827
  • [Journal-full-title] Progress in lipid research
  • [ISO-abbreviation] Prog. Lipid Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS041233-04; United States / NINDS NIH HHS / NS / R01 NS041233; United States / NINDS NIH HHS / NS / NS41233; United States / NINDS NIH HHS / NS / R01 NS041233-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Leptin; 0 / Receptors, Leptin
  • [Number-of-references] 209
  • [Other-IDs] NLM/ NIHMS23764; NLM/ PMC1976277
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25. 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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26. Kreutzer JN, Ruzzene M, Guerra B: Enhancing chemosensitivity to gemcitabine via RNA interference targeting the catalytic subunits of protein kinase CK2 in human pancreatic cancer cells. BMC Cancer; 2010;10:440
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  • [Title] Enhancing chemosensitivity to gemcitabine via RNA interference targeting the catalytic subunits of protein kinase CK2 in human pancreatic cancer cells.
  • BACKGROUND: Pancreatic cancer is a complex genetic disorder that is characterized by rapid progression, invasiveness, resistance to treatment and high molecular heterogeneity.
  • Various agents have been used in clinical trials showing only modest improvements with respect to gemcitabine-based chemotherapy, which continues to be the standard first-line treatment for this disease.
  • However, owing to the overwhelming molecular alterations that have been reported in pancreatic cancer, there is increasing focus on targeting molecular pathways and networks, rather than individual genes or gene-products with a combination of novel chemotherapeutic agents.
  • METHODS: Cells were transfected with small interfering RNAs (siRNAs) targeting the individual CK2 subunits.
  • The CK2 protein expression levels were determined and the effect of its down-regulation on chemosensitization of pancreatic cancer cells was investigated.
  • RESULTS: The present study examined the impact on cell death following depletion of the individual protein kinase CK2 catalytic subunits alone or in combination with gemcitabine and the molecular mechanisms by which this effect is achieved.
  • Depletion of the CK2alpha or -alpha' subunits in combination with gemcitabine resulted in marked apoptotic and necrotic cell death in PANC-1 cells.
  • We show that the mechanism of cell death is associated with deregulation of distinct survival signaling pathways.
  • CONCLUSIONS: Results reported here show that the two catalytic subunits of CK2 contribute differently to enhance gemcitabine-induced cell death, the reduced level of CK2alpha' being the most effective and that simultaneous reduction in the expression of CK2 and other survival factors might be an effective therapeutic strategy for enhancing the sensitivity of human pancreatic cancer towards chemotherapeutic agents.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Pancreatic Ductal / drug therapy. Casein Kinase II / antagonists & inhibitors. Casein Kinase II / genetics. Deoxycytidine / analogs & derivatives. Pancreatic Neoplasms / drug therapy. RNA, Small Interfering / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects

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  • (PMID = 20718998.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.7.11.1 / Casein Kinase II
  • [Other-IDs] NLM/ PMC2931491
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27. Park SJ, Seo SW, Choi OS, Park CS: Alpha-lipoic acid protects against cholecystokinin-induced acute pancreatitis in rats. World J Gastroenterol; 2005 Aug 21;11(31):4883-5
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  • [Title] Alpha-lipoic acid protects against cholecystokinin-induced acute pancreatitis in rats.
  • AIM: Alpha-lipoic acid (ALA) has been used as an antioxidant.
  • The aim of this study was to investigate the effect of alpha-lipoic acid on cholecystokinin (CCK)-octapeptide induced acute pancreatitis in rats.
  • We checked the pancreatic weight/body weight ratio, the secretion of pro-inflammatory cytokines and the levels of lipase, amylase of serum.
  • RESULTS: ALA significantly decreased the pancreatic weight/body weight ratio and serum amylase and lipase in CCK octapeptide-induced acute pancreatitis.
  • However, the secretion of IL-1beta, IL-6, and TNF-alpha were comparable in CCK octapeptide-induced acute pancreatitis.
  • [MeSH-minor] Acute Disease. Animals. Hyperlipidemias / prevention & control. Injections, Intraperitoneal. Interleukin-1 / secretion. Interleukin-6 / secretion. Male. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 16097064.001).
  • [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 / Interleukin-1; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 73Y7P0K73Y / Thioctic Acid; 9011-97-6 / Cholecystokinin
  • [Other-IDs] NLM/ PMC4398742
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28. 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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29. Lamba S, Felicioni L, Buttitta F, Bleeker FE, Malatesta S, Corbo V, Scarpa A, Rodolfo M, Knowles M, Frattini M, Marchetti A, Bardelli A: Mutational profile of GNAQQ209 in human tumors. PLoS One; 2009;4(8):e6833
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  • [Title] Mutational profile of GNAQQ209 in human tumors.
  • BACKGROUND: Frequent somatic mutations have recently been identified in the ras-like domain of the heterotrimeric G protein alpha-subunit (GNAQ) in blue naevi 83%, malignant blue naevi (50%) and ocular melanoma of the uvea (46%).
  • METHODOLOGY: To assess if the mutations are present in other tumor types we performed a systematic mutational profile of the GNAQ exon 5 in a panel of 922 neoplasms, including glioblastoma, gastrointestinal stromal tumors (GIST), acute myeloid leukemia (AML), blue naevi, skin melanoma, bladder, breast, colorectal, lung, ovarian, pancreas, and thyroid carcinomas.
  • Changes affecting Q209 were not found in any of the other tumors.
  • Our data indicate that the occurrence of GNAQ mutations display a unique pattern being present in a subset of melanocytic tumors but not in malignancies of glial, epithelial and stromal origin analyzed in this study.

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  • (PMID = 19718445.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.1 / Heterotrimeric GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2730032
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30. Seo DW: EUS-Guided Antitumor Therapy for Pancreatic Tumors. Gut Liver; 2010 Sep;4 Suppl 1:S76-81
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  • [Title] EUS-Guided Antitumor Therapy for Pancreatic Tumors.
  • Endoscopic ultrasound (EUS) is a very useful modality for the diagnosis and staging of pancreatic masses.
  • With the advent of EUS-guided fine-needle aspiration technology, this modality has made a tremendous leap from imaging modality to histologic diagnosis and therapeutic intervention.
  • EUS offers high-resolution images of and unparalleled access to the pancreas.
  • After locating the tip of the echoendoscope in the duodenum or stomach, several drugs or local treatment modalities can be delivered directly into the pancreas.
  • EUS-guided ethanol lavage with/without paclitaxel injection has been tested for the treatment of cystic tumors of the pancreas, with complete resolution of cystic tumor being observed in up to 70-80% of patients.
  • Ethanol injection is also performed for the management of solid neuroendocrine tumors of the pancreas.
  • Various type of EUS-guided injection have also been investigated for the treatment of pancreatic cancer.
  • An activated allogenic mixed lymphocyte culture (Cytoimplant) was injected in patients with advanced pancreatic cancer.
  • A replication-deficient adenovirus vector carrying the tumor necrosis factor-alpha gene was also delivered intratumorally by EUS.
  • ONYX-015 is an oncolytic attenuated adenovirus that exhibits replication preferentially in malignant cells, causing cell death, and this has also been injected into pancreatic cancers under EUS guidance.
  • This article reviews the various applications of EUS for the treatment of pancreatic tumors.

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  • (PMID = 21103299.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2989554
  • [Keywords] NOTNLM ; Brachytherapy / Cystic tumor / Cytoimplant / Endoscopic ultrasonography / Immunotherapy / Pancreas cancer / Photodynamic therapy / Radiofrequency ablation
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31. Song JM, Liu HX, Li Y, Zeng YJ, Zhou ZG, Liu HY, Xu B, Wang L, Zhou B, Wang R: Extracellular heat-shock protein 70 aggravates cerulein-induced pancreatitis through toll-like receptor-4 in mice. Chin Med J (Engl); 2008 Aug 5;121(15):1420-5
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  • BACKGROUND: In patients suffering from acute pancreatitis, the pathogenesis is not completely understood, and several recent studies in vitro suggested that heat shock proteins might play an important role in cell signaling.
  • Histologic alteration of the pancreas was evaluated.
  • Tumor necrosis factor alpha (TNF-alpha) concentrations and myeloperoxidase (MPO) activity in both pancreas and lungs were analyzed.
  • The nuclear factor kappa B (NF-kappaB) activation in pancreatic tissue was measured using a sensitive RelA enzyme-linked immunosorbent assay.
  • RESULTS: Treatment with recombinant Hsp70 to wild-type mice in CIP resulted in significant aggravation of inflammation in pancreas, elevated levels of serum cytokines, up-regulation of pulmonary MPO activity and increase of lung tissues TNF-alpha concentrations.
  • In contrast, treatment with Hsp70 to TLR4-deficient mice had little effect on serum cytokines levels, pancreatic inflammation, pulmonary MPO activity and TNF-alpha concentrations.
  • CONCLUSIONS: The results suggest that extracellular Hsp70 might induce systemic inflammatory response syndrome (SIRS)-like response in vivo and TLR4 might be involved in the Hsp70-mediated activation of inflammatory reaction in the progression of CIP without infection.
  • [MeSH-minor] Acute Disease. Animals. Female. Male. Mice. Mice, Inbred C57BL. Systemic Inflammatory Response Syndrome / etiology

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  • (PMID = 18959120.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; 0 / Tlr4 protein, mouse; 0 / Toll-Like Receptor 4; 888Y08971B / Ceruletide
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32. 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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33. Sato K, Arai H, Mizuno A, Fukaya M, Sato T, Koganei M, Sasaki H, Yamamoto H, Taketani Y, Doi T, Takeda E: Dietary palatinose and oleic acid ameliorate disorders of glucose and lipid metabolism in Zucker fatty rats. J Nutr; 2007 Aug;137(8):1908-15
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  • After 8 wk, palatinose feeding (PO and PL) led to significant reductions in visceral fat mass, adipocyte cell size, hyperglycemia, and hyperlipidemia compared with sucrose feeding (SO and SL); pancreatic islet hypertrophy was also prevented by palatinose feeding.
  • Linoleic-acid-fed rats (PL and SL) exhibited reduced insulin-immunoreactive staining of the pancreatic islets, enhanced macrophage infiltration in adipose tissue, and an elevated plasma tumor necrosis factor-alpha concentration when compared with oleic-acid-fed rats (PO and SO).
  • [MeSH-minor] Adipose Tissue / drug effects. Adipose Tissue / pathology. Animals. Blood Glucose / drug effects. Body Weight. Gene Expression Regulation / drug effects. Inflammation / pathology. Liver / drug effects. Liver / metabolism. Male. Pancreas / drug effects. Rats. Rats, Zucker. Triglycerides / blood

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  • (PMID = 17634263.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Triglycerides; 2UMI9U37CP / Oleic Acid; 43360LXH8N / isomaltulose; 67I334IX2M / Isomaltose; IY9XDZ35W2 / Glucose
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34. Matsuda T, Almasan A, Tomita M, Uchihara JN, Masuda M, Ohshiro K, Takasu N, Yagita H, Ohta T, Mori N: Resistance to Apo2 ligand (Apo2L)/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis and constitutive expression of Apo2L/TRAIL in human T-cell leukemia virus type 1-infected T-cell lines. J Virol; 2005 Feb;79(3):1367-78
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  • [Title] Resistance to Apo2 ligand (Apo2L)/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis and constitutive expression of Apo2L/TRAIL in human T-cell leukemia virus type 1-infected T-cell lines.
  • Adult T-cell leukemia (ATL), a CD4+-T-cell malignancy caused by human T-cell leukemia virus type 1 (HTLV-1), is difficult to cure, and novel treatments are urgently needed.
  • Apo2 ligand (Apo2L; also tumor necrosis factor-related apoptosis-inducing ligand [TRAIL]) has been implicated in antitumor therapy.
  • We found that HTLV-1-infected T-cell lines and primary ATL cells were more resistant to Apo2L-induced apoptosis than uninfected cells.
  • Interestingly, HTLV-1-infected T-cell lines and primary ATL cells constitutively expressed Apo2L mRNA.
  • Inducible expression of the viral oncoprotein Tax in a T-cell line up-regulated Apo2L mRNA.
  • NF-kappaB plays a crucial role in the pathogenesis and survival of ATL cells.
  • [MeSH-major] Gene Expression Regulation. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / pathogenicity. Membrane Glycoproteins / metabolism. NF-kappa B / metabolism. T-Lymphocytes / virology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Apoptosis. Apoptosis Regulatory Proteins. Cell Line. Humans. Leukemia-Lymphoma, Adult T-Cell. Ligands. TNF-Related Apoptosis-Inducing Ligand. Transcriptional Activation

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  • (PMID = 15650163.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Gene Products, tax; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / NF-kappa B; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC544134
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35. 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


36. Patel M, Fine DR: Fibrogenesis in the pancreas after acinar cell injury. Scand J Surg; 2005;94(2):108-11
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  • [Title] Fibrogenesis in the pancreas after acinar cell injury.
  • Fibrosis within the pancreas is a key feature of chronic pancreatitis and pancreatic cancer.
  • It has now been well demonstrated that following injury to acinar cells, pancreatic stellate cell activation, migration and proliferation is the key mediator of this process.
  • The pancreatic stellate cell is likely to play an important role in maintaining the normal extracellular matrix; we speculate that the dysregulation of this process is an important factor in chronic pancreatitis.
  • [MeSH-major] Pancreas / cytology. Pancreas / pathology
  • [MeSH-minor] Apoptosis / physiology. Apoptosis Regulatory Proteins. Chronic Disease. Fibrosis. Humans. Membrane Glycoproteins / metabolism. Metalloproteases / physiology. Pancreatitis / physiopathology. TNF-Related Apoptosis-Inducing Ligand. Transforming Growth Factor beta / physiology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16111091.001).
  • [ISSN] 1457-4969
  • [Journal-full-title] Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society
  • [ISO-abbreviation] Scand J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; EC 3.4.- / Metalloproteases
  • [Number-of-references] 22
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37. Santini D, Poli F, Lega S: Solid-papillary tumors of the pancreas: histopathology. JOP; 2006;7(1):131-6
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  • [Title] Solid-papillary tumors of the pancreas: histopathology.
  • A solid-pseudopapillary tumor is an uncommon and "enigmatic" pancreatic neoplasm, and the term encompasses the two most conspicuous histological features: solid and pseudopapillary areas.
  • Histologically, solid-pseudopapillary tumors are generally characterized by solid areas alternating with a pseudopapillary pattern, and cystic spaces which are the results of degenerative changes occurring in the solid neoplasm.
  • Its immunohistochemical pattern is very distinctive and neoplastic cells are consistently vimentin-, CD10- and CD56-positive.
  • Some cases express focal positivity for alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase and synaptophysin.
  • Endocrine and pancreatic enzyme markers are absent; the origin of solid-pseudopapillary tumors has not yet been clarified.
  • Many investigators favor the theory that solid-pseudopapillary tumors originate from multipotent primordial cells while others suggest an extra-pancreatic origin from genital ridge angle-related cells.
  • Solid-pseudopapillary tumors appear as a low malignancy tumor and only a small number of cases recur or develop metastases after resection.
  • [MeSH-major] Carcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antigens, CD56 / analysis. Cell Proliferation. Humans. Immunohistochemistry. Neoplasm Invasiveness. Neprilysin / analysis. Receptors, Progesterone / analysis. Vimentin / analysis

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  • (PMID = 16407635.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Receptors, Progesterone; 0 / Vimentin; EC 3.4.24.11 / Neprilysin
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38. Hernández-Espinosa D, Miñano A, Martínez C, Pérez-Ceballos E, Heras I, Fuster JL, Vicente V, Corral J: L-asparaginase-induced antithrombin type I deficiency: implications for conformational diseases. Am J Pathol; 2006 Jul;169(1):142-53
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  • We studied the consequences of this drug on antithrombin levels, activity, conformation, and immunohistological and ultrastructural features in plasma from acute lymphoblastic leukemia patients, HepG2 cells, and plasma and livers from mice treated with this drug.
  • Moreover, l-asparaginase impaired secretion of antithrombin by HepG2 cells.
  • Similar effects were observed for alpha1-antitrypsin in plasma, cells, and livers, and intracellular aggregates of additional proteins were observed in frontal cortex and pancreas.
  • This is the first report of a conformational drug-associated effect on serpins without genetic factors involved. l-Asparaginase treatment induces severe, acquired, and transient type I deficiency of antithrombin (and alpha1-antitrypsin) with intracellular accumulation of the nascent molecule, increasing the risk of thrombosis.
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Line, Tumor. Electrophoresis, Polyacrylamide Gel. Factor Xa / drug effects. Factor Xa / metabolism. Humans. Liver / chemistry. Liver / metabolism. Male. Mice. Microscopy, Electron, Transmission. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Conformation. alpha 1-Antitrypsin / drug effects. alpha 1-Antitrypsin / metabolism

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  • (PMID = 16816368.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha 1-Antitrypsin; 9001-31-4 / Fibrin; EC 3.4.21.6 / Factor Xa; EC 3.5.1.1 / Asparaginase
  • [Other-IDs] NLM/ PMC1698772
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39. Carvalho KM, Morais TC, de Melo TS, de Castro Brito GA, de Andrade GM, Rao VS, Santos FA: The natural flavonoid quercetin ameliorates cerulein-induced acute pancreatitis in mice. Biol Pharm Bull; 2010;33(9):1534-9
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  • Cerulein significantly enhanced the serum levels of amylase and lipase, and pancreatic myeloperoxidase activities, malondialdehyde and the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6, as well as the pancreatic wet weight/body weight ratio.
  • Histological assessment of the pancreas showed tissue edema, neutrophil infiltration, acinar vacuolization, and cell necrosis and a marked increase in the immunoreactivity staining for TNF-alpha.
  • Pretreatment with quercetin or thalidomide significantly attenuated the severity of cerulein-induced acute pancreatitis as evidenced by effective reductions in the pancreatic wet weight/body weight ratio, biochemical indices, proinflammatory cytokines, myeloperoxidase activity, malondialdehyde formation, and an increase in antiinflammatory cytokine IL-10.
  • Quercetin treatment also markedly suppressed the histological changes such as pancreatic edema, inflammatory cell infiltration, acinar cell necrosis, and the expression of TNF-alpha.

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  • (PMID = 20823570.001).
  • [ISSN] 1347-5215
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Flavonoids; 888Y08971B / Ceruletide; 9IKM0I5T1E / Quercetin
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40. Hirashima K, Takamori H, Hirota M, Tanaka H, Ichihara A, Sakamoto Y, Ikuta Y, Karashima R, Watanabe M, Iyama K, Baba H: Multiple gastrointestinal stromal tumors in neurofibromatosis type 1: report of a case. Surg Today; 2009;39(11):979-83
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  • [Title] Multiple gastrointestinal stromal tumors in neurofibromatosis type 1: report of a case.
  • This report presents a case of multiple gastrointestinal stromal tumors (GIST) with neurofibromatosis type 1 (NF1).
  • A 68-year-old woman was admitted to the hospital because of a tumor close to the head of the pancreas.
  • Imaging studies revealed submucosal tumors of the duodenum.
  • The retroperitoneal tumor was diagnosed before surgery.
  • Besides the main tumor in the duodenum, multiple small submucosal tumors were found in the duodenum and upper part of the jejunum during the operation.
  • All of these tumors were resected.
  • The histological diagnosis of all these tumors was GISTs.
  • These tumors were immunohistochemically positive for KIT, but they demonstrated no mutation in c-kit exons 9, 11, 13, and 17, and platelet-derived growth factor receptor alpha exons 12 and 18.
  • [MeSH-major] Digestive System Surgical Procedures / methods. Duodenum / pathology. Gastrointestinal Stromal Tumors / complications. Jejunum / pathology. Neurofibromatosis 1 / complications
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans


46. Jeong DH, Kim HK, Prince AE, Lee DS, Kim YN, Han J, Kim KT: Plasma proteomic analysis of patients with squamous cell carcinoma of the uterine cervix. J Gynecol Oncol; 2008 Sep;19(3):173-80
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  • [Title] Plasma proteomic analysis of patients with squamous cell carcinoma of the uterine cervix.
  • OBJECTIVE: To compare plasma protein expression between patients with squamous cell carcinoma (SCC) of the cervix and normal controls.
  • METHODS: Plasma samples from patients with benign gynecological disease (normal cervix, n=6) and cervical cancer (SCC, n=6) were subjected to plasma proteomic analysis using two dimensional gel electrophoresis (2-DE) and matrix-assisted laser desorption/ionization mass spectroscopy (MALDI-MS).
  • Western blotting and immunoturbidimetric assay were performed to validate the results of 2-DE.
  • RESULTS: Eight proteins showed differential expression between controls and SCC patients; six (ceruloplasmin, complement C3, afamin precursor, alpha-1-B-glycoprotein, transferrin, alpha-fibrinogen precursor) were up-regulated, while two (chain A, crystal structure of antithrombin and apolipoprotein A-IV precursor) were down-regulated in the plasma of SCC patients.
  • Western blotting analysis revealed significant elevation of ceruloplasmin, complement C3, afamin, and alpha-1-B-glycoprotein in the plasma of SCC patients in comparison to controls.
  • Immunoturbidimetric assay of a larger group confirmed the results of 2-DE and Western blotting, and showed that ceruloplasmin and complement C3 were significantly elevated in the plasma of SCC patients in comparison with controls and patients with carcinoma in situ (CIS) of the uterine cervix.
  • CONCLUSION: Plasma protein expression determined using 2-DE and MALDI-MS will give a chance to identify tumor-specific biomarkers for SCC of the cervix.

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  • (PMID = 19471570.001).
  • [ISSN] 2005-0380
  • [Journal-full-title] Journal of gynecologic oncology
  • [ISO-abbreviation] J Gynecol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2676467
  • [Keywords] NOTNLM ; MALDI-MS / Plasma proteins / Squamous cell carcinoma / Two dimensional gel electrophoresis / Uterine cervical cancer
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47. 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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48. Wang F, Li SS, Segersvärd R, Strömmer L, Sundqvist KG, Holgersson J, Permert J: Hypoxia inducible factor-1 mediates effects of insulin on pancreatic cancer cells and disturbs host energy homeostasis. Am J Pathol; 2007 Feb;170(2):469-77
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  • [Title] Hypoxia inducible factor-1 mediates effects of insulin on pancreatic cancer cells and disturbs host energy homeostasis.
  • Intratumoral hypoxia and paracrine insulin stimulate the expression of hypoxia inducible factor-1alpha (HIF-1alpha) in pancreatic cancer cells.
  • In the present studies, we investigated whether insulin-induced HIF-1alpha expression is a prerequisite for insulin to induce other trophic effects in MiaPaCa2 human pancreatic cancer cells and whether inhibition of HIF-1alpha expression would decrease tumor glycolysis and improve host energy homeostasis.
  • We found that hypoxia was a prerequisite for induction of HIF-1alpha mRNA expression by insulin in MiaPaCa2 cells.
  • Under hypoxic conditions, insulin stimulated glycolysis, cell proliferation, and the secretion of vascular endothelial growth factor in regular MiaPaCa2 cells but not in a MiaPaCa2 variant (si-MiaPaCa2) that expressed specific short interfering RNA for HIF-1alpha and therefore lacked HIF-1alpha protein.
  • When si-MiaPaCa2 cells were transplanted into the pancreas of athymic mice, they were less tumorigenic and expressed less hexokinase than regular MiaPaCa2 cells.
  • Body weight gain was attenuated in mice hosting tumors composed of regular MiaPaCa2 but not si-MiaPaCa2 cells.
  • These results suggest that an interaction between insulin and HIF-1alpha helps sustain pancreatic cancer cells and disturbs host energy homeostasis.
  • [MeSH-major] Glycolysis / drug effects. Homeostasis / drug effects. Hypoglycemic Agents / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Insulin / pharmacology. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Animals. Cell Hypoxia. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Regulation / drug effects. Hexokinase / biosynthesis. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 17255315.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoglycemic Agents; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Insulin; 0 / Vascular Endothelial Growth Factor A; EC 2.7.1.1 / Hexokinase
  • [Other-IDs] NLM/ PMC1851851
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49. Shimizu K, Kobayashi M, Tahara J, Shiratori K: Cytokines and peroxisome proliferator-activated receptor gamma ligand regulate phagocytosis by pancreatic stellate cells. Gastroenterology; 2005 Jun;128(7):2105-18
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  • [Title] Cytokines and peroxisome proliferator-activated receptor gamma ligand regulate phagocytosis by pancreatic stellate cells.
  • BACKGROUND & AIMS: Pancreatic stellate cells have been characterized as the major source of extracellular matrix and cytokine production in the pancreas.
  • This study showed that pancreatic stellate cells have a phagocytic function.
  • METHODS: The morphological features of periacinar phagocytic cells were investigated by immunohistochemically staining serial sections of the pancreas from male WBN/Kob rats and an animal model of acute pancreatitis for glial fibrillary acidic protein and alpha-smooth muscle actin.
  • Pancreatic stellate cells were assayed for phagocytic activity by incubating them with senescent polymorphonuclear neutrophils or fluorescence-labeled latex beads in the presence or absence of cytokines, growth factors, and peroxisome proliferator-activated receptor gamma ligand.
  • RESULTS: Phagocytic cells were observed in areas of inflammation, and they were identical to the glial fibrillary acidic protein-positive and alpha-smooth muscle actin-positive cells, thus suggesting that they were pancreatic stellate cells.
  • Aged polymorphonuclear neutrophils were ingested into the cytoplasm of the pancreatic stellate cells.
  • Transforming growth factor beta, tumor necrosis factor alpha, and interleukin 1beta decreased the phagocytic activity of pancreatic stellate cells, whereas troglitazone induced a dose-dependent increase in both phagocytic activity and expression of CD36.
  • CONCLUSIONS: Pancreatic stellate cells act as resident phagocytic cells, and CD36 promotes troglitazone-induced phagocytic activity via peroxisome proliferator-activated receptor gamma transactivation.
  • Because phagocytosis is essential to limit the extent of inflammation, enhancement of phagocytic activity may provide an important approach to the treatment of pancreatic diseases.
  • [MeSH-major] PPAR gamma / physiology. Pancreas / cytology. Phagocytosis / physiology
  • [MeSH-minor] Animals. Antigens, CD36 / physiology. Cell Culture Techniques. Immunohistochemistry. Inflammation. Ligands. Male. Pancreatic Diseases / therapy. Rats

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  • [ErratumIn] Gastroenterology. 2005 Aug;129(2):775
  • (PMID = 15940641.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD36; 0 / Ligands; 0 / PPAR gamma
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50. 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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51. Ebert C, Nebe B, Walzel H, Weber H, Jonas L: Inhibitory effect of the lectin wheat germ agglutinin (WGA) on the proliferation of AR42J cells. Acta Histochem; 2009;111(4):335-42
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  • [Title] Inhibitory effect of the lectin wheat germ agglutinin (WGA) on the proliferation of AR42J cells.
  • The rat pancreatic acinar tumour cell line AR42J is a widely used model to study the secretion, proliferation and differentiation of cells under the influence of hormones.
  • These so-called amphicrine cells synthesize and secrete digestive enzymes as well as neuroendocrine peptides.
  • They possess both subtypes of the highly glycosylated cholecystokinin (CCK) receptor which are important for the regulation of secretion and for cell growth.
  • AR42J cells extrude CCK and gastrin-like hormone peptides and have the ability of an autostimulation (autocrine loop).
  • The lectins wheat germ agglutinin (WGA) and Ulex europaeus agglutinin (UEA-I) bind to the glycosylated sites of these CCK receptors with the effect inhibiting CCK binding and thus inhibiting the CCK-induced Ca2+ release and alpha-amylase secretion.
  • The so-called trophic hormones CCK and gastrin stimulate the secretion and proliferation of AR42J cells within the autocrine loop via autostimulation of their CCK receptors.
  • In preceding papers, we described the inhibitory effect of WGA on the binding of 125I-CCK-8s to the CCK-A and -B receptors and the subsequent enzyme secretion of AR42J cells.
  • In the present work, we studied the influence of the lectins WGA, UEA-I and galectin-1, as well as of the lectin-like enzyme alpha-amylase, on the proliferation of AR42J cells and prevention of autostimulation.
  • Whereas WGA inhibited the growth fraction significantly, UEA-I, human galectin-1 and human alpha-amylase had no significant effect.
  • In transmission electron microscopy, we observed the accumulation of typical zymogen granules under the effect of WGA and a better differentiation of cells.
  • [MeSH-major] Cell Proliferation / drug effects
  • [MeSH-minor] Animals. Cell Line, Tumor. Flow Cytometry. Galectin 1 / pharmacology. Glycosylation / drug effects. Humans. Microscopy, Electron, Transmission. Pancreas / pathology. Pancreas / ultrastructure. Plant Lectins / pharmacology. Rats. Receptors, Cholecystokinin / chemistry. Secretory Vesicles / ultrastructure. Wheat Germ Agglutinins / pharmacology. alpha-Amylases / pharmacology

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  • (PMID = 19195686.001).
  • [ISSN] 1618-0372
  • [Journal-full-title] Acta histochemica
  • [ISO-abbreviation] Acta Histochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Galectin 1; 0 / Plant Lectins; 0 / Receptors, Cholecystokinin; 0 / Ulex europaeus lectins; 0 / Wheat Germ Agglutinins; EC 3.2.1.1 / alpha-Amylases
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52. Park D, Ryu KS, Choi D, Kwak J, Park C: Characterization and role of fucose mutarotase in mammalian cells. Glycobiology; 2007 Sep;17(9):955-62
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  • [Title] Characterization and role of fucose mutarotase in mammalian cells.
  • L-Fucose for mammalian glycosylation contains an anomeric carbon atom generating alpha- and beta-L-fucoses.
  • Based on sequence comparison of mouse and human homologs with the prokaryotic fucose mutarotases (FucU) characterized previously, we investigated their function in mammalian cells.
  • The mouse gene was widely expressed in various tissues and cell lines, including kidney, liver, and pancreas, although expression was marginal in muscle and testis.
  • By generating stably expressed cell lines for mutarotase genes in HepG2, it was shown that fucose incorporations into cellular proteins were increased as demonstrated by an incorporation of radiolabeled fucose into the cells.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor. Escherichia coli / metabolism. Guinea Pigs. Humans. Magnetic Resonance Spectroscopy / methods. Mice. Molecular Sequence Data. Protein Structure, Tertiary. Sequence Homology, Amino Acid. Tissue Distribution


53. 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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54. Sener G, Kabasakal L, Yüksel M, Gedik N, Alican Y: Hepatic fibrosis in biliary-obstructed rats is prevented by Ginkgo biloba treatment. World J Gastroenterol; 2005 Sep 21;11(35):5444-9
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  • Tumor necrosis factor-alpha (TNF-alpha) was also assayed in serum samples.
  • Serum AST, ALT, LDH, and TNF-alpha levels were elevated in the BDL group as compared to control group and were significantly decreased by EGb treatment.

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  • (PMID = 16222734.001).
  • [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 / Antioxidants; 0 / Ginkgo biloba extract 761; 0 / Plant Extracts
  • [Other-IDs] NLM/ PMC4320351
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55. Urano N, Fujiwara Y, Doki Y, Tsujie M, Yamamoto H, Miyata H, Takiguchi S, Yasuda T, Yano M, Monden M: Overexpression of hypoxia-inducible factor-1 alpha in gastric adenocarcinoma. Gastric Cancer; 2006;9(1):44-9
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  • [Title] Overexpression of hypoxia-inducible factor-1 alpha in gastric adenocarcinoma.
  • In addition to its regulation by oncogenes or tumor suppressor genes such as HER2, p53, VHL, and PTEN, overexpression of HIF-1alpha is induced by hypoxia.
  • [MeSH-major] Adenocarcinoma / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Stomach Neoplasms / metabolism
  • [MeSH-minor] Cell Differentiation. Humans. Immunoenzyme Techniques. Lymph Nodes. Lymphatic Metastasis. Neoplasm Invasiveness / pathology. Survival Rate. Tumor Suppressor Protein p53 / metabolism. Up-Regulation. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16557436.001).
  • [ISSN] 1436-3291
  • [Journal-full-title] Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association
  • [ISO-abbreviation] Gastric Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Tumor Suppressor Protein p53; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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56. 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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57. Li Q, Feng FY, Chen Q, Jiao SC, Li F, Wang HQ, Huang WX, Ling CQ, Li MZ, Ren J, Zhang Y, Qin FZ, Zhou MZ, Zhu RZ: [Multicenter phase II clinical trial of uroacitides injection in the treatment for advanced malignant tumors]. Zhonghua Zhong Liu Za Zhi; 2008 Jul;30(7):534-7
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  • [Title] [Multicenter phase II clinical trial of uroacitides injection in the treatment for advanced malignant tumors].
  • OBJECTIVE: To investigate the efficacy, safety and the life quality improvement of uroacitides injection in the treatment for patients with advanced malignant tumors.
  • METHODS: A total of 160 patients with advanced stage cancers were enrolled into this multicenter, open and non-randomized phase II clinical trial, including cancers of the lung (33 cases), liver (45 cases), breast (17 cases), esophagus (11 cases), stomach (18 cases), colon (19 cases), pancreas (3 cases) and kidney (4 cases), and glioma (10 cases).
  • The total objective response rate (ORR, CR + PR)) and tumor control rate (CR + PR + MR + SD) of the 138 evaluable patients were 5.8% and 65.2%, respectively.
  • [MeSH-minor] Breast Neoplasms / blood. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. Carcinoma, Non-Small-Cell Lung / blood. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Catheterization, Central Venous. Colorectal Neoplasms / blood. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / pathology. Humans. Nausea / chemically induced. Neoplasm Staging. Quality of Life. Remission Induction. Salvage Therapy. Treatment Outcome. Vomiting / chemically induced. alpha-Fetoproteins / metabolism

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  • (PMID = 19062723.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] Clinical Trial, Phase II; English Abstract; Journal Article; Multicenter Study
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 0 / Peptides; 0 / Phenylacetates; 0 / alpha-Fetoproteins; 0 / cell differentiation agent II; EC 2.1.1.- / Methyltransferases
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58. 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


59. Vervoort L, Burvenich I, Staelens S, Dumolyn C, Waegemans E, Van Steenkiste M, Baird SK, Scott AM, De Vos F: Preclinical evaluation of monoclonal antibody 14C5 for targeting pancreatic cancer. Cancer Biother Radiopharm; 2010 Apr;25(2):193-205
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  • [Title] Preclinical evaluation of monoclonal antibody 14C5 for targeting pancreatic cancer.
  • The use of radiolabeled antibodies that are able to target primary tumors as well as metastatic tumor sites with minimal reactivity to normal tissues is a promising approach for treating pancreatic cancer.
  • In this study, the integrin alpha(v)beta(5) is studied as a target for the diagnosis of and potential therapy for human pancreatic cancer by using the radiolabeled murine monoclonal antibody (mAb) 14C5.
  • Biopsy specimens from human pancreatic tumors were examined for the expression of the integrin alpha(v)beta(5).
  • The pancreatic tumor cell line Capan-1 was used to test the in vitro targeting potency of mAb 14C5 labeled with 125/131-iodine and 111-indium.
  • Biodistribution and tumor-targeting characteristics were studied in Capan-1 xenografts.
  • All tumor sections were positive for the integrin alpha(v)beta(5), with an extensive positive staining of the stroma.
  • In vivo radioisotope tumor uptake was maximum at 48-72 hours, with the uptake of (111)In-p-SCN-Bz-DOTA-14C5 (35.84 +/- 8.64 percentage of injected dose per g [%ID/g]) being 3.9- and 2.2-folds higher than (131)I-14C5 (12.16 +/- 1.03%ID/g) and (111)In-p-SCN-Bz-DTPA-14C5 (14.30 +/- 3.76%ID/g), respectively.
  • Planar gamma imaging with mAb 14C5 indicated clear localization of the pancreatic tumors versus minimal normal tissue uptake. mAb 14C5 is a promising new antibody for targeting the integrin alpha(v)beta(5) for the diagnosis of and potential therapy for pancreatic cancer.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Pancreatic Neoplasms / therapy. Radiopharmaceuticals. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Female. Humans. Iodine Radioisotopes. Mice. Mice, Nude. Pancreas / immunology. Pancreas / metabolism. Pancreas / pathology. Pentetic Acid / analogs & derivatives. Pentetic Acid / pharmacokinetics. Radioimmunoassay. Receptors, Vitronectin / immunology. Receptors, Vitronectin / metabolism. Tissue Distribution. Tumor Cells, Cultured

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  • (PMID = 20423233.001).
  • [ISSN] 1557-8852
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 14C5 monoclonal antibody; 0 / Antibodies, Monoclonal; 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptors, Vitronectin; 0 / integrin alphaVbeta5; 102650-30-6 / 1-(4-isothiocyanatobenzyl)diethylenetriaminepentaacetic acid; 7A314HQM0I / Pentetic Acid
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60. Zhang XP, Tian H, Lai YH, Chen L, Zhang L, Cheng QH, Yan W, Li Y, Li QY, He Q, Wang F: Protective effects and mechanisms of Baicalin and octreotide on renal injury of rats with severe acute pancreatitis. World J Gastroenterol; 2007 Oct 14;13(38):5079-89
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  • The mortality, plasma endotoxin level, contents of blood urea nitrogen (BUN), creatinine (CREA), phospholipase A2 (PLA2), nitrogen monoxide (NO), tumor necrosis factor (TNF)-alpha, IL-6 and endothelin-1 (ET-1) in serum, expression levels of renal Bax and Bcl-2 protein, apoptotic indexes and pathological changes of kidney were observed at 3, 6 and 12 h after operation.
  • The contents of IL-6, ET-1, TNF-alpha (at 6 h) and PLA2 (at 6 h and 12 h) were lower in treated groups than in model group [P<0.001, 3.031 (0.870) and 2.646 (1.373) pg/mL vs 5.437 (1.025) pg/mL; 2.882 (1.392) and 3.076 (1.205) pg/mL vs 6.817 (0.810) pg/mL; 2.832 (0.597) and 2.462 (1.353) pg/mL vs 5.356 (0.747) pg/mL; 16.226 (3.174) and 14.855 (5.747) pg/mL vs 25.625 (7.973) pg/mL; 18.625 (5.780) and 15.185 (1.761) pg/mL vs 24.725 (3.759) pg/mL; 65.10 (27.51) and 47.60 (16.50) pg/mL vs 92.15 (23.12) pg/mL; 67.91+/-20.61 and 66.86+/-22.10 U/mL, 63.13+/-26.31 and 53.63+/-12.28 U/mL vs 101.46+/-14.67 and 105.33+/-18.10 U/mL, respectively].
  • [MeSH-minor] Acute Disease. Animals. Apoptosis / drug effects. Creatinine / blood. Dose-Response Relationship, Drug. Endothelin-1 / blood. Interleukin-6 / blood. Male. Nitric Oxide / blood. Phospholipases A2 / blood. Proto-Oncogene Proteins c-bcl-2 / metabolism. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / blood. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17876873.001).
  • [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 / Anti-Infective Agents; 0 / Bax protein, rat; 0 / Endothelin-1; 0 / Flavonoids; 0 / Gastrointestinal Agents; 0 / Interleukin-6; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Necrosis Factor-alpha; 0 / bcl-2-Associated X Protein; 31C4KY9ESH / Nitric Oxide; 347Q89U4M5 / baicalin; AYI8EX34EU / Creatinine; EC 3.1.1.4 / Phospholipases A2; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ PMC4434637
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61. Korkolis DP, Aggeli C, Plataniotis GD, Gontikakis E, Zerbinis H, Papantoniou N, Xinopoulos D, Apostolikas N, Vassilopoulos PP: Successful en bloc resection of primary hepatocellular carcinoma directly invading the stomach and pancreas. World J Gastroenterol; 2009 Mar 7;15(9):1134-7
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  • [Title] Successful en bloc resection of primary hepatocellular carcinoma directly invading the stomach and pancreas.
  • Multivisceral surgical resection for cure was successfully performed in a 70-year-old man suffering from a primary hepatocellular carcinoma (HCC) associated with direct invasion to the stomach and pancreas.
  • The patient presented with gastric outlet obstruction, upper abdominal pain and a history of chronic liver disease due to hepatitis B virus (HBV) infection.
  • Upper gastrointestinal (GI) endoscopy revealed an infiltrating tumor protruding through the gastric wall and obliterating the lumen.
  • Computer tomograghy (CT) and magnetic resonance imaging (MRI) scan demonstrated a 15-cm tumor in the left lateral segment of the liver with invasion to the stomach and pancreas.
  • Alpha-foetoprotein (AFP) levels and liver function tests were normal.
  • Pathology revealed a poorly differentiated, giant cell HCC involving the stomach and pancreas.
  • Disease-free margins of resection were achieved.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Liver Neoplasms / surgery. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery

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  • (PMID = 19266609.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2655177
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62. Qu CF, Song EY, Li Y, Rizvi SM, Raja C, Smith R, Morgenstern A, Apostolidis C, Allen BJ: Pre-clinical study of 213Bi labeled PAI2 for the control of micrometastatic pancreatic cancer. Clin Exp Metastasis; 2005;22(7):575-86
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  • [Title] Pre-clinical study of 213Bi labeled PAI2 for the control of micrometastatic pancreatic cancer.
  • PURPOSE: The urokinase plasminogen activator (uPA) and its receptor (uPAR) are expressed by pancreatic cancer cells and can be targeted by the plasminogen activator inhibitor type 2 (PAI2).
  • We have labeled PAI2 with (213)Bi to form the alpha conjugate (AC), and have studied its in vitro cytotoxicity and in vivo efficacy.
  • METHODS AND MATERIALS: The expression of uPA/uPAR on pancreatic cell lines, human pancreatic cancer tissues, lymph node metastases, and mouse xenografts were detected by immunohistochemistry, confocal microscopy, and flow cytometry.
  • At 2 days post-cancer cell subcutaneous inoculation, mice were injected with AC by local or systemic injection.
  • RESULTS: uPA/uPAR is strongly expressed on pancreatic cancer cell lines and cancer tissues.
  • The AC can target and kill cancer cells in vitro in a concentration-dependent fashion.
  • Some 90% of TUNEL positive cells were found after incubation with 1.2 MBq/ml of AC.
  • A single local injection of approximately 222 MBq/kg 2 days post-cell inoculation can completely inhibit tumor growth over 12 weeks, and an intraperitoneal injection of 111 MBq/kg causes significant tumor growth delay.
  • CONCLUSIONS: (213)Bi-PAI2 can specifically target pancreatic cancer cells in vitro and inhibit tumor growth in vivo. (213)Bi-PAI2 may be a useful agent for the treatment of post-surgical pancreatic cancer patients with minimum residual disease.
  • [MeSH-major] Bismuth / therapeutic use. Neoplasm Metastasis / radiotherapy. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / radiotherapy. Plasminogen Activator Inhibitor 2 / therapeutic use. Radioisotopes / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / radiation effects. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Microscopy, Confocal. Radiopharmaceuticals / therapeutic use. Transplantation, Heterologous. Urokinase-Type Plasminogen Activator / metabolism

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  • (PMID = 16475028.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Plasminogen Activator Inhibitor 2; 0 / Radioisotopes; 0 / Radiopharmaceuticals; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; U015TT5I8H / Bismuth
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63. Wei H, Wang C, Chen L: Proliferating cell nuclear antigen, survivin, and CD34 expressions in pancreatic cancer and their correlation with hypoxia-inducible factor 1alpha. Pancreas; 2006 Mar;32(2):159-63
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  • [Title] Proliferating cell nuclear antigen, survivin, and CD34 expressions in pancreatic cancer and their correlation with hypoxia-inducible factor 1alpha.
  • OBJECTIVE: Hypoxia-inducible factor 1alpha (HIF-1alpha) has been universally detected in many types of cells and plays a key role in modulation of tumor-related genes.
  • The purpose of this study was to explore the relationship between HIF-1alpha messenger RNA (mRNA) expression and biologic characteristics in pancreatic cancer, such as tumor angiogenesis, tumor cell proliferation, differentiation, apoptosis, and metastasis.
  • The expressions of survivin, proliferating cell nuclear antigen (PCNA), and CD34 proteins were measured immunohistochemically.
  • RESULTS: There was very significant difference in the expression of HIF-1alpha between the pancreatic cancer tissue and adjacent normal tissue (P < 0.01), but no significant difference was found among tumor histopathologic grades (P > 0.05).
  • There was significant difference in the expression of HIF-1alpha mRNA between Japanese Pancreatic Society stages I to II and stages III to IV (P < 0.05).
  • CONCLUSION: The expression level of HIF-1alpha mRNA is surmised to have a significant correlation with tumor angiogenesis, cell proliferation, apoptosis, and metastasis.
  • Inhibition of HIF-1alpha may be an important and approachable therapeutic target for pancreatic cancer.
  • [MeSH-major] Antigens, CD34 / genetics. Microtubule-Associated Proteins / genetics. Neoplasm Proteins / genetics. Pancreatic Neoplasms / genetics. Proliferating Cell Nuclear Antigen / genetics
  • [MeSH-minor] DNA Primers. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Inhibitor of Apoptosis Proteins. Neoplasm Staging. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis

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  • (PMID = 16552335.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BIRC5 protein, human; 0 / DNA Primers; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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64. Tapia B, Ahrens W, Kenney B, Touloukian R, Reyes-Múgica M: Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature. Pediatr Dev Pathol; 2008 Sep-Oct;11(5):384-90
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  • [Title] Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature.
  • Primary epithelial tumors of the pancreas are extremely uncommon in children, and among these, acinar cell carcinoma (ACC) is the most rare.
  • Here we describe our recent observations in the case of a 10-year-old boy with one of these exceptional examples.
  • The histologic diagnosis of ACC was supported by both immunohistochemistry and electron microscopy.
  • Despite its rarity, ACC should be kept in the differential diagnosis of pediatric pancreatic exocrine tumors.
  • We also provide a comparison with an example of solid pseudopapillary tumor, another relatively infrequent epithelial tumor of the pancreas in the young.
  • We review the relevant literature addressing the clinical and pathologic features of ACC and its distinction from other pancreatic neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Pancreatic Cyst / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Child. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Pancreatectomy. Treatment Outcome. alpha 1-Antitrypsin / metabolism

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  • (PMID = 19006424.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
  • [Number-of-references] 37
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65. Gin VC, Zacharias M: Glucagonoma: anaesthetic management. Anaesth Intensive Care; 2009 Mar;37(2):329-30
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  • [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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66. 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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67. Mukherjee S, Das D, Mukherjee M, Das AS, Mitra C: Synergistic effect of folic acid and vitamin B12 in ameliorating arsenic-induced oxidative damage in pancreatic tissue of rat. J Nutr Biochem; 2006 May;17(5):319-27
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  • [Title] Synergistic effect of folic acid and vitamin B12 in ameliorating arsenic-induced oxidative damage in pancreatic tissue of rat.
  • The efficacies of two nutritional factors, folic acid and vitamin B12, were assessed in this study against arsenic-induced islet cellular toxicity.
  • Results showed that, compared to control group, there was a significant increase in the levels of nitric oxide (NO), malondialdehyde (MDA) and hydroxyl radical (OH-) formation in the pancreatic tissue of arsenic-treated rats, while the activity of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), and cellular content of antioxidant glutathione (GSH) were low in these animals.
  • The serum level of tumor necrosis factor-alpha (TNF-alpha) and IL-6 was significantly high in these animals.
  • Light microscopic examination showed a marked fall in the number of islet cells.
  • Although folic acid alone could not restore the normal level of TNF-alpha and IL-6, combined folic acid and vitamin B12 could restore it.
  • Folic acid and vitamin B12 combined also could recover islet cell count.
  • [MeSH-major] Arsenic / toxicity. Folic Acid / administration & dosage. Oxidative Stress / drug effects. Pancreas / drug effects. Vitamin B 12 / administration & dosage
  • [MeSH-minor] Animals. Catalase / metabolism. Drug Synergism. Glutathione / analysis. Hydroxyl Radical / metabolism. Interleukin-6 / blood. Islets of Langerhans / cytology. Islets of Langerhans / drug effects. Male. Malondialdehyde / metabolism. Nitric Acid / metabolism. Rats. Superoxide Dismutase / metabolism. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16214333.001).
  • [ISSN] 0955-2863
  • [Journal-full-title] The Journal of nutritional biochemistry
  • [ISO-abbreviation] J. Nutr. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 3352-57-6 / Hydroxyl Radical; 411VRN1TV4 / Nitric Acid; 4Y8F71G49Q / Malondialdehyde; 935E97BOY8 / Folic Acid; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione; N712M78A8G / Arsenic; P6YC3EG204 / Vitamin B 12
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68. Li Z, Fallon J, Mandeli J, Wetmur J, Woo SL: A genetically enhanced anaerobic bacterium for oncopathic therapy of pancreatic cancer. J Natl Cancer Inst; 2008 Oct 1;100(19):1389-400
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  • [Title] A genetically enhanced anaerobic bacterium for oncopathic therapy of pancreatic cancer.
  • BACKGROUND: A major obstacle in treatment of solid tumors is the inefficient delivery of therapeutic agents to the hypoxic cores.
  • Hypoxia offers the potential for anaerobic bacteria colonization and tumor destruction by the bacteria, and dormant spores of wild-type Clostridium perfringens (Cp) germinate and proliferate within the hypoxic cores of pancreatic tumors in mice.
  • METHODS: Recombinant Cp strains in which superoxide dismutase, a major oxygen tolerance gene, was deleted (Cp/sod(-)) were constructed to enhance its selective growth in tumors.
  • The ability of the recombinant Cp strains to kill tumors was investigated in C57/BL6 mice bearing murine PANC02 tumors.
  • RESULTS: Cp/sod(-) showed reduced toxic effects compared with wild-type Cp when spores were administered intravenously into PANC02 tumor-bearing mice.
  • Mice treated with Cp/sod(-)/PVL spores demonstrated a reduction in neutrophils and macrophages in tumors, logarithmically elevated growth of intratumoral bacteria, enhanced tumor necrosis, and substantially prolonged survival without apparent systemic and organ toxic effects, compared with mice treated with both wild-type Cp and Cp/sod(-) spores.
  • Accordingly, 47% of Cp/sod(-)/PVL-treated mice (n = 15) achieved tumor-free survival for over 120 days, whereas all mice treated with Cp/sod(-) or phosphate-buffered saline (n = 10 per group) died within 50 days.
  • CONCLUSIONS: Cp/sod(-)/PVL provides a prototype for a novel class of oncopathic microbes that may have potential for the safe and effective treatment of pancreatic cancer and other poorly vascularized tumors.

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  • [CommentIn] NIH Guide Grants Contracts. 2016 Jul 29;:NOT-OD-16-124 [27483554.001]
  • [RetractionIn] Li Z, Fallon J, Mandeli J, Wetmur J, Woo SL. J Natl Cancer Inst. 2010 Feb 24;102(4):283 [20176752.001]
  • [CommentIn] Fed Regist. 2016 Jul 25;81(142):48426-48427 [27737274.001]
  • (PMID = 18812551.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-120017
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Biomarkers, Tumor; 0 / Exotoxins; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Leukocidins; 0 / Panton-Valentine leukocidin; EC 1.15.1.1 / Superoxide Dismutase
  • [Other-IDs] NLM/ PMC2720732
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69. Graham KL, Sanders N, Tan Y, Allison J, Kay TW, Coulson BS: Rotavirus infection accelerates type 1 diabetes in mice with established insulitis. J Virol; 2008 Jul;82(13):6139-49
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  • Infection modulates type 1 diabetes, a common autoimmune disease characterized by the destruction of insulin-producing islet beta cells in the pancreas.
  • Childhood rotavirus infections have been associated with exacerbations in islet autoimmunity.
  • Nonobese diabetic (NOD) mice develop lymphocytic islet infiltration (insulitis) and then clinical diabetes, whereas NOD8.3 TCR mice, transgenic for a T-cell receptor (TCR) specific for an important islet autoantigen, show more rapid diabetes onset.
  • Infected males showed increased CD8(+) T-cell proportions in islets.
  • Levels of beta-cell major histocompatibility complex class I expression and islet tumor necrosis factor alpha mRNA were elevated in at least one model.
  • Thus, rotavirus infection after beta-cell autoimmunity is established affects insulitis and exacerbates diabetes.
  • A possible mechanism involves increased exposure of beta cells to immune recognition and activation of autoreactive T cells by proinflammatory cytokines.
  • [MeSH-minor] Age Factors. Analysis of Variance. Animals. Antibodies, Viral / blood. CD8-Positive T-Lymphocytes / immunology. Flow Cytometry. Male. Mice. Mice, Inbred BALB C. Mice, Inbred NOD. Receptors, Antigen, T-Cell / genetics. Receptors, Antigen, T-Cell / immunology


70. 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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71. Samuel I, Tephly L, Williard DE, Carter AB: Enteral exclusion increases MAP kinase activation and cytokine production in a model of gallstone pancreatitis. Pancreatology; 2008;8(1):6-14
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  • BACKGROUND: We have previously demonstrated that enteral exclusion augments pancreatic p38 mitogen-activated protein (MAP) kinase activation and tumor necrosis factor-alpha (TNF-alpha) production after bile-pancreatic duct ligation in rats.
  • METHODS: In the present study, we evaluated c-Jun NH(2)-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) activation, and cytokine production, in pancreata of duct-ligated rats with and without duodenal bile-pancreatic juice replacement from a donor rat.
  • We hypothesized that enteral exclusion of bile-pancreatic juice activates stress kinases and induces cytokine production in ligation-induced acute pancreatitis.
  • RESULTS: Increased JNK and ERK activation after ligation are inhibited by bile-pancreatic juice replacement.
  • Increases in pancreatic production of IL-1beta and IL-12 after ligation are significantly subdued by replacement.
  • In additional in vitro studies, we show that cholecystokinin- or TNF-alpha-stimulated nuclear transcription factor kappa-B activation in AR42J cells is inhibited by dominant negative ERK2.
  • CONCLUSIONS: Our novel findings using our Donor Rat Model indicate that bile-pancreatic juice exclusion induces MAP kinase activation and exacerbates cell stress and inflammation in this experimental model of gallstone pancreatitis. and IAP.

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
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  • (PMID = 18235211.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK062805; United States / NIEHS NIH HHS / ES / R01 ES014871; United States / NIDDK NIH HHS / DK / DK062805
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cytokines; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2829292
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72. Kitamura Y, Sato M, Hatamochi A, Yamazaki S: Necrolytic migratory erythema without glucagonoma associated with hepatitis B. Eur J Dermatol; 2005 Jan-Feb;15(1):49-51
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  • [Title] Necrolytic migratory erythema without glucagonoma associated with hepatitis B.
  • We report a case of necrolytic migratory erythema (NME) without glucagonoma associated with hepatitis B.
  • Although the most common cause of NME is a glucagon-secreting alpha-islet cell tumor of the pancreas, a dermatitis clinically and histologicaly identical to NME has been described in patients without glucagonoma.
  • We added some discussion on the terminology of this disease.

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  • (PMID = 15701595.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
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73. 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


74. 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


75. 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


76. Sun LK, Reding T, Bain M, Heikenwalder M, Bimmler D, Graf R: Prostaglandin E2 modulates TNF-alpha-induced MCP-1 synthesis in pancreatic acinar cells in a PKA-dependent manner. Am J Physiol Gastrointest Liver Physiol; 2007 Dec;293(6):G1196-204
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  • [Title] Prostaglandin E2 modulates TNF-alpha-induced MCP-1 synthesis in pancreatic acinar cells in a PKA-dependent manner.
  • We recently demonstrated in a model of chronic pancreatitis (WBN/Kob rat) that inhibition of COX-2 activity reduces and delays pancreatic inflammation and fibrosis.
  • MCP-1 plays an important role in the recruitment of macrophages to the site of tissue injury.
  • The aim of our study is to identify mechanisms by which macrophages and acinar cells maintain an inflammatory reaction.
  • The expression profile of E prostanoid receptors EP(1-4) and MCP-1 was analyzed by RT-PCR from pancreatic specimens and AR42J cells.
  • MCP-1 secretion was detected by ELISA from rat pancreatic lobuli.
  • We determined EP(1-4) mRNA levels in WBN/Kob rats with chronic pancreatic inflammation.
  • Individual isoforms were highly increased in rat pancreas, concurrent with MCP-1 mRNA expression.
  • In supernatants of pancreatic lobuli and AR42J cells, MCP-1 was detectable by ELISA.
  • In the presence of TNF-alpha, MCP-1 was upregulated.
  • Coincubation with PGE(2) enhanced the TNF-alpha-induced MCP-1 synthesis significantly.
  • Similarly, TNF-alpha mRNA was synergistically upregulated by TNF-alpha and PGE(2).
  • Furthermore, the synergistic effect of TNF-alpha and PGE(2) was abolished by inhibition of PKA but not of PKC.
  • We conclude that EP receptors are upregulated during chronic pancreatic inflammation.
  • PGE(2) modulates the TNF-alpha-induced MCP-1 synthesis and secretion from acinar cells.
  • This mechanism might explain the COX-2-dependent propagation of pancreatic inflammation.
  • [MeSH-major] Chemokine CCL2 / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Dinoprostone / metabolism. Pancreas / metabolism. Pancreatitis / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Rats. Rats, Wistar

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  • (PMID = 17916652.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [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 / Tumor Necrosis Factor-alpha; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; K7Q1JQR04M / Dinoprostone
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77. Tascilar O, Cakmak GK, Tekin IO, Emre AU, Ucan BH, Bahadir B, Acikgoz S, Irkorucu O, Karakaya K, Balbaloglu H, Kertis G, Ankarali H, Comert M: Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis. World J Gastroenterol; 2007 Dec 14;13(46):6172-82
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  • Tissue levels of TNF-alpha, IL-2 and IL-6 were screened immunohistochemically.
  • The level of tumor necrosis factor-alpha (TNF-alpha) and IL-6 and accumulation of ox-LDL were evident in the lung tissues of ANP groups when compared to EPO groups, particularly at 72 h.
  • CONCLUSION: EPO administration leads to a significant decrease in ALI parameters by inhibiting polymorphonuclear leukocyte (PMNL) accumulation, decreasing the levels of proinflammatory cytokines in circulation, preserving microvascular endothelial cell integrity and reducing oxidative stress-associated lipid peroxidation and therefore, can be regarded as a cytoprotective agent in ANP-induced ALI.
  • [MeSH-major] Erythropoietin / pharmacology. Pancreatitis, Acute Necrotizing / complications. Respiratory Distress Syndrome, Adult / etiology. Respiratory Distress Syndrome, Adult / prevention & control
  • [MeSH-minor] Amylases / blood. Animals. Body Weight. Disease Models, Animal. Interleukin-2 / blood. Interleukin-6 / blood. Lipoproteins, LDL / metabolism. Lung / metabolism. Lung / pathology. Male. Malondialdehyde / metabolism. Neutrophils / pathology. Pleural Effusion. Pulmonary Alveoli / pathology. Rats. Rats, Wistar. Taurodeoxycholic Acid

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  • (PMID = 18069756.001).
  • [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 / Interleukin-2; 0 / Interleukin-6; 0 / Lipoproteins, LDL; 0 / oxidized low density lipoprotein; 11096-26-7 / Erythropoietin; 4Y8F71G49Q / Malondialdehyde; 516-50-7 / Taurodeoxycholic Acid; EC 3.2.1.- / Amylases
  • [Other-IDs] NLM/ PMC4171226
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78. Szabo G, Mandrekar P, Oak S, Mayerle J: Effect of ethanol on inflammatory responses. Implications for pancreatitis. Pancreatology; 2007;7(2-3):115-23
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  • BACKGROUND/AIMS: Alcohol use alters inflammatory cell responses.
  • While alcohol has direct effects on pancreatic acinar cells, activation of inflammatory cells is a major component of the pathology of alcoholic pancreatitis.
  • Our results support the hypothesis that both acute alcohol intake in the presence of complex stimuli (such as necrotic cells) and chronic alcohol exposure result in hyper-responsiveness of monocytes to inflammatory signals and may contribute to increased inflammation in pancreatitis.

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  • [Copyright] (c) 2007 S. Karger AG, Basel and IAP.
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  • (PMID = 17592223.001).
  • [ISSN] 1424-3903
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / R01 AA011576; United States / NIAAA NIH HHS / AA / AA00577; United States / NIAAA NIH HHS / AA / AA011576
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / TLR2 protein, human; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 3K9958V90M / Ethanol
  • [Number-of-references] 45
  • [Other-IDs] NLM/ PMC2790780
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