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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. 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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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

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

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

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  • (PMID = 17158765.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Indium Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptor, Cholecystokinin B; 0 / Receptors, Somatostatin; 142694-57-3 / SDZ 215-811; 7A314HQM0I / Pentetic Acid; RWM8CCW8GP / Octreotide
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6. Manna P, Sinha M, Sil PC: Protective role of arjunolic acid in response to streptozotocin-induced type-I diabetes via the mitochondrial dependent and independent pathways. Toxicology; 2009 Mar 4;257(1-2):53-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pancreatic beta-cell death is the cause of decreased insulin production in diabetes.
  • Streptozotocin (STZ) is widely used to induce experimental diabetes due to its ability to selectively target and destroy insulin producing pancreatic beta-cells via the formation of both reactive oxygen species (ROS) and RNS (reactive nitrogen species).
  • This study investigated the prophylactic role of arjunolic acid (AA) against STZ-induced diabetes in the pancreas tissue of the Swiss albino rats (as a working model).
  • We observed that STZ administration (at a dose of 65mg/kg body weight, injected in the tail vain) caused increased production of both ROS and RNS in the pancreas tissue of experimental animals.
  • Formation of these reactive intermediates decreased the intracellular antioxidant defense, increased the levels of lipid peroxidation, protein carbonylation, serum glucose and TNF-alpha.
  • Investigating the signaling pathways, we found that STZ administration caused the activation of phospho-ERK1/2, phospho-p38, NF-kappaB and destruction of mitochondrial transmembrane potential, release of cytochrome c as well as activation of caspase 3 in the pancreas tissue keeping the levels of total ERK1/2 and p38 significantly unchanged.
  • Treatment of animals with AA (at a dose of 20mg/kg body weight, orally) both prior and post to the STZ administration effectively reduced these adverse effects by inhibiting the excessive ROS and RNS formation as well as by down-regulating the activation of phospho-ERK1/2, phospho-p38, NF-kappaB and mitochondrial dependent signal transduction pathways leading to apoptotic cell death.
  • [MeSH-major] Antioxidants / pharmacology. Diabetes Mellitus, Experimental / drug therapy. Diabetes Mellitus, Type 1 / drug therapy. Hypoglycemic Agents / pharmacology. Mitochondria / drug effects. Pancreas / drug effects. Triterpenes / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blood Glucose / drug effects. Caspase 3 / metabolism. Cytochromes c / metabolism. Dose-Response Relationship, Drug. Lipid Peroxidation / drug effects. Male. Membrane Potential, Mitochondrial / drug effects. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. NF-kappa B / metabolism. Oxidative Stress / drug effects. Phosphorylation. Protein Carbonylation / drug effects. Rats. Reactive Nitrogen Species / metabolism. Reactive Oxygen Species / metabolism. Time Factors. Tumor Necrosis Factor-alpha / blood. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19133311.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Blood Glucose; 0 / Hypoglycemic Agents; 0 / NF-kappa B; 0 / Reactive Nitrogen Species; 0 / Reactive Oxygen Species; 0 / Triterpenes; 0 / Tumor Necrosis Factor-alpha; 465-00-9 / arjunolic acid; 9007-43-6 / Cytochromes c; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3
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7. Hsieh PS: Inflammatory change of fatty liver induced by intraportal low-dose lipopolysaccharide infusion deteriorates pancreatic insulin secretion in fructose-induced insulin-resistant rats. Liver Int; 2008 Sep;28(8):1167-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inflammatory change of fatty liver induced by intraportal low-dose lipopolysaccharide infusion deteriorates pancreatic insulin secretion in fructose-induced insulin-resistant rats.
  • BACKGROUND: This study tested whether subacute inflammatory change of fatty liver induced by portal endotoxaemia is detrimental to pancreatic insulin secretion in fructose-fed rats (FFRs) with fatty liver.
  • In another set of experiments, the liver and pancreatic tissues were obtained for histological examination in these four groups.
  • Pancreatic insulin secretion was evaluated by in vivo hyperglycaemic clamp study.
  • The increased white blood cell count was also noted in rats after intraportal LPS infusion for 2 and 4 weeks.
  • Increased histopathological scores of liver and pancreas shown in FFRs were further increased in those combined with portal endotoxaemia.
  • CONCLUSION: This study demonstrates that the chronic subacute inflammatory change of fatty liver induced by mild portal endotoxaemia could deteriorate insulin secretion in a rodent model of metabolic syndrome and fatty liver.
  • [MeSH-major] Fatty Liver / physiopathology. Insulin / secretion. Metabolic Syndrome X / physiopathology. Pancreas / physiopathology
  • [MeSH-minor] Animals. Blood Pressure. Endotoxins / blood. Fructose / adverse effects. Glucose / administration & dosage. Glucose / adverse effects. Glucose Clamp Technique. Hyperglycemia / chemically induced. Infusions, Parenteral. Interleukin-6 / blood. Lipopolysaccharides / administration & dosage. Lipopolysaccharides / toxicity. Liver / pathology. Male. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 18397237.001).
  • [ISSN] 1478-3231
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endotoxins; 0 / Insulin; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 30237-26-4 / Fructose; IY9XDZ35W2 / Glucose
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8. Flohé SB, Agrawal H, Flohé S, Rani M, Bangen JM, Schade FU: Diversity of interferon gamma and granulocyte-macrophage colony-stimulating factor in restoring immune dysfunction of dendritic cells and macrophages during polymicrobial sepsis. Mol Med; 2008 May-Jun;14(5-6):247-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diversity of interferon gamma and granulocyte-macrophage colony-stimulating factor in restoring immune dysfunction of dendritic cells and macrophages during polymicrobial sepsis.
  • The development of immunosuppression during polymicrobial sepsis is associated with the failure of dendritic cells (DC) to promote the polarization of T helper (Th) cells toward a protective Th1 type.
  • The aim of the study was to test potential immunomodulatory approaches to restore the capacity of splenic DC to secrete interleukin (IL) 12 that represents the key cytokine in Th1 cell polarization.
  • DC from septic mice showed an impaired capacity to release the pro-inflammatory and Th1-promoting cytokines tumor necrosis factor alpha, IFN-gamma, and IL-12 in response to bacterial stimuli, but secreted IL-10.
  • [MeSH-major] Dendritic Cells / drug effects. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Interferon-gamma / pharmacology. Macrophages / drug effects. Sepsis / prevention & control

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  • (PMID = 18297128.001).
  • [ISSN] 1076-1551
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Antigens, CD86; 0 / Receptors, Interferon; 0 / interferon gamma receptor; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2249752
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9. Huang CJ, Gurlo T, Haataja L, Costes S, Daval M, Ryazantsev S, Wu X, Butler AE, Butler PC: Calcium-activated calpain-2 is a mediator of beta cell dysfunction and apoptosis in type 2 diabetes. J Biol Chem; 2010 Jan 1;285(1):339-48
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  • [Title] Calcium-activated calpain-2 is a mediator of beta cell dysfunction and apoptosis in type 2 diabetes.
  • The islet in type 2 diabetes (T2DM) and the brain in neurodegenerative diseases share progressive cell dysfunction, increased apoptosis, and accumulation of locally expressed amyloidogenic proteins (islet amyloid polypeptide (IAPP) in T2DM).
  • Excessive activation of the Ca(2+)-sensitive protease calpain-2 has been implicated as a mediator of oligomer-induced cell death and dysfunction in neurodegenerative diseases.
  • To establish if human IAPP toxicity is mediated by a comparable mechanism, we overexpressed human IAPP in rat insulinoma cells and freshly isolated human islets.
  • Pancreas was also obtained at autopsy from humans with T2DM and nondiabetic controls.
  • We report that overexpression of human IAPP leads to the formation of toxic oligomers and increases beta cell apoptosis mediated by increased cytosolic Ca(2+) and hyperactivation of calpain-2.
  • Cleavage of alpha-spectrin, a marker of calpain hyperactivation, is increased in beta cells in T2DM.
  • We conclude that overactivation of Ca(2+)-calpain pathways contributes to beta cell dysfunction and apoptosis in T2DM.

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  • (PMID = 19861418.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK059579; United States / NIDDK NIH HHS / DK / DK059579
  • [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 / Amyloid; 0 / Dipeptides; 0 / Islet Amyloid Polypeptide; 0 / Recombinant Fusion Proteins; 117591-20-5 / calpeptin; 12634-43-4 / Spectrin; EC 3.4.22.- / Calpain; EC 3.4.22.53 / calpain 2, human; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2804181
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10. Viterbo D, Zenilman ME, Bluth MH: Comparison of His and GST tagged versions of recombinant pancreatitis associated protein 2 in modulation of inflammatory responses. Inflamm Res; 2010 Oct;59(10):827-35
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  • However, continued study of PAP has been hampered by the ability to effectively isolate appropriate amounts of protein from pancreatic juice or efficient generation of recombinant proteins.
  • METHODS: His or GST tagged rPAP2 were generated, cultured with clonal (NR8383) macrophages and compared with respect to inflammatory cytokine expression (IL-1alpha, IL-1beta, IL-6, and TNF-alpha) and bacterial (E. coli) agglutination.
  • RESULTS: PAP2His treatment induced a 3.6, 2.8, 13.0, 3.5 fold induction of IL-1alpha, IL-1beta, TNF-alpha and IL-6, respectively; similar cytokine expression changes were observed with PAP2GST treatment (3.9, 2.6, 12.2, and 3.0 fold induction of IL-1alpha, IL-1beta, TNF-alpha and IL-6, respectively) (P<0.05).
  • [MeSH-major] Antigens, Neoplasm / immunology. Biomarkers, Tumor / immunology. Inflammation / immunology. Lectins, C-Type / immunology. Protein Isoforms / immunology

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  • (PMID = 20396928.001).
  • [ISSN] 1420-908X
  • [Journal-full-title] Inflammation research : official journal of the European Histamine Research Society ... [et al.]
  • [ISO-abbreviation] Inflamm. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Protein Isoforms; 0 / Recombinant Fusion Proteins; 0 / pancreatitis-associated protein
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11. Guzy RD, Sharma B, Bell E, Chandel NS, Schumacker PT: Loss of the SdhB, but Not the SdhA, subunit of complex II triggers reactive oxygen species-dependent hypoxia-inducible factor activation and tumorigenesis. Mol Cell Biol; 2008 Jan;28(2):718-31
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  • Mitochondrial complex II is a tumor suppressor comprised of four subunits (SdhA, SdhB, SdhC, and SdhD).
  • Mutations in any of these should disrupt complex II enzymatic activity, yet defects in SdhA produce bioenergetic deficiency while defects in SdhB, SdhC, or SdhD induce tumor formation.
  • We show that the inhibition of distal subunits of complex II, either pharmacologically or via RNA interference of SdhB, increases normoxic reactive oxygen species (ROS) production, increases hypoxia-inducible factor alpha (HIF-alpha) stabilization in an ROS-dependent manner, and increases growth rates in vitro and in vivo without affecting hypoxia-mediated activation of HIF-alpha.
  • Proximal pharmacologic inhibition or RNA interference of complex II at SdhA, however, does not increase normoxic ROS production or HIF-alpha stabilization and results in decreased growth rates in vitro and in vivo.
  • Furthermore, the enhanced growth rates resulting from SdhB suppression are inhibited by the suppression of HIF-1alpha and/or HIF-2alpha, indicating that the mechanism of SdhB-induced tumor formation relies upon ROS production and subsequent HIF-alpha activation.
  • Therefore, differences in ROS production, HIF proliferation, and cell proliferation contribute to the differences in tumor phenotype in cells lacking SdhB as opposed to those lacking SdhA.

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  • (PMID = 17967865.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL35440; United States / NHLBI NIH HHS / HL / HL079650; United States / NHLBI NIH HHS / HL / R01 HL079650; United States / NHLBI NIH HHS / HL / HL32646; United States / NHLBI NIH HHS / HL / R01 HL035440
  • [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 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Iron-Sulfur Proteins; 0 / Protein Subunits; 0 / Reactive Oxygen Species; EC 1.3.5.1 / Electron Transport Complex II; EC 1.3.5.1 / SDHA protein, human; EC 1.3.5.1 / SDHB protein, human; EC 1.3.99.1 / Succinate Dehydrogenase
  • [Other-IDs] NLM/ PMC2223429
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12. Hauge-Evans AC, Richardson CC, Milne HM, Christie MR, Persaud SJ, Jones PM: A role for kisspeptin in islet function. Diabetologia; 2006 Sep;49(9):2131-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A role for kisspeptin in islet function.
  • AIMS/HYPOTHESIS: We investigated the production of kisspeptin (KISS1) and the KISS1 receptor, GPR54, in pancreatic islets and determined the effects of exogenous kisspeptin on insulin secretion.
  • METHODS: RT-PCR and immunohistochemistry were used to detect expression of KISS1 and GPR54 mRNAs and the production of KISS1 and GPR54 in human and mouse islets and in beta (MIN6) and alpha- (alphaTC1) cell lines.
  • RESULTS: KISS1 and GPR54 mRNAs were both detected in human and mouse islets, and GPR54 mRNA expression was also found in the MIN6 and alphaTC1 endocrine cell lines.
  • In sections of mouse pancreas, KISS1 and GPR54 immunoreactivities were co-localised in both beta and alpha cells within islets, but were not detected in the exocrine pancreas.
  • In contrast, KISS1 inhibited insulin secretion from MIN6 cells at both 2 and 20 mmol/l glucose.
  • KISS1 had no significant effect on glucagon secretion from mouse islets.
  • CONCLUSIONS/INTERPRETATION: This is the first report to show that the GPR54/KISS1 system is expressed in the endocrine pancreas, where it influences beta cell secretory function.
  • These observations suggest an important role for this system in the normal regulation of islet function.
  • [MeSH-major] Islets of Langerhans / metabolism. Proteins / physiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Gene Expression. Glucagon / metabolism. Humans. Immunohistochemistry. In Vitro Techniques. Insulin / secretion. Kisspeptins. Mice. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Receptors, G-Protein-Coupled / physiology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16826407.001).
  • [ISSN] 0012-186X
  • [Journal-full-title] Diabetologia
  • [ISO-abbreviation] Diabetologia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Insulin; 0 / KISS1 protein, human; 0 / KISS1R protein, human; 0 / Kiss1 protein, mouse; 0 / Kiss1r protein, mouse; 0 / Kisspeptins; 0 / Proteins; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Proteins; 9007-92-5 / Glucagon
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13. 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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14. Li W, Nakagawa T, Koyama N, Wang X, Jin J, Mizuno-Horikawa Y, Gu J, Miyoshi E, Kato I, Honke K, Taniguchi N, Kondo A: Down-regulation of trypsinogen expression is associated with growth retardation in alpha1,6-fucosyltransferase-deficient mice: attenuation of proteinase-activated receptor 2 activity. Glycobiology; 2006 Oct;16(10):1007-19
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  • Consistently, the expression of trypsinogen proteins was found to be lower in Fut8-/- mice in the duodenum, small intestine, and pancreas.
  • Trypsin, an active form of trypsinogen, regulates cell growth through a G-protein-coupled receptor, the proteinase-activated receptor 2 (PAR-2).
  • In a cell culture system, a Fut8 knockdown mouse pancreatic acinar cell carcinoma, TGP49-Fut8-KDs, showed decreased growth rate, similar to that seen in Fut8-/- mice, and the decreased growth rate was rescued by the application of the PAR-2-activating peptide (SLIGRL-NH2).
  • Our findings clearly demonstrate a relationship between Fut8 and the regulation of EGF receptor (EGFR)-trypsin-PAR-2 pathway in controlling cell growth and that the EGFR-trypsin-PAR-2 pathway is suppressed in TGP49-Fut8-KDs as well as in Fut8-/- mice.
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Down-Regulation. Embryo, Mammalian / metabolism. Male. Mice. Mice, Knockout. Oligopeptides / pharmacology. Phosphorylation. Receptor, Epidermal Growth Factor / metabolism. Tumor Cells, Cultured

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  • (PMID = 16861703.001).
  • [ISSN] 0959-6658
  • [Journal-full-title] Glycobiology
  • [ISO-abbreviation] Glycobiology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Receptor, PAR-2; 0 / seryl-leucyl-isoleucyl-glycyl--arginyl-leucinamide; 9002-08-8 / Trypsinogen; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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15. Li BZ, Zhu L, Duan W: [Clinicopathologic study of tumors of intermediate trophoblasts]. Zhonghua Bing Li Xue Za Zhi; 2006 Dec;35(12):722-6
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  • [Title] [Clinicopathologic study of tumors of intermediate trophoblasts].
  • OBJECTIVE: To study the clinicopathologic features and immunophenotype of placental site trophoblastic tumor (PSTT) and epithelioid trophoblastic tumor (ETT).
  • METHODS: During the period from 1959 to 2005, a total of 1012 cases of gestational trophoblastic disease were diagnosed in Beijing Obstetrics and Gynecology Hospital.
  • Immunohistochemical study for cytokeratin 18, human chorionic gonadotropin (hCG), human placental lactogen (hPL), Mel-CAM (CD146), placental-like alkaline phosphatase (PLAP), epithelial membrane antigen (EMA), inhibin-alpha and proliferative cell nuclear antigen (PCNA) were performed.
  • The morphologic features and immunohistochemical findings were compared with those of the controlled group which consisted of 20 cases of early gestational villi with decidua basalis and 20 cases of hydatidiform moles with implantation site.
  • Uterine curettage could achieve an accurate pathologic diagnosis in 60% of cases.
  • Histologically, PSTT cells permeated between the myometrial fibers and vessels either individually or connecting in cords or sheets in a manner reminiscent of the implantation site reaction.
  • ETT composed of a relatively uniform population of mononuclear trophoblastic cells, clumping together in nests as the cell islets associating with eosinophilic, fibrillary and hyaline material and necrotic debris, forming a "geographic map" like pattern.
  • Immunohistochemical study for hPL, hCG, Mel-CAM (CD146) and PLAP was most helpful for the differential diagnosis.
  • One case of PSTT developed metastasis in pancreas, 5 months after the operation.
  • The remaining patients survived without tumor recurrence.
  • CONCLUSIONS: PSTT is a tumor of implantation site intermediate trophoblasts while ETT differentiates towards chorionic-type intermediate trophoblasts.
  • The different pathologic features and immunophenotype observed were closely related with the difference in tumor cell differentiation.
  • An accurate pathologic diagnosis of the uterine curettage material is important for the clinical management.
  • [MeSH-major] Trophoblastic Neoplasms / pathology. Trophoblastic Tumor, Placental Site / pathology. Uterine Neoplasms / pathology
  • [MeSH-minor] Adult. Alkaline Phosphatase / metabolism. Antigens, CD146 / metabolism. Chorionic Gonadotropin / metabolism. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Hysterectomy / methods. Immunohistochemistry. Isoenzymes / metabolism. Middle Aged. Placental Lactogen / metabolism. Pregnancy. Prognosis

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  • (PMID = 17374255.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD146; 0 / Chorionic Gonadotropin; 0 / Isoenzymes; 0 / MCAM protein, human; 0 / germ-cell AP isoenzyme; 9035-54-5 / Placental Lactogen; EC 3.1.3.1 / Alkaline Phosphatase
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16. Harikumar KB, Sung B, Tharakan ST, Pandey MK, Joy B, Guha S, Krishnan S, Aggarwal BB: Sesamin manifests chemopreventive effects through the suppression of NF-kappa B-regulated cell survival, proliferation, invasion, and angiogenic gene products. Mol Cancer Res; 2010 May;8(5):751-61
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  • [Title] Sesamin manifests chemopreventive effects through the suppression of NF-kappa B-regulated cell survival, proliferation, invasion, and angiogenic gene products.
  • Because the transcription factor NF-kappaB has been associated with inflammation, carcinogenesis, tumor cell survival, proliferation, invasion, and angiogenesis of cancer, we postulated that sesamin might mediate its effect through the modulation of the NF-kappaB pathway.
  • We found that sesamin inhibited the proliferation of a wide variety of tumor cells including leukemia, multiple myeloma, and cancers of the colon, prostate, breast, pancreas, and lung.
  • Sesamin also potentiated tumor necrosis factor-alpha-induced apoptosis and this correlated with the suppression of gene products linked to cell survival (e.g., Bcl-2 and survivin), proliferation (e.g., cyclin D1), inflammation (e.g., cyclooxygenase-2), invasion (e.g., matrix metalloproteinase-9, intercellular adhesion molecule 1), and angiogenesis (e.g., vascular endothelial growth factor).

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  • [Copyright] (c)2010 AACR.
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  • (PMID = 20460401.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-124787-01A2; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P01 CA124787; United States / NCI NIH HHS / CA / P01 CA091844-020004; United States / NCI NIH HHS / CA / P01 CA091844; United States / NCI NIH HHS / CA / CA-16 672; United States / NCI NIH HHS / CA / CA124787-020002; United States / NCI NIH HHS / CA / CA091844-010004; United States / NCI NIH HHS / CA / P01 CA124787-01A20002; United States / NCI NIH HHS / CA / P01 CA091844-010004; United States / NCI NIH HHS / CA / CA091844-020004; United States / NCI NIH HHS / CA / CA124787-01A20002; United States / NCI NIH HHS / CA / P01 CA124787-020002
  • [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 / Angiogenic Proteins; 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / Dioxoles; 0 / Growth Inhibitors; 0 / Lignans; 0 / NF-kappa B; 8008-74-0 / Sesame Oil; S7946O4P76 / sesamin
  • [Other-IDs] NLM/ NIHMS196068; NLM/ PMC2895997
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17. 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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18. 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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19. Pejcić I, Vrbić S, Filipović S, Sćekić M, Petković I, Pejcić L, Djenić N: [Significance of serum tumor markers monitoring metastases in carcinomas of unknown primary site]. Vojnosanit Pregl; 2010 Sep;67(9):723-31
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  • [Title] [Significance of serum tumor markers monitoring metastases in carcinomas of unknown primary site].
  • BACKGROUND/AIM: Unknown primary tumors represent a heterogeneous group of malignancies that are indicative of ominous prognosis.
  • Cancer of unknown primary site (CUP) is defined as the lack of any detectable primary site after full evaluation, and accounts for approximately 3-5% of all newly diagnosed patients with malignancies.
  • The aim of this report was to present the prognostic and predictive value of 8 serum tumor markers in this group of patients.
  • On histological examination, all the patients were presented with metastatic tumors whose primary site (origin) could not be detected with noninvasive diagnostic techniques.
  • In all the cases we evaluated 8 serum tumor markers: alpha-fetoproteins (AFP), chronic gonadotrophin beta submit, human (beta-HCG), neuron specific enolase (NSE), marker of malignant ovarian tumors (CA 125), prostate-specific antigene (PSA), marker of malignant brest tumor (CA 15-3), marker of malignant pancreas tumor and gastrointestinal tumor (Ca 19-9), carcinoembryonic antigen (CEA) at the time of diagnosis.
  • The patients responding to chemotherapy with complete response (CR), partial response (PR) or stable disease (SD) had the markers determined after three-month periods until the time of relapse or progression.
  • Average tumor marker values before and after the chemotherapy were significantly lower for NSE and CA 125.
  • CONCLUSION: Increased values of serum tumor markers are very often in CUP.
  • The tumors show nonspecific overexpression of tumor markers.
  • However, a routine evaluation of commonly used serum tumor markers has not been proven of any prognostic and predictive assistance.
  • [MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / blood. Carcinoma / secondary. Carcinoma, Squamous Cell / secondary. Neoplasms, Unknown Primary / pathology


20. 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


21. 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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22. Yang L, Kang WK: The effect of HIF-1alpha siRNA on growth and chemosensitivity of MIA-paca cell line. Yonsei Med J; 2008 Apr 30;49(2):295-300
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  • [Title] The effect of HIF-1alpha siRNA on growth and chemosensitivity of MIA-paca cell line.
  • HIF-1alpha induction by various stimuli contributes to cell proliferation and survival.
  • To investigate the effect of HIF-1alpha, we used small interfering RNA (siRNA), and expected that cell apoptosis and sensitivity to chemotherapeutic drug increase, when we blocked the HIF-1alpha gene.
  • Thus we performed in vitro and in vivo experiment to clarify the effect of hypoxia-inducible factor-1alpha on tumor growth.
  • MATERIALS AND METHODS: We made control and HIF-1alpha siRNA using vector plasmid and then transfected Mia-paca cell lines with these RNAs.
  • After selection with geneticin, two new cell lines were made, confirmed via immunoblotting.
  • After treating with gemcitabine, each cell line was assayed to confirm the effect of HIF-1alpha siRNA using the cell proliferation assay and capase-3 assay.
  • After subcutaneously injecting each new cell lines, intraperitoneal gemicitabine chemotherapy was performed for 3 weeks.
  • During that period, we analyzed the difference of tumor growth rate.
  • RESULTS: The tumor growth of HIF-1alpha siRNA-transfected group was slower than that of the control group both in vitro and in vivo experiment.
  • CONCLUSION: The suppression of HIF-1alpha results in decrease of cell proliferation and increase of chemosensitivity of pancreatic cancer cell line.
  • Therefore, targeting the HIF-1alpha may be useful treatment modality for some pancreatic cancers.
  • [MeSH-major] Cell Proliferation. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. RNA Interference. RNA, Small Interfering / genetics
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / pharmacology. Blotting, Western. Caspase 3 / metabolism. Cell Hypoxia. Cell Line, Tumor. Cell Survival / drug effects. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Female. Humans. Mice. Random Allocation. Transfection

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  • (PMID = 18452268.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095643
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ PMC2615320
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23. Ferrand A, Vatinel S, Kowalski-Chauvel A, Bertrand C, Escrieut C, Fourmy D, Dufresne M, Seva C: Mechanism for Src activation by the CCK2 receptor: Patho-physiological functions of this receptor in pancreas. World J Gastroenterol; 2006 Jul 28;12(28):4498-503
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  • [Title] Mechanism for Src activation by the CCK2 receptor: Patho-physiological functions of this receptor in pancreas.
  • AIM: To investigate in vivo, whether CCK2 receptors (CCK2R) regulate proteins known to play a crucial role in cell proliferation and cancer development and analyse in vitro the molecular mechanisms that lead to Src activation; in particular, to identify the domains within the CCK2R sequence that are implicated in this activation.
  • We used pancreatic tissues derived from wild type or Elas-CCK2 mice that expressed the CCK2R in pancreatic acini, displayed an increased pancreatic growth and developed preneoplastic lesions.
  • The pancreatic tumor cell line AR4-2J expressing the endogenous CCK2R or COS-7 cells transiently transfected with wild type or mutant CCK2R were used as in vitro models to study the mechanism of Src activation.
  • Src activation was measured by in vitro kinase assays, ERK activation by western blot using anti-phospho-ERK antibodies and the involvement of Src in gastrin-induced cell proliferation by MTT test.
  • RESULTS: We showed in vivo that the targeted CCK2R expression in the pancreas of Elas-CCK2 mice, led to the activation of Src and the ERK pathway.
  • Src was activated upstream of the ERK pathway by the CCK2R in pancreatic tumoral cells and contributed to the proliferative effects mediated by this receptor.
  • CONCLUSION: Deregulation of the Src/ERK pathway by the CCK2R might represent an early step that contributes to cell proliferation, formation of preneoplastic lesions and pancreatic tumor development.
  • [MeSH-major] Pancreas / metabolism. Pancreatic Neoplasms / physiopathology. Precancerous Conditions / physiopathology. Receptor, Cholecystokinin B / physiology. src-Family Kinases / metabolism
  • [MeSH-minor] Amino Acid Motifs / physiology. Animals. Cell Line. Cell Proliferation. Cell Transformation, Neoplastic. Enzyme Activation / physiology. Extracellular Signal-Regulated MAP Kinases / metabolism. GTP-Binding Protein alpha Subunits, Gq-G11 / physiology. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Mice. Mice, Transgenic. Protein Structure, Tertiary / physiology. Signal Transduction / physiology

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  • (PMID = 16874861.001).
  • [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 / Receptor, Cholecystokinin B; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11
  • [Other-IDs] NLM/ PMC4125636
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24. 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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25. Thirabanjasak D, Basturk O, Altinel D, Cheng JD, Adsay NV: Is serous cystadenoma of the pancreas a model of clear-cell-associated angiogenesis and tumorigenesis? Pancreatology; 2009;9(1-2):182-8
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  • [Title] Is serous cystadenoma of the pancreas a model of clear-cell-associated angiogenesis and tumorigenesis?
  • BACKGROUND: Similar to the other von Hippel-Lindau (VHL)-related tumors such as renal cell carcinomas and capillary hemangioblastomas, serous cystadenomas (SCAs) of the pancreas are also characterized by clear cells.
  • Over the years, we have also noticed that the tumor epithelium shows a prominent capillary network.
  • METHODS: Eighteen cases of SCA were reviewed histologically, and immunohistochemical analysis was performed for CD31 and vascular endothelial growth factor (VEGF) as well as the molecules implicated in clear-cell tumorigenesis: GLUT-1, hypoxia-inducible factor-1 (HIF-1alpha), and carbonic anhydrase IX (CA IX).
  • RESULTS: There was an extensively rich capillary network that appears almost intraepithelially in all cases of SCA, which was confirmed by CD31 stain that showed, on average, 26 capillaries per every 100 epithelial cells.
  • Among the clear-cell tumorigenesis markers, CA IX was detected in all cases, GLUT-1 and HIF-1alpha in most cases.
  • CONCLUSION: As in other VHL-related clear-cell tumors, there is a prominent capillary network immediately adjacent to the epithelium of SCA, confirming that the clear-cell- angiogenesis association is also valid for this tumor type.
  • Molecules implicated in clear-cell tumorigenesis are also consistently expressed in SCA.
  • More importantly, SCA may also serve as a model of clear-cell-associated angiogenesis and tumorigenesis, and the information gained from this tumor type may also be applicable to other clear-cell tumors.

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  • [Copyright] Copyright 2008 S. Karger AG, Basel and IAP.
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  • (PMID = 19077470.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA101936; United States / NCI NIH HHS / CA / CA101936
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Glucose Transporter Type 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC2835376
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26. 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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27. 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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28. Liao SY, Lerman MI, Stanbridge EJ: Expression of transmembrane carbonic anhydrases, CAIX and CAXII, in human development. BMC Dev Biol; 2009 Mar 16;9:22
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  • BACKGROUND: Transmembrane CAIX and CAXII are members of the alpha carbonic anhydrase (CA) family.
  • Expression of CAIX and CAXII proteins in tumor tissues is primarily induced by hypoxia and this is particularly true for CAIX, which is regulated by the transcription factor, hypoxia inducible factor-1 (HIF-1).
  • Their distributions in normal adult human tissues are restricted to highly specialized cells that are not always hypoxic.
  • RESULTS: The co-localization of CAIX and HIF-1alpha was limited to certain cell types in embryonic and early fetal tissues.
  • Those cells comprised the primitive mesenchyma or involved chondrogenesis and skin development.
  • Transient CAIX expression was limited to immature tissues of mesodermal origin and the skin and ependymal cells.
  • The only tissues that persistently expressed CAIX protein were coelomic epithelium (mesothelium) and its remnants, the epithelium of the stomach and biliary tree, glands and crypt cells of duodenum and small intestine, and the cells located at those sites previously identified as harboring adult stem cells in, for example, the skin and large intestine.
  • CAXII expression is restricted to cells involved in secretion and water absorption such as parietal cells of the stomach, acinar cells of the salivary glands and pancreas, epithelium of the large intestine, and renal tubules.
  • 3) CAIX and CAXII expression is closely related to cell origin and secretory activity involving proton transport, respectively.
  • The intriguing finding of rare CAIX-expressing cells in those sites corresponding to stem cell niches requires further investigation.

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  • (PMID = 19291313.001).
  • [ISSN] 1471-213X
  • [Journal-full-title] BMC developmental biology
  • [ISO-abbreviation] BMC Dev. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-56000; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2666674
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29. 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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30. 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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31. Marsh WL, Colonna J, Yearsley M, Bloomston M, Frankel WL: Calponin is expressed in serous cystadenomas of the pancreas but not in adenocarcinomas or endocrine tumors. Appl Immunohistochem Mol Morphol; 2009 May;17(3):216-9
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  • [Title] Calponin is expressed in serous cystadenomas of the pancreas but not in adenocarcinomas or endocrine tumors.
  • The diagnosis of serous microcystic adenoma (SMA) is usually straightforward.
  • For small biopsies and/or unusual variants, the differential diagnosis includes other pancreatic or metastatic neoplasms showing cystic or clear cell features.
  • We evaluated immunostains for potential use in the diagnosis of SMA.
  • Additionally, microarrays previously constructed from 56 pancreatic adenocarcinomas (PACs) and 64 pancreatic endocrine tumors (PENs) were studied.
  • The microarrays were stained with calponin, chromogranin, CD10, alpha-inhibin, and monoclonal neuron-specific enolase (m-NSE).
  • For SMAs, staining was seen with calponin (85.2%), alpha-inhibin (96.2%), and m-NSE (96.2%).
  • Staining for alpha-inhibin was absent in PACs and present in 4.1% of PENs; whereas immunoreactivity for m-NSE was present in 26.8% of PACs and 73.7% of PENs.
  • An immunohistochemical profile of staining with calponin, alpha-inhibin, and m-NSE and absent staining with chromogranin supports the diagnosis of SMA, and distinguishes SMA from PAC and PEN.
  • Calponin and alpha-inhibin are the most useful positive markers for SMA, and are negative in most entities in the differential diagnosis.

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  • (PMID = 19391217.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Microfilament Proteins; 0 / calponin; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins; EC 4.2.1.11 / Phosphopyruvate Hydratase
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32. Nishiuchi T, Imachi H, Murao K, Fujiwara M, Muraoka T, Kikuchi F, Nishiuchi Y, Kushida Y, Haba R, Ishida T: Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1). Endocrine; 2009 Aug;36(1):20-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1).
  • Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by tumors of the parathyroid glands, the anterior pituitary, and the endocrine pancreas.
  • He was admitted to our hospital because of recurrent hypoglycemia and a growth of pancreatic tumors.
  • He subsequently underwent surgery for the pancreatic tumors.
  • The majority of these tumor cells were immunohistochemically positive for insulin and negative for glucagon.
  • A few nodules showed immunohistochemical staining positivity for glucagon but they were negative for insulin.
  • Although it is uncommon for patients with MEN1 to exhibit insulinoma and glucagonoma, this case suggests the need for careful analysis of pancreatic tumors in patients with MEN1.
  • [MeSH-major] Glucagonoma / pathology. Insulinoma / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / pathology


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

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  • (PMID = 17193820.001).
  • [ISSN] 0740-2570
  • [Journal-full-title] Seminars in diagnostic pathology
  • [ISO-abbreviation] Semin Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 91
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34. van Grevenstein WM, Hofland LJ, Jeekel J, van Eijck CH: The expression of adhesion molecules and the influence of inflammatory cytokines on the adhesion of human pancreatic carcinoma cells to mesothelial monolayers. Pancreas; 2006 May;32(4):396-402
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of adhesion molecules and the influence of inflammatory cytokines on the adhesion of human pancreatic carcinoma cells to mesothelial monolayers.
  • OBJECTIVES: Pancreatic cancer has a tremendously deplorable prognosis.
  • Peritoneal dissemination frequently occurs after surgical resection of the tumor.
  • Specific adhesion molecules may be of great importance in local tumor recurrence.
  • The aim of this study was to investigate the effects of inflammatory cytokines, interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha), on the interaction between pancreatic tumor cells and mesothelial cells.
  • METHODS: An experimental in vitro model was designed using Panc-1, MiaPaCa-2, and BxPC-3 pancreatic carcinoma cell lines.
  • Primary cultures of mesothelial cells were incubated with the inflammatory cytokines, and after the incubation, the adherence of the different pancreatic cell lines was measured.
  • RESULTS: Preincubation of the mesothelial monolayer with IL-1beta or TNF-alpha resulted in enhanced tumor cell adhesion of the MiaPaCa-2 and BxPC-3 cells.
  • The amount of stimulation for the MiaPaCa-2 cells was more than 100% versus the control situation and for BxPC-3 cells between 20% to 35%.
  • IL-6 did not affect the tumor cell adhesion of the MiaPaCa-2 and BxPC-3 cells.
  • Mesothelial cells show a significant enhancement of expression of ICAM-1, VCAM-1, and CD44 after stimulation with IL-1beta and TNF-alpha.
  • CONCLUSIONS: The presented results prove that IL-1beta and TNF-alpha are significant stimulating factors in pancreatic tumor cell adhesion in vitro and may therefore account for tumor recurrence to the peritoneum in vivo.
  • The immunocytochemical staining results demonstrate that ICAM-1 and CD44 important adhesion molecules and interference with their function may decrease the incidence of peritoneal tumor recurrence after curative resection of pancreatic cancer.
  • [MeSH-major] Cell Adhesion Molecules / analysis. Cytokines / pharmacology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antigens, CD44 / analysis. Cell Adhesion / drug effects. Cell Line, Tumor. Epithelial Cells / pathology. Humans. Immunohistochemistry. Intercellular Adhesion Molecule-1 / analysis. Vascular Cell Adhesion Molecule-1 / analysis

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  • (PMID = 16670622.001).
  • [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, CD44; 0 / CD44 protein, human; 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1
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35. Matsueda K, Yamamoto H, Yoshida Y, Notohara K: Hepatoid carcinoma of the pancreas producing protein induced by vitamin K absence or antagonist II (PIVKA-II) and alpha-fetoprotein (AFP). J Gastroenterol; 2006 Oct;41(10):1011-9
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  • [Title] Hepatoid carcinoma of the pancreas producing protein induced by vitamin K absence or antagonist II (PIVKA-II) and alpha-fetoprotein (AFP).
  • We describe a rare case of hepatoid carcinoma of the pancreas with production of protein induced by vitamin K absence or antagonist II (PIVKA-II) and alpha-fetoprotein (AFP).
  • The patient was a 49-year-old woman admitted because of high serum levels of PIVKA-II (1.63 AU/ml) and AFP (623 ng/ml) and abnormal ultrasonographic findings of the pancreas, found incidentally at medical checkup.
  • Both ultrasonography and computed tomography showed swelling of the pancreas with small areas of low density, but no hepatic lesions.
  • A PIVKA-II and AFP-producing pancreatic cancer was strongly suspected, and total pancreatectomy was performed.
  • Pathological examination showed that the tumor cells were arranged in trabecular and solid patterns with bile production, and were immunohistochemically positive for PIVKA-II and AFP, resembling hepatocellular carcinoma cells.
  • The tumor was diagnosed as hepatoid carcinoma of the pancreas, and the patient has survived 48 months after initial diagnosis.
  • It is important that hepatoid carcinoma be considered as a possible malignant tumor of the pancreas, and simultaneous measurement of the serum levels of AFP and PIVKA-II will enable earlier diagnosis.
  • This is the first report describing hepatoid carcinoma of the pancreas producing PIVKA-II.
  • [MeSH-major] Biomarkers, Tumor / blood. Carcinoma, Hepatocellular / secretion. Pancreatic Neoplasms / secretion. Protein Precursors / secretion. Prothrombin / secretion. Vitamin K Deficiency / complications. alpha-Fetoproteins / secretion
  • [MeSH-minor] Biomarkers / blood. Cholangiopancreatography, Endoscopic Retrograde. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Immunohistochemistry. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 17096071.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Protein Precursors; 0 / alpha-Fetoproteins; 53230-14-1 / acarboxyprothrombin; 9001-26-7 / Prothrombin
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36. Ikemoto T, Yamaguchi T, Morine Y, Imura S, Soejima Y, Fujii M, Maekawa Y, Yasutomo K, Shimada M: Clinical roles of increased populations of Foxp3+CD4+ T cells in peripheral blood from advanced pancreatic cancer patients. Pancreas; 2006 Nov;33(4):386-90
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  • [Title] Clinical roles of increased populations of Foxp3+CD4+ T cells in peripheral blood from advanced pancreatic cancer patients.
  • OBJECTIVES: Further metastasis should be avoided in pancreatic cancer (PC) patients for effective surgical treatment.
  • Regulatory T cells (Foxp3CD4 T cells including CD4CD25 T cells and CD4CD25 T cells) play important roles in tumor immunity.
  • This study aimed to investigate whether regulatory T cells participate in metastasis.
  • The peripheral blood mononuclear cells (PBMCs) were subjected to FACScan analysis after labeling with anti-CD4, anti-CD25, and anti-Foxp3 antibodies.
  • Tumor markers, including DUPAN2 and CA19-9, surface markers, such as the CD4/CD8 ratio, and the CD57 cell population were assessed.
  • RESULTS: The Foxp3CD4 T-cell population among the PBMCs was significantly increased in PC patients (8.10% +/- 4.65%) compared with healthy donors (2.47 +/- 0.78%) (P < 0.001).
  • No significant relationships existed for the tumor markers, CD4/CD8 ratio, and CD57 cells.
  • However, a significant correlation was found between Foxp3CD4 T cells among the PBMCs and the TNM stage (P < 0.05).
  • CONCLUSIONS: Foxp3CD4 T cells are good markers for metastasis detection in PC patients and more accurate than other conventional tumor markers, especially at advanced stages of the disease.
  • [MeSH-major] Forkhead Transcription Factors / analysis. Pancreatic Neoplasms / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Aged. Female. Humans. Interleukin-2 Receptor alpha Subunit / analysis. Male. Middle Aged. Neoplasm Staging. T-Lymphocyte Subsets / immunology

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  • (PMID = 17079944.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit
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37. Eastham LL, Mills CN, Niles RM: PPARalpha/gamma expression and activity in mouse and human melanocytes and melanoma cells. Pharm Res; 2008 Jun;25(6):1327-33
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  • [Title] PPARalpha/gamma expression and activity in mouse and human melanocytes and melanoma cells.
  • PURPOSE: We examined the expression of PPARs and the effects of PPARalpha and PPARgamma agonists on growth of mouse and human melanocytes and melanoma cells.
  • METHODS: PPARalpha,beta, and PPARgamma mRNA qualitative expression in melan-a mouse melanocytes, B16 mouse melanoma, human melanocytes, and A375 and SK-mel28 human melanoma cells was determined by RT-PCR, while quantitative PPARalpha mRNA levels were determined by QuantiGene assay.
  • The effect of natural and synthetic PPAR ligands on cell growth was determined by either hemocytometer counting or crystal violet assay.
  • RESULTS: Both mouse and human melanoma cells produced more PPARalpha and PPARgamma protein compared to melanocytes.
  • PPARalpha mRNA levels were elevated in human melanoma cells, but not in mouse melanoma cells relative to melanocytes.
  • Silencing of PPARalpha in human melanoma cells did not alter cell proliferation or morphology.
  • PPARgamma-selective agonists inhibited the growth of both mouse and human melanoma cells, while PPARalpha-selective agonists had limited effects.
  • [MeSH-major] Melanocytes / metabolism. Melanoma / metabolism. PPAR alpha / physiology. PPAR gamma / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. RNA, Messenger / analysis. Transcriptional Activation

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

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  • (PMID = 16720919.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha
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39. Stone SP, Buescher LS: Life-threatening paraneoplastic cutaneous syndromes. Clin Dermatol; 2005 May-Jun;23(3):301-6
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  • [Title] Life-threatening paraneoplastic cutaneous syndromes.
  • Paraneoplastic syndromes are diseases or symptom complexes associated with malignancy, usually internal.
  • In this article, we discuss the link between malignancy and such dermatologic disorders as acanthosis nigricans, acrokeratosis paraneoplastica of Bazex, dermatomyositis, erythema gyratum repens, necrolytic migratory erythema (glucagonoma syndrome), and paraneoplastic pemphigus and discuss, where such information is known, the mechanism by which these paraneoplastic diseases occur.
  • [MeSH-major] Paraneoplastic Syndromes / diagnosis. Skin Diseases / diagnosis
  • [MeSH-minor] Critical Illness. Erythema / diagnosis. Humans. Neoplasms / diagnosis. Pemphigus / diagnosis

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  • (PMID = 15896545.001).
  • [ISSN] 0738-081X
  • [Journal-full-title] Clinics in dermatology
  • [ISO-abbreviation] Clin. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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40. Cheshire H, Stather P, Vorster J: Acquired acrodermatitis enteropathica due to zinc deficiency in a patient with pre-existing Darier's disease. J Dermatol Case Rep; 2009 Nov 28;3(3):41-3
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  • [Title] Acquired acrodermatitis enteropathica due to zinc deficiency in a patient with pre-existing Darier's disease.
  • Typically these patches start near the body's orifices before migrating to other sites, however in this patient the presentation was atypical thus delaying the diagnosis.
  • OBSERVATIONS: We report a case of an atypical presentation of acrodermatitis enteropathica (AE) due to acquired zinc deficiency in a 65 year old female patient with a previous diagnosis of histologically confirmed Darier's disease.
  • Acrodermatitis enteropathica typically presents in infants, either due to an autosomal recessive genetic disorder, or after the cessation of breast feeding.
  • In adults acquired zinc deficiency can be caused by glucagonoma syndrome, poor nutritional state, intestinal malabsorption, nephrotic syndrome and after major trauma (i.e. burns or significant surgery).
  • In our patient low zinc levels confirmed hypozincaemia and the diagnosis of acrodermatitis enteropathica.
  • CONCLUSION: We believe this to be an unusual presentation of acrodermatitis enteropathica due to a probable dietary zinc deficiency in a lady with pre-existing Darier's disease which may possibly have influenced the uncharacteristic clinical presentation.

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  • (PMID = 21886729.001).
  • [ISSN] 1898-7249
  • [Journal-full-title] Journal of dermatological case reports
  • [ISO-abbreviation] J Dermatol Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Other-IDs] NLM/ PMC3157796
  • [Keywords] NOTNLM ; Darier's disease / acrodermatitis enteropathica / hair loss / mucous membranes / zinc
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41. 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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42. Ma RY, Tam TS, Suen AP, Yeung PM, Tsang SW, Chung SK, Thomas MK, Leung PS, Yao KM: Secreted PDZD2 exerts concentration-dependent effects on the proliferation of INS-1E cells. Int J Biochem Cell Biol; 2006;38(5-6):1015-22
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  • [Title] Secreted PDZD2 exerts concentration-dependent effects on the proliferation of INS-1E cells.
  • PDZD2 (PDZ domain containing 2) is a multi-PDZ protein expressed in pancreas and many other tissues.
  • To understand the possible functional role of PDZD2 in pancreas, we investigated the cellular distribution of PDZD2 in adult pancreas using an antiserum that recognizes both the full-length and secreted forms of PDZD2.
  • Immunohistochemical analysis revealed a strong expression of PDZD2 in pancreatic islet beta cells but not alpha cells.
  • Consistent with the beta-cell-enriched expression of PDZD2, immunoblot analysis indicated expression of both full-length PDZD2 and sPDZD2 in the insulinoma cell line INS-1E.
  • A recombinant sPDZD2 protein was synthesized for study of its functional effect on INS-1E cells.
  • In culture media with limiting serum, co-incubation with sPDZD2 stimulated the proliferation of INS-1E cells.
  • As a potential mitogen of beta-like cells, sPDZD2 may be useful for the optimization of beta-cell growth and differentiation in vitro.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adult. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Insulin-Secreting Cells / metabolism. Mitogens / pharmacology. Neoplasm Proteins. Pancreas / metabolism

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  • (PMID = 16413998.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Intracellular Signaling Peptides and Proteins; 0 / Mitogens; 0 / Neoplasm Proteins; 0 / PDZD2 protein, human
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43. Nishida A, Andoh A, Inatomi O, Fujiyama Y: Interleukin-32 expression in the pancreas. J Biol Chem; 2009 Jun 26;284(26):17868-76
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  • [Title] Interleukin-32 expression in the pancreas.
  • We studied IL-32 expression in human pancreatic tissue and pancreatic cancer cell lines.
  • IL-32 was weakly immunoexpressed by pancreatic duct cells.
  • In the inflamed lesions of chronic pancreas, the ductal expression of IL-32 was markedly increased.
  • A strong expression of IL-32alpha was detected in the pancreatic cancer cells.
  • In pancreatic cancer cell lines (PANC-1, MIA PaCa-2, and BxPC-3 cells), the expression of IL-32 mRNA and protein was enhanced by IL-1beta, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha.
  • An inhibitor of phosphatidylinositol 3-kinase (LY294002) significantly suppressed the IL-1beta-, IFN-gamma- and TNF-alpha-induced IL-32 mRNA expression.
  • The blockade of NF-kappaB and activated protein-1 activation markedly suppressed the IL-1beta-, IFN-gamma-, and/or TNF-alpha-induced IL-32 mRNA expression.
  • Furthermore, IL-32-specific small interfering RNA significantly decreased the uptake of [3H]thymidine and increased the annexin V-positive population (apoptotic cells) in PANC-1 cells.
  • Pancreatic duct cells are the local source of IL-32, and IL-32 may play an important role in inflammatory responses and pancreatic cancer growth.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Gene Expression Regulation, Neoplastic. Interleukins / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Apoptosis. Blotting, Northern. Blotting, Western. Cell Proliferation. Cells, Cultured. Electrophoretic Mobility Shift Assay. Enzyme-Linked Immunosorbent Assay. Humans. Immunoenzyme Techniques. Interferon-gamma / genetics. Interferon-gamma / metabolism. Interleukin-1beta / genetics. Interleukin-1beta / metabolism. NF-kappa B / antagonists & inhibitors. NF-kappa B / genetics. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism. Transfection. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19386602.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL32 protein, human; 0 / Interleukin-1beta; 0 / Interleukins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Other-IDs] NLM/ PMC2719425
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44. Takahashi H, Funahashi H, Sawai H, Matsuo Y, Yamamoto M, Okada Y, Takeyama H, Manabe T: Synthetic serine protease inhibitor, gabexate mesilate, prevents nuclear factor-kappaB activation and increases TNF-alpha-mediated apoptosis in human pancreatic cancer cells. Dig Dis Sci; 2007 Oct;52(10):2646-52
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  • [Title] Synthetic serine protease inhibitor, gabexate mesilate, prevents nuclear factor-kappaB activation and increases TNF-alpha-mediated apoptosis in human pancreatic cancer cells.
  • Gabexate mesilate (GM), a synthetic serine protease inhibitor, suppresses nuclear factor-kappaB (NF-kappaB) activity in human monocytes or human umbilical vein endothelial cells (HUVECs).
  • In this study we examine whether GM also suppresses NF-kappaB activation and induces apoptosis in human pancreatic cancer cell lines.
  • The addition of tumor necrosis factor alpha (TNF-alpha) did not change the rates of growth of BxPC-3 and MIA PaCa-2.
  • However, in the presence of GM and TNF-alpha, proliferation decreased in a dose-dependent manner.
  • GM- and TNF-alpha-treated cells exhibited morphologic changes indicative of apoptosis, including chromatin condensation and nuclear fragmentation.
  • The NF-kappaB activity of both cell lines was increased by the addition of TNF-alpha, while TNF-alpha-induced NF-kappaB activity was suppressed by prestimulation with GM in a dose-dependent manner.
  • Caspase 3 and 7 activity was significantly increased by TNF-alpha with GM stimulation.
  • Furthermore, GM also suppressed the invasive potential of both cell lines.
  • These results indicate that GM inhibits TNF-alpha-induced NF-kappaB activation and enhances apoptosis in human pancreatic cancer cell lines.
  • [MeSH-major] Apoptosis / drug effects. Gabexate / pharmacology. NF-kappa B / drug effects. Pancreatic Neoplasms / drug therapy. Serine Proteinase Inhibitors / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Humans

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  • (PMID = 17357832.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Serine Proteinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 4V7M9137X9 / Gabexate
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45. Lewis RB, Lattin GE Jr, Paal E: Pancreatic endocrine tumors: radiologic-clinicopathologic correlation. Radiographics; 2010 Oct;30(6):1445-64
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  • [Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
  • Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.
  • They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and glucagonoma are the most common functioning PETs.
  • Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.
  • At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.
  • Cystic change, calcification, and necrosis are common in large tumors, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller tumors.
  • Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such tumors have a poor prognosis.
  • Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

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  • [Copyright] © RSNA, 2010.
  • (PMID = 21071369.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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46. Barth BM, Gustafson SJ, Young MM, Fox TE, Shanmugavelandy SS, Kaiser JM, Cabot MC, Kester M, Kuhn TB: Inhibition of NADPH oxidase by glucosylceramide confers chemoresistance. Cancer Biol Ther; 2010 Dec 1;10(11):1126-36
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  • The bioactive sphingolipid ceramide induces oxidative stress by disrupting mitochondrial function and stimulating NADPH oxidase (NOX) activity, both implicated in cell death mechanisms.
  • Many anticancer chemotherapeutics (anthracyclines, Vinca alkaloids, paclitaxel, and fenretinide), as well as physiological stimuli such as tumor necrosis factor α (TNFα), stimulate ceramide accumulation and increase oxidative stress in malignant cells.
  • Consequently, ceramide metabolism in malignant cells and, in particular the up-regulation of glucosylceramide synthase (GCS), has gained considerable interest in contributing to chemoresistance.
  • We further showed, in both glioblastoma and neuroblastoma cells that glucosylceramide directly interfered with NOX assembly, hence delineating a direct resistance mechanism.

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  • (PMID = 20935456.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM077391; United States / NINDS NIH HHS / NS / U54 NS041069; United States / NIGMS NIH HHS / GM / GM77391; United States / NINDS NIH HHS / NS / U54 NS41069
  • [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] United States
  • [Chemical-registry-number] 0 / Glucosylceramides; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 80168379AG / Doxorubicin; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.6.3.1 / NADPH Oxidase; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase
  • [Other-IDs] NLM/ PMC3047104
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47. He J, Haskins K: Pathogenicity of T helper 2 T-cell clones from T-cell receptor transgenic non-obese diabetic mice is determined by tumour necrosis factor-alpha. Immunology; 2008 Jan;123(1):108-17
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  • [Title] Pathogenicity of T helper 2 T-cell clones from T-cell receptor transgenic non-obese diabetic mice is determined by tumour necrosis factor-alpha.
  • Although T cells producing Th2 cytokines are generally thought to counter a Th1 response, there have been reports of Th2 T-cell clones with pathogenic activity, including one previously reported by us in which the Th2 T-cell clone was derived from a T-cell receptor transgenic (TCR-Tg) mouse bearing pathogenic TCR.
  • In this study, our goal was to determine whether Th2 T-cell clones derived from a TCR-Tg in which the autoantigen was absent would be pathogenic and if so, to investigate possible mechanisms by which the Th2 T-cell clone could promote disease.
  • We found that a Th2 T-cell clone derived from the 6.9 TCR-Tg/non-obese diabetic (NOD).C6 mouse in which 6.9 T cells do not encounter autoantigen, produced Th2 cytokines but not interferon-gamma.
  • This Th2 T-cell clone, like the previous one we had isolated from the 2.5 TCR-Tg/NOD mouse, also turned out to be pathogenic.
  • Intracellular staining revealed that these Th2 T-cell clones produce low levels of tumour necrosis factor-alpha (TNF-alpha) in vitro, and after adoptive transfer, they migrate to the pancreas where they produce TNF-alpha as well as Th2 cytokines (interleukin (IL)-4, IL-10).
  • Induction of disease was prevented by administration of soluble TNF-alpha receptor to recipient mice, suggesting that the diabetogenicity of these Th2 T-cell clones is caused by their low level production of TNF-alpha.

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  • (PMID = 17983440.001).
  • [ISSN] 1365-2567
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK050561; United States / NIDDK NIH HHS / DK / R56 DK050561; United States / NIDDK NIH HHS / DK / R01DK50561
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Cytokines; 0 / Icos protein, mouse; 0 / Inducible T-Cell Co-Stimulator Protein; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Tumor Necrosis Factor; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide
  • [Other-IDs] NLM/ PMC2433281
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48. 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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49. Mastrandrea LD, Sessanna SM, Del Toro A, Laychock SG: ATP-independent glucose stimulation of sphingosine kinase in rat pancreatic islets. J Lipid Res; 2010 Aug;51(8):2171-80
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  • [Title] ATP-independent glucose stimulation of sphingosine kinase in rat pancreatic islets.
  • Sphingosine kinase (SPHK) catalyzes sphingosine 1-phosphate production, promoting cell survival and reducing apoptosis in isolated rat pancreatic islets.
  • Glucose, the primary islet beta-cell growth factor and insulin secretagogue, increased islet SPHK activity by 3- to 5-fold following acute (1 h) or prolonged (7 days) stimulation.
  • In contrast, 3-o-methylglucose (3-oMeG), which is transported but neither phosphorylated nor metabolized, did not increase islet SPHK activity.
  • Glyceraldehyde and alpha-ketoisocaproic acid (KIC), metabolites that stimulate glycolysis and the citric acid cycle, respectively, did not activate islet SPHK.
  • A role for SPHK activity in beta-cell growth was confirmed when small interfering (si)SPHK2 RNA transfection reduced rat insulinoma INS-1e cell SPHK levels and activity and cell growth.
  • Glucose induced an early and sustained increase in islet SPHK activity that was dependent on glucose phosphorylation, but independent of ATP generation or new protein biosynthesis.
  • Glucose-supported beta-cell growth appears to be in part mediated by SPHK activity.
  • [MeSH-major] Adenosine Triphosphate. Glucose / pharmacology. Insulin-Secreting Cells / drug effects. Insulin-Secreting Cells / metabolism. Phosphotransferases (Alcohol Group Acceptor) / genetics. Phosphotransferases (Alcohol Group Acceptor) / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Enzymologic / genetics. Gene Knockdown Techniques. RNA, Small Interfering / genetics. Rats. Time Factors

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  • (PMID = 20371493.001).
  • [ISSN] 1539-7262
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.- / sphingosine kinase; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2903817
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50. Büyükberber M, Savaş MC, Bağci C, Koruk M, Gülşen MT, Tutar E, Bilgiç T, Deveci R, Küçük C: The beneficial effect of propolis on cerulein-induced experimental acute pancreatitis in rats. Turk J Gastroenterol; 2009 Jun;20(2):122-8
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  • Serum amylase and lipase levels, white blood cell count and serum tumor necrosis factor-alpha levels were measured and pancreatic tissue was evaluated histologically.
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Disease Models, Animal. Edema. Lipase / blood. Male. Pancreas / drug effects. Pancreas / pathology. Rats. Rats, Wistar. Treatment Outcome

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  • (PMID = 19530045.001).
  • [ISSN] 2148-5607
  • [Journal-full-title] The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
  • [ISO-abbreviation] Turk J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Gastrointestinal Agents; 888Y08971B / Ceruletide; 9009-62-5 / Propolis; EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases
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51. Dubova EA, Shchegolev AI, Mishnev OD, Egorov VI: [Solid pseudopapillary tumor of the pancreas]. Arkh Patol; 2008 Jan-Feb;70(1):49-52
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  • [Title] [Solid pseudopapillary tumor of the pancreas].
  • The paper reviews the data available in the literature and describes the authors' observation of solid pseudopapillary tumor of the pancreas in a 33-year-old woman.
  • Microscopically, the tumor, 2.5 x 2.5 x 2 cm in size, appeared predominantly as solid areas and solitary pseudopapillae comprising monomorphic round and oval cells with a light cytoplasm and round nuclei.
  • Immunohistochemical study revealed diffuse cytoplasmic tumor cell staining in response to vimentin, alpha-antitrypsin, neuronspecific enolase, and cytokeratin 18; focal expression of synaptophysin and CD117; a negative reaction with antibodies to epithelial membrane antigen, S-100 protein, cytokeratins 7, 8, and 19, and CD57.
  • Progesterone receptors were detectable in the nuclei of solitary tumor cells and the reaction with estrogen receptor was negative.
  • [MeSH-major] Carcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18368811.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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52. 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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53. Ito T, Omori K, Rawson J, Todorov I, Asari S, Kuroda A, Shintaku J, Itakura S, Ferreri K, Kandeel F, Mullen Y: Improvement of canine islet yield by donor pancreas infusion with a p38MAPK inhibitor. Transplantation; 2008 Jul 27;86(2):321-9
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  • [Title] Improvement of canine islet yield by donor pancreas infusion with a p38MAPK inhibitor.
  • The islet isolation process, from pancreas procurement through islet collection, may activate p38MAPK leading to cytokine release and islet damage.
  • METHODS: Pancreata removed from Beagle dogs were infused with University of Wisconsin solution containing the p38IH, SB203580, and Pefabloc (n=6) or vehicle (dimethyl sulfoxide and Pefabloc) alone (n=7), through the pancreatic duct and preserved using the two-layer method.
  • RESULTS: p38IH-treated pancreata yielded significantly more islets than control pancreata (IEQ/g: 2134+/-297 vs. 1477+/-145 IEQ/g or 65,012+/-9385 vs. 45,700+/-5103 IEQ/pancreas; P<0.05).
  • Apoptotic beta-cell percentages assessed by laser scanning cytometry were lower in p38IH-treated than the controls (44%+/-9.4% vs. 61.6%+/-4.8%, P<0.05).
  • Tumor necrosis factor-alpha expression assessed by real-time reverse transcription polymerase chain reaction was significantly lower in the p38IH-treated group than controls.
  • Plasma C-peptide levels after glucagon challenge were higher in animals receiving p38IH-treated islets (n=5) versus untreated islets (n=4) (0.40+/-0.78 vs. 0.21+/-0.05 ng/mL, P<0.05).
  • CONCLUSIONS: Infusion of pancreata with University of Wisconsin solution containing p38IH through the duct before preservation suppresses cytokine release, prevents beta-cell apoptosis, and improves islet yield significantly with no adverse effect on islet function after transplantation. p38IH treatment of human pancreata may improve islet yield for use in clinical transplantation.

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  • (PMID = 18645497.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / U42 RR016607; United States / NCRR NIH HHS / RR / U42 RR 16607
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Insulin; 0 / Organ Preservation Solutions; 0 / University of Wisconsin-lactobionate solution; 63CZ7GJN5I / Allopurinol; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; GAN16C9B8O / Glutathione; K72T3FS567 / Adenosine; N5O3QU595M / Raffinose
  • [Other-IDs] NLM/ NIHMS83977; NLM/ PMC3791927
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54. Arlen M, Arlen P, Tsang A, Wang X, Gupta R: The therapeutic value of monoclonal antibodies directed against immunogenic tumor glycoproteins. J Cancer; 2010;1:209-22
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  • [Title] The therapeutic value of monoclonal antibodies directed against immunogenic tumor glycoproteins.
  • Monoclonal antibodies developed against immunogenic proteins (Tumor Specific Antigens/TSA's) that are expressed in human cancers, display a unique behavioral pattern.
  • This includes the early recognition of these immunogenic membrane proteins that can serve as diagnostic markers, and the targeting of such markers for the destruction of the tumor, primarily thru ADCC.The monoclonals (mAbs) that we have developed against specific immunogenic tumor membrane proteins have been studied in detail.
  • These tumor proteins, when first defined, were referred to as tumor associated antigens.
  • With the ability of the mAbs to demonstrate therapeutic antitumor activity in those patients with relatively advanced malignancies, the term tumor specific was introduced.
  • Monoclonals that we were able to develop from tumor specific proteins derived from colon and pancreas cancer were found capable of targeting those tumors to induce apoptosis.
  • Monoclonals developed from these tumor antigens are in the initial phases of investigation with regard to their specificity and antitumor activity.Mabs capable of targeting the malignancies noted above were produced following immunization of BALBc mice with the Tumor Specific Antigens.
  • The resulting mAbs were found to switch their isotypes to an IgG1 subsequent to chimerization and or humanization, when expressed in CHO cells.
  • The monoclonals, so produced, were not only more efficient in controlling tumor growth but minimized the development of a HAMA response.Because of 1) the specificity of this group of monoclonal antibodies in targeting well defined immunogenic proteins that were expressed on the tumor cell membrane,2) their lack of cross reactivity to normal tissue, 3) relatively low toxicity when delivered intravenously, 4) rapid targeting of tumor cell populations (4-6 hrs in vitro) and their 5) ability to destroy xenograft transplants (in vivo) within days of delivery, these mAbs were felt to be ideal for possible use in the treatment of patients with recurrent and or metastatic tumors.Initial clinical studies have been planned for following the filing of an IND.
  • It is required by FDA that the potential effects of tumor control and toxicity be defined using the naked antibodies produced under GMP conditions, In those situations where patients with recurrent malignancies are to be studied we have come to realize that a number of factors can influence the response to monoclonal therapy.
  • As such we plan to eventually employ the therapeutic mAbs in combination with chemotherapy as a means of enhancing the immunogenicity of the tumor system being treated and to possibly weaken the malignant growth for easier destruction by the mAb.
  • We will also look at the combination of mAbs with immunostimulants such as GMCSF and IL-2 (fusion proteins) and eventual conjugation of the mAbs with alpha and possibly B-emitters to help in targeting bystander cells.

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  • (PMID = 21060731.001).
  • [ISSN] 1837-9664
  • [Journal-full-title] Journal of Cancer
  • [ISO-abbreviation] J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Other-IDs] NLM/ PMC2974238
  • [Keywords] NOTNLM ; ADCC / Monoclonal antibodies / apoptosis / chimeric antibodies / hybridomas / tumor specific antigens (TSA).
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55. Serra S, Salahshor S, Fagih M, Niakosari F, Radhi JM, Chetty R: Nuclear expression of E-cadherin in solid pseudopapillary tumors of the pancreas. JOP; 2007;8(3):296-303
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  • [Title] Nuclear expression of E-cadherin in solid pseudopapillary tumors of the pancreas.
  • CONTEXT: Solid pseudopapillary tumors of the pancreas are rare and have recently been shown to harbor mutations of the beta-catenin gene with resultant nuclear localization of beta-catenin protein to the nucleus.
  • OBJECTIVE: To explore the protein expression of E-cadherin in a series of solid pseudopapillary tumors of the pancreas.
  • PARTICIPANTS: Eighteen cases of solid pseudopapillary tumors of the pancreas.
  • Tissue cores from normal pancreas were used as controls and for orientation purposes.
  • MAIN OUTCOME MEASURES: The slides were stained with the following commercially available antibodies: CD10, CD56, vimentin, alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase, chromogranin, synaptophysin, beta-catenin and E-cadherin.
  • RESULTS: All the tumors were CD10, vimentin, alpha-1-antitrypsin and alpha-1-antichymotrypsin diffusely positive (50% or more of the tumor cells staining) and CD56 showed focal positivity in all cases with 5-10% of tumor cells displaying immunolabeling.
  • Similarly, E-cadherin protein was localized to the nucleus in all 18 cases, with loss of the characteristic membranous decoration of cells.
  • CONCLUSION: This study is the first demonstration of aberrant nuclear localization of E-cadherin protein in solid pseudopapillary tumors of the pancreas.
  • Whilst the exact mechanism is not know and nuclear E-cadherin is not related to tumor aggression, this staining pattern may be of diagnostic value in concert with beta-catenin staining.
  • [MeSH-major] Cadherins / analysis. Carcinoma, Papillary / chemistry. Cell Nucleus / chemistry. Pancreatic Neoplasms / chemistry

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  • (PMID = 17495358.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Cadherins; 0 / beta Catenin; EC 3.4.24.11 / Neprilysin
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56. Bancila V, Cens T, Monnier D, Chanson F, Faure C, Dunant Y, Bloc A: Two SUR1-specific histidine residues mandatory for zinc-induced activation of the rat KATP channel. J Biol Chem; 2005 Mar 11;280(10):8793-9
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  • Zinc at micromolar concentrations hyperpolarizes rat pancreatic beta-cells and brain nerve terminals by activating ATP-sensitive potassium channels (KATP).
  • The molecular determinants of this effect were analyzed using insulinoma cell lines and cells transfected with either wild type or mutated KATP subunits.
  • Zinc activated KATP in cells co-expressing rat Kir6.2 and SUR1 subunits, as in insulinoma cell lines.
  • In contrast, zinc exerted an inhibitory action on SUR2A-containing cells.
  • The five SUR1-specific extracellular histidine residues were submitted to site-directed mutagenesis.
  • Thereby zinc could exert a negative control on cell excitability and secretion process of pancreatic beta-and alpha-cells.
  • In fact, we have recently shown that such a mechanism occurs in hippocampal mossy fibers, a brain region characterized, like the pancreas, by an important accumulation of zinc and a high density of SUR1-containing KATP.
  • [MeSH-minor] ATP-Binding Cassette Transporters. Animals. Cell Line. Cell Line, Tumor. Humans. Insulinoma. Kidney. Multidrug Resistance-Associated Proteins. Mutagenesis, Site-Directed. Pancreatic Neoplasms. Rats. Receptors, Drug. Recombinant Proteins / chemistry. Recombinant Proteins / metabolism. Sulfonylurea Receptors

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  • (PMID = 15613469.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCC8 protein, human; 0 / ABCC9 protein, human; 0 / ATP-Binding Cassette Transporters; 0 / Abcc8 protein, rat; 0 / Kir6.2 channel; 0 / Multidrug Resistance-Associated Proteins; 0 / Potassium Channels, Inwardly Rectifying; 0 / Receptors, Drug; 0 / Recombinant Proteins; 0 / Sulfonylurea Receptors; 4QD397987E / Histidine; J41CSQ7QDS / Zinc
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57. Esposito I, Penzel R, Chaib-Harrireche M, Barcena U, Bergmann F, Riedl S, Kayed H, Giese N, Kleeff J, Friess H, Schirmacher P: Tenascin C and annexin II expression in the process of pancreatic carcinogenesis. J Pathol; 2006 Apr;208(5):673-85
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  • [Title] Tenascin C and annexin II expression in the process of pancreatic carcinogenesis.
  • Cell surface annexin II is a high-affinity receptor for large TNC splice variants.
  • The aim of this study was to analyse whether TNC and annexin II play a role in the development of pancreatic ductal adenocarcinoma (PDAC).
  • PDAC is characterized by a rich ECM populated by pancreatic stellate cells, which play a crucial role in pancreatic desmoplasia.
  • The mRNA and protein levels of TNC and of annexin II were analysed in pancreatic tissues by DNA array, quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) and immunohistochemistry.
  • TNC and annexin II mRNA levels were significantly higher in pancreatic cancer tissues than in the normal pancreas.
  • TNC expression was detected with increased frequency in the progression from PanIN-1 lesions to PDAC, and a parallel switch from cytoplasmic to cell surface expression of annexin II was observed.
  • Large TNC transcripts were found in pancreatic cancer and in chronic pancreatitis, but not in the normal pancreas.
  • TNC expression was demonstrated in pancreatic stellate cells, where it could be induced by tumour necrosis factor alpha (TNFalpha), transforming growth factor beta1 (TGF-beta1) and by cancer cell supernatants supplemented with TGF-beta1.
  • In conclusion, the expression of TNC and cell surface annexin II increases in the progression from low-grade PanIN lesions to pancreatic cancer.
  • Pancreatic stellate cells are identified as a source of TNC in pancreatic tissues, possibly under the influence of soluble factors released by the tumour cells.
  • [MeSH-major] Adenocarcinoma / metabolism. Annexin A2 / metabolism. Cell Transformation, Neoplastic / metabolism. Pancreatic Neoplasms / metabolism. Tenascin / metabolism
  • [MeSH-minor] Blotting, Western. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunoenzyme Techniques. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Pancreatitis, Chronic / metabolism. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Transforming Growth Factor beta / pharmacology. Transforming Growth Factor beta1. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16450333.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A2; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TGFB1 protein, human; 0 / Tenascin; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha
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58. Kolb-van Harten P, Rosien U, Klöppel G, Layer P: Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression. Pancreatology; 2007;7(4):370-2
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  • [Title] Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression.
  • We report a case of acinar cell carcinoma of the pancreas associated with excessively elevated levels of serum alpha-fetoprotein (>32,000 ng/ml).
  • Abdominal computed tomography scan revealed a large pancreatic mass with infiltration of the splenic artery.
  • This regimen was associated with clinical improvement and dramatic decreases in both tumor size and serum alpha-fetoprotein.
  • [MeSH-major] Carcinoma, Acinar Cell / metabolism. Pancreatic Neoplasms / metabolism. alpha-Fetoproteins / metabolism

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  • [Copyright] 2007 S. Karger AG, Basel and IAP
  • (PMID = 17703084.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha-Fetoproteins; 0W860991D6 / Deoxycytidine; 50SG953SK6 / Mitomycin; B76N6SBZ8R / gemcitabine
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59. 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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60. 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


61. Koehler JA, Baggio LL, Lamont BJ, Ali S, Drucker DJ: Glucagon-like peptide-1 receptor activation modulates pancreatitis-associated gene expression but does not modify the susceptibility to experimental pancreatitis in mice. Diabetes; 2009 Sep;58(9):2148-61
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  • [Title] Glucagon-like peptide-1 receptor activation modulates pancreatitis-associated gene expression but does not modify the susceptibility to experimental pancreatitis in mice.
  • OBJECTIVE: Clinical reports link use of the glucagon-like peptide-1 receptor (GLP-1R) agonists exenatide and liraglutide to pancreatitis.
  • However, whether these agents act on the exocrine pancreas is poorly understood.
  • The importance of endogenous GLP-1R signaling for gene expression in the exocrine pancreas and the severity of pancreatitis was assessed in Glp1r(-/-) mice.
  • RESULTS: Acute administration of Ex-4 increased expression of egr-1 and c-fos in the exocrine pancreas.
  • Administration of Ex-4 or liraglutide for 1 week increased pancreas weight and induced expression of mRNA transcripts encoding the anti-inflammatory proteins pancreatitis-associated protein (PAP) (RegIIIbeta) and RegIIIalpha.
  • Chronic Ex-4 treatment of high-fat-fed mice increased expression of PAP and reduced pancreatic expression of mRNA transcripts encoding for the proinflammatory monocyte chemotactic protein-1, tumor necrosis factor-alpha, and signal transducer and activator of transcription-3.
  • Sitagliptin and metformin did not significantly change pancreatic gene expression profiles.
  • Ex-4 administered before or after caerulein did not modify the severity of experimental pancreatitis, and levels of pancreatic edema and serum amylase were comparable in caerulein-treated Glp1r(-/-) versus Glp1r(+/+) mice.
  • CONCLUSIONS: These findings demonstrate that GLP-1 receptor activation increases pancreatic mass and selectively modulates the expression of genes associated with pancreatitis.
  • [MeSH-major] Glucagon-Like Peptide 1 / metabolism. Pancreatitis / metabolism. Pancreatitis / physiopathology. Receptors, Glucagon / genetics. Receptors, Glucagon / metabolism
  • [MeSH-minor] Animals. Ceruletide / toxicity. Dietary Fats / pharmacology. Disease Models, Animal. Early Growth Response Protein 1 / genetics. Gene Expression / drug effects. Gene Expression / physiology. Genes, fos / physiology. Glucagon-Like Peptide-1 Receptor. Hypoglycemic Agents / toxicity. Liraglutide. Male. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. Pancreas, Exocrine / drug effects. Pancreas, Exocrine / physiology. Peptides / toxicity. Severity of Illness Index. Signal Transduction / drug effects. Signal Transduction / physiology. Venoms / toxicity

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  • (PMID = 19509017.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse; 0 / Glp1r protein, mouse; 0 / Glucagon-Like Peptide-1 Receptor; 0 / Hypoglycemic Agents; 0 / Peptides; 0 / Receptors, Glucagon; 0 / Venoms; 839I73S42A / Liraglutide; 888Y08971B / Ceruletide; 89750-14-1 / Glucagon-Like Peptide 1; 9P1872D4OL / exenatide
  • [Other-IDs] NLM/ PMC2731518
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62. Long C, Yin B, Lu Q, Zhou X, Hu J, Yang Y, Yu F, Yuan Y: Promoter hypermethylation of the RUNX3 gene in esophageal squamous cell carcinoma. Cancer Invest; 2007 Dec;25(8):685-90
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  • [Title] Promoter hypermethylation of the RUNX3 gene in esophageal squamous cell carcinoma.
  • Alteration in transforming growth factor-beta (TGF-beta) signaling pathway is one of the main causes of esophageal squamous cell carcinoma (ESCC).
  • Hypermethylation of RUNX3 promoter was frequently found in gastrointestinal cancers, including those of stomach, liver, colon and pancreas.
  • The aim of this study was to determine whether promoter methylation of the RUNX3 gene correlates with ESCC tumor progression.Accordingly, we first determined RUNX3 mRNA expression and methylation status of its promoter region in 42 primary tumors with ESCC and Eca-109, an ESCC cell line.
  • Loss of RUNX3 mRNA expression was detected by RT-PCR in 23 out of 42 (54.8%) ESCC specimens and Eca-109 cells.
  • The Promoter hypermethylation was detected by Methylation Specific Polymerase Chain Reaction (MS-PCR) in 27 out of 42 (64.3%) ESCC specimen and Eca-109 cells.
  • Importantly, we found positive correlations, not only between the promoter hypermethylation and tumor clinical pathologic stages (P = 0.003), but also between the loss of RUNX3 mRNA expression and the tumor progression (P = 0.016).
  • Finally, we observed that the loss of RUNX3 mRNA expression is statistically correlated with the promoter hypermethylation in these tumors (P < 0.001).
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Core Binding Factor Alpha 3 Subunit / genetics. DNA Methylation. Esophageal Neoplasms / genetics. Promoter Regions, Genetic
  • [MeSH-minor] Aged. Azacitidine / pharmacology. Cell Line, Tumor. Female. Humans. Male. Middle Aged. RNA, Messenger / analysis. Signal Transduction. Transforming Growth Factor beta / physiology

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  • (PMID = 18058463.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit; 0 / RNA, Messenger; 0 / Runx3 protein, human; 0 / Transforming Growth Factor beta; M801H13NRU / Azacitidine
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63. Stehr SN, Heller AR: Omega-3 fatty acid effects on biochemical indices following cancer surgery. Clin Chim Acta; 2006 Nov;373(1-2):1-8
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  • Mechanisms accounting for these anti-tumor effects are reduced levels of PGE(2) and inducible NO synthase as well as an increased lipid peroxidation, or translation inhibition with subsequent cell cycle arrest.
  • Further, omega-3 eicosapentaenoic acid is capable of down-regulating the production and effect of a number of mediators of cachexia, such as IL-1, IL-6, TNF-alpha and proteolysis-inducing factor.
  • In patients undergoing tumor resection surgery we observed improvement of liver and pancreas biochemical indices when omega-3 fatty acids were administered.

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

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  • (PMID = 18592007.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Platelet-Derived Growth Factor; 0 / Vascular Endothelial Growth Factors; 0 / platelet-derived growth factor A; 103107-01-3 / Fibroblast Growth Factor 2
  • [Other-IDs] NLM/ PMC2435004
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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. Ralhan R, Desouza LV, Matta A, Tripathi SC, Ghanny S, Datta Gupta S, Bahadur S, Siu KW: Discovery and verification of head-and-neck cancer biomarkers by differential protein expression analysis using iTRAQ labeling, multidimensional liquid chromatography, and tandem mass spectrometry. Mol Cell Proteomics; 2008 06;7(6):1162-73
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  • Multidimensional LC-MS/MS has been used for the analysis of biological samples labeled with isobaric mass tags for relative and absolute quantitation (iTRAQ) to identify proteins that are differentially expressed in human head-and-neck squamous cell carcinomas (HNSCCs) in relation to non-cancerous head-and-neck tissues (controls) for cancer biomarker discovery.
  • Some of the proteins include stratifin (14-3-3sigma); YWHAZ (14-3-3zeta); three calcium-binding proteins of the S100 family, S100-A2, S100-A7 (psoriasin), and S100-A11 (calgizarrin); prothymosin alpha (PTHA); L-lactate dehydrogenase A chain; glutathione S-transferase Pi; APC-binding protein EB1; and fascin.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromatography, Liquid / methods. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Head and Neck Neoplasms / metabolism. Proteomics / methods. Tandem Mass Spectrometry / methods


67. Srivastava S, Li Z, Yang X, Yedwabnick M, Shaw S, Chan C: Identification of genes that regulate multiple cellular processes/responses in the context of lipotoxicity to hepatoma cells. BMC Genomics; 2007 Oct 09;8:364
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  • [Title] Identification of genes that regulate multiple cellular processes/responses in the context of lipotoxicity to hepatoma cells.
  • Exposure to elevated levels of free fatty acids (FFAs) and tumor necrosis factor alpha (TNF-alpha) alters multiple cellular processes, causing lipotoxicity.
  • RESULTS: As a model system to test this hypothesis, human hepatoblastoma cells (HepG2) were exposed to elevated physiological levels of FFAs and TNF-alpha.
  • The aim of the current study is to identify the genes that could be altered to treat or ameliorate the cellular responses affected by a complex disease rather than to identify the causal genes.
  • The analyses identified NADH dehydrogenase and mitogen activated protein kinases (MAPKs) as important regulators of both cytotoxicity and lipid accumulation in response to FFA and TNF-alpha exposure.

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  • (PMID = 17925029.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM079688; United States / NCI NIH HHS / CA / R21 CA126136; United States / NIGMS NIH HHS / GM / 1R01GM079688-01; United States / NCI NIH HHS / CA / 1R21CA126136-01
  • [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] England
  • [Chemical-registry-number] 0 / Fatty Acids, Nonesterified; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; EC 1.6.99.3 / NADH Dehydrogenase; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2110894
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68. Chow JY, Ban M, Wu HL, Nguyen F, Huang M, Chung H, Dong H, Carethers JM: TGF-beta downregulates PTEN via activation of NF-kappaB in pancreatic cancer cells. Am J Physiol Gastrointest Liver Physiol; 2010 Feb;298(2):G275-82
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  • [Title] TGF-beta downregulates PTEN via activation of NF-kappaB in pancreatic cancer cells.
  • TGF-beta utilizes receptor-activated SMAD signaling to mediate growth suppression; however, non-SMAD signaling that modulates the TGF-beta response in epithelial cells become apparent when the SMAD signaling is abrogated, a common occurrence in pancreatic cancers.
  • Here, we examined whether TGF-beta utilized NF-kappaB to downregulate PTEN, a gene that is rarely mutated in pancreatic cancers.
  • SMAD4-null BxPc3 and CAPAN-1 pancreatic cancer cells were treated with TGF-beta (10 ng/ml) and lysed, and cellular proteins were analyzed by Western blots using p-IkappaB, p65, and PTEN antibodies.
  • Dominant negative p-IkappaB-alpha-M (NF-kappaB superrepressor) was used to block activation of NF-kappaB.
  • Cell motility was assessed by Boyden chamber migration assay.
  • TGF-beta induced IkappaB-alpha phosphorylation followed by NF-kappaB p65 subunit nuclear translocation and increased NF-kappaB activity.
  • IkappaB-alpha-M blocked TGF-beta-induced NF-kappaB activity, reversed downregulated PTEN promoter activity and PTEN expression, and prevented augmentation of cell motility induced by TGF-beta.
  • Thus TGF-beta suppresses PTEN in pancreatic cancer cells through NF-kappaB activation and enhances cell motility and invasiveness in a SMAD4-independent manner that can be counteracted when TGF-beta-SMAD signaling is restored.
  • The TGF-beta/NF-kappaB/PTEN cascade may be a critical pathway for pancreatic cancer cells to proliferate and metastasize.