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1. Vosters O, Beuneu C, Goldman M, Verhasselt V: N-acetylcysteine derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells. Pancreas; 2008 May;36(4):363-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: We recently observed that duct cells constitutively express CD40, a membrane molecule whose engagement results in duct cell activation and proinflammatory cytokine secretion.
  • This observation suggests a potential role of this pathway in the pathogenesis of type 1 diabetes, islet graft rejection, or acute pancreatitis.
  • METHODS: We assessed the effects of Nacystelyn on CD40 expression and function in human caucasian pancreatic adenocarcinoma, ATCC n degrees THB-80 (CAPAN-2) cells, a human pancreatic duct cell line.
  • To assess CAPAN-2 cell responses to CD40 engagement, we looked at nuclear factor-kappaB transcription factor activation using enzyme-linked immunosorbent assay and electrophoretic mobility shift assay and cytokine mRNA levels by quantitative real-time reverse transcriptase polymerase chain reaction.
  • [MeSH-minor] Adenocarcinoma / pathology. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. NF-kappa B / drug effects. NF-kappa B / genetics. Pancreatic Neoplasms / pathology. Transcription, Genetic / drug effects

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  • (PMID = 18437082.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / N-acetylcysteine lysinate; 0 / NF-kappa B; K3Z4F929H6 / Lysine; WYQ7N0BPYC / Acetylcysteine
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2. Dietrich CF: Comments and illustrations regarding the guidelines and good clinical practice recommendations for contrast-enhanced ultrasound (CEUS)--update 2008. Ultraschall Med; 2008 Sep;29 Suppl 4:S188-202
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The recently published EFSUMB guidelines and recommendations provide general advice for the use of ultrasound contrast agents to improve the management of patients.
  • The recommendations also deal with the uses of ultrasound contrast agents for the evaluation of the microvasculature and macrovasculature of the kidneys, including the characterization of focal renal lesions, the detection of lesions and the monitoring of local treatment.
  • Ductal adenocarcinoma as the most common tumor of the pancreas is typically hypoenhanced compared to the adjacent pancreatic tissue in all phases.
  • Neuroendocrine tumors and serous microcystic adenoma of the pancreas are characterized by hypervascularization appearing typically hyperenhanced during CEUS.
  • [MeSH-minor] Adenoma, Islet Cell / ultrasonography. Carcinoma, Pancreatic Ductal / ultrasonography. Endosonography / standards. Humans. Liver Diseases / ultrasonography. Liver Neoplasms / ultrasonography. Neuroendocrine Tumors / ultrasonography. Pancreatic Diseases / ultrasonography. Pancreatic Neoplasms / ultrasonography

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  • (PMID = 18833497.001).
  • [ISSN] 1438-8782
  • [Journal-full-title] Ultraschall in der Medizin (Stuttgart, Germany : 1980)
  • [ISO-abbreviation] Ultraschall Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media
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3. Hong X, Michalski CW, Kong B, Zhang W, Raggi MC, Sauliunaite D, De Oliveira T, Friess H, Kleeff J: ALCAM is associated with chemoresistance and tumor cell adhesion in pancreatic cancer. J Surg Oncol; 2010 Jun 1;101(7):564-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ALCAM is associated with chemoresistance and tumor cell adhesion in pancreatic cancer.
  • AIMS: Cell-cell adhesion is a major factor in integrity of epithelia which is frequently disturbed in cancer leading to local invasion and distant metastasis.
  • METHODS: To define expression and function of activated leukocyte cell adhesion molecule (ALCAM, CD166) in pancreatic cancer and in pancreatic neuroendocrine tumors (PNET), microarray analyses, RT-PCR, immunohistochemistry, RNAi, adhesion, migration, invasion, and chemoresistance assays were used.
  • RESULTS: We demonstrate that expression of ALCAM is altered and its serum levels are increased in pancreatic ductal adenocarcinoma (PDAC).
  • ALCAM was expressed on the membranes of islet cells in the normal pancreas whereas normal pancreatic ducts were ALCAM-negative.
  • PNET were mostly ALCAM-positive with a cytoplasmic staining pattern which was in contrast to the membrane expression observed in non-transformed islet cells.
  • In vitro, ALCAM silencing using RNAi had no effects on growth or invasion of pancreatic cancer cells but reduced cell adhesion and induced chemoresistance.
  • In neuroendocrine tumor cell lines, silencing of ALCAM decreased cell growth.
  • CONCLUSIONS: We propose ALCAM as a novel serum biomarker in human pancreatic tumors which is associated with cell adhesion, growth and chemoresistance.
  • [MeSH-major] Activated-Leukocyte Cell Adhesion Molecule / blood. Biomarkers, Tumor / blood. Carcinoma, Pancreatic Ductal / pathology. Neuroendocrine Tumors / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Case-Control Studies. Cell Adhesion. Cell Line, Tumor. Cell Transformation, Neoplastic. Drug Resistance, Neoplasm. Humans. Middle Aged. Survival Analysis

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  • (PMID = 20461761.001).
  • [ISSN] 1096-9098
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Activated-Leukocyte Cell Adhesion Molecule; 0 / Biomarkers, Tumor
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4. Bockman DE: Transition to pancreatic cancer in response to carcinogen. Langenbecks Arch Surg; 2008 Jul;393(4):557-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: It has become obvious that the traditional assumptions about the transition from normal pancreas to pancreatic cancer are incomplete.
  • Experimental studies reveal that the earliest changes during transition to pancreatic adenocarcinoma involve premalignant lesions that are derived from acinar, islet, and ductal cells.
  • As part of redifferentiation and transformation to adenocarcinoma, cells regain the characteristics of developing pancreas.
  • Elements significant in identifying precursor cell types include Pdx1, hedgehog signaling, notch signaling, and nestin, an intermediate filament expressed by precursor cell types.
  • CONCLUSIONS: Thus pancreatic carcinogenesis is not simply a matter of transition of ductal cells to cancer cells months after insult by the carcinogen; ductal cells are not the sole source transitioning to cancer, and PanINs are not the sole route to adenocarcinoma.
  • Tubular complexes, derived from multiple cell sources, are included in routes to pancreatic cancer.
  • Markers characteristic of developing pancreas are consistent with this transition.
  • [MeSH-major] Carcinogens. Cell Transformation, Neoplastic / chemically induced. Pancreatic Neoplasms / chemically induced. Precancerous Conditions / chemically induced
  • [MeSH-minor] Animals. Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / pathology. Gene Expression Regulation, Neoplastic / genetics. Hedgehog Proteins / genetics. Homeodomain Proteins / genetics. Humans. Intermediate Filament Proteins / genetics. Nerve Tissue Proteins / genetics. Nestin. Receptors, Notch / genetics. Signal Transduction / drug effects. Signal Transduction / genetics. Smoking / adverse effects. Stem Cells / drug effects. Stem Cells / pathology. Trans-Activators / genetics

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  • [Cites] Development. 2001 Mar;128(6):871-81 [11222142.001]
  • [Cites] Differentiation. 1996 Oct;61(1):67-75 [8921586.001]
  • [Cites] Genes Dev. 2001 Jan 15;15(2):111-27 [11157769.001]
  • [Cites] Diabetes. 2001 Feb;50 Suppl 1:S5-9 [11272202.001]
  • [Cites] J Cell Biochem. 2005 Jul 1;95(4):649-56 [15849724.001]
  • [Cites] Dig Dis Sci. 1989 Jan;34(1):46-55 [2535980.001]
  • [Cites] Am J Surg. 1982 Aug;144(2):243-9 [7102934.001]
  • [Cites] Pancreas. 2005 Aug;31(2):108-18 [16024996.001]
  • [Cites] J Pathol. 1992 Feb;166(2):97-103 [1373187.001]
  • [Cites] Diabetologia. 2000 Jul;43(7):907-14 [10952464.001]
  • [Cites] J Endocrinol. 2001 Nov;171(2):309-18 [11691651.001]
  • [Cites] Lab Invest. 2003 Jun;83(6):853-9 [12808120.001]
  • [Cites] Development. 1995 Jun;121(6):1569-80 [7600975.001]
  • [Cites] Lab Invest. 2005 May;85(5):675-88 [15765120.001]
  • [Cites] J Natl Cancer Inst. 1976 Oct;57(4):931-6 [187782.001]
  • [Cites] Genes Dev. 1998 Jun 1;12(11):1705-13 [9620856.001]
  • [Cites] Pancreas. 2006 Mar;32(2):119-29 [16552330.001]
  • [Cites] Am J Pathol. 1999 Apr;154(4):1223-9 [10233860.001]
  • [Cites] Nature. 1999 Aug 26;400(6747):877-81 [10476967.001]
  • [Cites] Genes Dev. 2001 Feb 1;15(3):286-93 [11159909.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):728-41 [15765408.001]
  • [Cites] Annu Rev Cell Dev Biol. 2003;19:71-89 [14570564.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):851-6 [14520413.001]
  • [Cites] J Natl Cancer Inst. 1975 Oct;55(4):857-64 [810597.001]
  • [Cites] Am J Pathol. 1978 Mar;90(3):645-58 [415616.001]
  • [Cites] Gastroenterology. 1998 Nov;115(5):1254-62 [9797382.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]
  • [Cites] Cell. 1990 Jun 15;61(6):1121-35 [1693546.001]
  • [Cites] Science. 2001 Oct 19;294(5542):564-7 [11577200.001]
  • [Cites] Cancer. 1981 Mar 15;47(6 Suppl):1528-34 [6268274.001]
  • [Cites] Eur J Cell Biol. 1990 Feb;51(1):64-75 [2184038.001]
  • [Cites] Lab Invest. 1993 Nov;69(5):518-30 [8246444.001]
  • [Cites] Dev Dyn. 2004 Jan;229(1):176-200 [14699589.001]
  • [Cites] Gastroenterology. 1992 Dec;103(6):1883-92 [1451981.001]
  • [Cites] Surgery. 1997 Jul;122(1):82-90 [9225919.001]
  • (PMID = 18189145.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Hedgehog Proteins; 0 / Homeodomain Proteins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Receptors, Notch; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein
  • [Number-of-references] 35
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5. Bockman DE, Guo J, Büchler P, Müller MW, Bergmann F, Friess H: Origin and development of the precursor lesions in experimental pancreatic cancer in rats. Lab Invest; 2003 Jun;83(6):853-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Notwithstanding the importance of understanding how pancreatic ductal adenocarcinoma develops, the process remains controversial.
  • A key question is whether the cells of origin of the tubular complexes that constitute precursor lesions are derived from a single cell type or from multiple types.
  • Animals were killed at intervals beginning 1 day after implantation of the carcinogen dimethylbenzanthracene.
  • Transdifferentiation of acinar cells to ductal cells does not require cell division.
  • Ductal adenocarcinoma is observed by 1 month after implantation of carcinogen.
  • Chymotrypsin and cytokeratin localized by immunocytochemistry indicate acinar and ductal cell characteristics.
  • Acino-ductal transdifferentiation persists in carcinogen-implanted animals, but not in controls implanted with sodium chloride crystals or subjected to sham implantation.
  • The precursor lesions (tubular complexes) are formed by the transdifferentiation of acinar cells and to a lesser extent islet cells, with the incorporation of the duct cells pre-existing in the lobules.
  • Therefore, cells that at one time were acinar cells, islet cells, and duct cells, provide the precursor cells for the ductal adenocarcinoma that develops from tubular complexes.
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene / toxicity. Animals. Carcinogens. Cell Cycle. Cell Differentiation. Male. Pancreas / drug effects. Pancreas / pathology. Pancreatic Ducts / drug effects. Pancreatic Ducts / pathology. Rats. Rats, Sprague-Dawley

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  • (PMID = 12808120.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
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6. Guo J, Kleeff J, Zhao Y, Li J, Giese T, Esposito I, Büchler MW, Korc M, Friess H: Yes-associated protein (YAP65) in relation to Smad7 expression in human pancreatic ductal adenocarcinoma. Int J Mol Med; 2006 May;17(5):761-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Yes-associated protein (YAP65) in relation to Smad7 expression in human pancreatic ductal adenocarcinoma.
  • Pancreatic ductal adenocarcinoma (PDAC) is characterized by multiple alterations in the TGF-beta signaling pathway.
  • YAP65 mRNA expression levels in human pancreatic tissue samples and cell lines were analyzed by Northern blotting and quantitative RT-PCR.
  • Enhanced expression of YAP65 mRNA was identified by Northern blotting and quantitative RT-PCR in PDAC in comparison to the normal pancreas (2.5-fold increase) and to chronic pancreatitis (1.3-fold increase).
  • In the normal pancreas, YAP65 was absent in acinar cells, large ducts and islet cells, but exhibited moderate to strong immunoreactivity in centroacinar cells and ductules.
  • In conclusion, YAP65 is expressed mainly in centroacinar and small ductal cells in the normal pancreas.
  • Together with the known function of YAP65 in different growth and differentiation regulating pathways, it is suggested that this gene plays a role in the normal and diseased pancreas.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Adenocarcinoma / pathology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology. Phosphoproteins / genetics. Smad7 Protein / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Blotting, Northern. Blotting, Western. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunohistochemistry. Male. Middle Aged. Mutation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Smad4 Protein / genetics. Transforming Growth Factor beta / pharmacology

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  • (PMID = 16596258.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-75059
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / SMAD4 protein, human; 0 / SMAD7 protein, human; 0 / Smad4 Protein; 0 / Smad7 Protein; 0 / Transforming Growth Factor beta; 0 / YAP1 (Yes-associated) protein, human
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