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11. Jankowski JA, Odze RD: Biomarkers in gastroenterology: between hope and hype comes histopathology. Am J Gastroenterol; 2009 May;104(5):1093-6
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  • Biomarkers are clinical variables associated with clinical outcomes.
  • In cancer biology, the best biomarkers are germline adenomatous polyposis coli mutations, which are highly predictive of colon cancer.
  • In other areas, such as Barrett's esophagus, despite early excellent success in identifying the importance of p16, p53, and aneuploidy in esophageal adenocarcinoma pathogenesis, useful biomarkers are still not widely used in clinical practice.
  • [MeSH-major] Biomarkers / analysis. Biomarkers, Tumor / analysis. Gastrointestinal Neoplasms / genetics. Gastrointestinal Neoplasms / pathology. Genes, APC. Precancerous Conditions / diagnosis
  • [MeSH-minor] Biopsy, Needle. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / genetics. Esophageal Neoplasms / pathology. Female. Gastroenterology / standards. Gastroenterology / trends. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease / epidemiology. Humans. Immunohistochemistry. Male. Molecular Biology. Prevalence. Reproducibility of Results. Risk Assessment. Sensitivity and Specificity. Stomach Neoplasms / epidemiology. Stomach Neoplasms / genetics. Stomach Neoplasms / pathology

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  • (PMID = 19417749.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor
  • [Number-of-references] 14
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12. De Groot CO, Jelesarov I, Damberger FF, Bjelić S, Schärer MA, Bhavesh NS, Grigoriev I, Buey RM, Wüthrich K, Capitani G, Akhmanova A, Steinmetz MO: Molecular insights into mammalian end-binding protein heterodimerization. J Biol Chem; 2010 Feb 19;285(8):5802-14
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  • [Title] Molecular insights into mammalian end-binding protein heterodimerization.
  • Microtubule plus-end tracking proteins (+TIPs) are involved in many microtubule-based processes.
  • End binding (EB) proteins constitute a highly conserved family of +TIPs.
  • Here we used a combination of methods to investigate the dimerization properties of the three human EB proteins EB1, EB2, and EB3.
  • Based on Förster resonance energy transfer, we demonstrate that the C-terminal dimerization domains of EBs (EBc) can readily exchange their chains in solution.
  • We further document that EB1c and EB3c preferentially form heterodimers, whereas EB2c does not participate significantly in the formation of heterotypic complexes.
  • Fluorescence spectroscopy and nuclear magnetic resonance studies in the presence of the cytoskeleton-associated protein-glycine-rich domains of either CLIP-170 or p150(glued) or of a fragment derived from the adenomatous polyposis coli tumor suppressor protein show that chain exchange of EBc domains can be controlled by binding partners.
  • Extension of these studies of the EBc domains to full-length EBs demonstrate that heterodimer formation between EB1 and EB3, but not between EB2 and the other two EBs, occurs both in vitro and in cells as revealed by live cell imaging.
  • [MeSH-major] Microtubule-Associated Proteins / metabolism. Models, Molecular. Protein Multimerization / physiology
  • [MeSH-minor] Animals. CHO Cells. Cell Line. Cricetinae. Cricetulus. Humans. Kinetics. Magnetic Resonance Spectroscopy. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Protein Structure, Quaternary. Protein Structure, Tertiary. Recombinant Proteins / chemistry. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Spectrometry, Fluorescence

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  • (PMID = 20008324.001).
  • [ISSN] 1083-351X
  • [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 / MAPRE1 protein, human; 0 / MAPRE3 protein, human; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; 144198-36-7 / dynactin; 148349-95-5 / cytoplasmic linker protein 170
  • [Other-IDs] NLM/ PMC2820806
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13. Sinicrope FA: Targeting cyclooxygenase-2 for prevention and therapy of colorectal cancer. Mol Carcinog; 2006 Jun;45(6):447-54
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  • A causal link for COX-2 in epithelial tumorigenesis was shown in genetically manipulated animal models of colon and breast carcinoma.
  • COX enzymes are targets for cancer prevention as shown by the observation that nonselective COX and selective COX-2 inhibitors have been reported to effectively prevent experimental colon cancer and can regress colorectal polyps in patients with familial adenomatous polyposis.

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  • (PMID = 16688727.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Prostaglandins; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 53
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4. Hendrix ND, Wu R, Kuick R, Schwartz DR, Fearon ER, Cho KR: Fibroblast growth factor 9 has oncogenic activity and is a downstream target of Wnt signaling in ovarian endometrioid adenocarcinomas. Cancer Res; 2006 Feb 1;66(3):1354-62
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  • [Title] Fibroblast growth factor 9 has oncogenic activity and is a downstream target of Wnt signaling in ovarian endometrioid adenocarcinomas.
  • Roughly 40% of ovarian endometrioid adenocarcinomas (OEA) have constitutive activation of Wnt signaling as a result of oncogenic mutations in the beta-catenin protein or inactivating mutations in key negative regulators of beta-catenin, such as the adenomatous polyposis coli and Axin tumor suppressor proteins.
  • Using microarray and quantitative PCR-based approaches, we found that fibroblast growth factor (FGF9) expression was increased >6-fold in primary OEAs with Wnt/beta-catenin pathway defects compared with OEAs lacking such defects.
  • [MeSH-major] Carcinoma, Endometrioid / genetics. Fibroblast Growth Factor 9 / genetics. Ovarian Neoplasms / genetics. Wnt1 Protein / metabolism

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  • (PMID = 16452189.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / PHS HHS / / NIH P30 46952; United States / NCI NIH HHS / CA / R01 CA 85463; United States / NCI NIH HHS / CA / R01 CA 94172; United States / NCI NIH HHS / CA / U19 CA 84953
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FGF9 protein, human; 0 / Fibroblast Growth Factor 9; 0 / RNA, Messenger; 0 / Wnt1 Protein; 0 / beta Catenin
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15. Wu JQ, Kornbluth S: Not-so-pseudo a substrate: Acm1-mediated inhibition of the APC. Mol Cell; 2008 Jun 6;30(5):543-4
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  • [Title] Not-so-pseudo a substrate: Acm1-mediated inhibition of the APC.
  • In a recent issue of Molecular Cell, Enquist-Newman et al. (2008) demonstrate that Acm1 is ubiquitinated by APC(Cdc20).
  • By contrast, the high-affinity interaction between Acm1 and APC(Cdh1) renders it a poor substrate, but a specific inhibitor, of the APC(Cdh1) complex.
  • [MeSH-major] Repressor Proteins / metabolism. Saccharomyces cerevisiae / metabolism. Saccharomyces cerevisiae Proteins / metabolism. Ubiquitin-Protein Ligase Complexes / antagonists & inhibitors. Ubiquitin-Protein Ligase Complexes / metabolism
  • [MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Cdc20 Proteins. Cdh1 Proteins. Cell Cycle Proteins / metabolism. Mitosis. Substrate Specificity. Ubiquitination

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  • [CommentOn] Mol Cell. 2008 May 23;30(4):437-46 [18498748.001]
  • (PMID = 18538651.001).
  • [ISSN] 1097-4164
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acm1 protein, S cerevisiae; 0 / CDC20 protein, S cerevisiae; 0 / CDH1 protein, S cerevisiae; 0 / Cdc20 Proteins; 0 / Cdh1 Proteins; 0 / Cell Cycle Proteins; 0 / Repressor Proteins; 0 / Saccharomyces cerevisiae Proteins; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
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16. Fouladkhah A, Avens JS: Effects of combined heat and acetic acid on natural microflora reduction on cantaloupe melons. J Food Prot; 2010 May;73(5):981-4
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  • High level of nutrients and water activity, direct contact with soil, and lack of thermal procedures during primary processing make fresh produce a potential food safety hazard.
  • Aerobic plate counts (APC) of dilutions were determined.
  • Statistical analysis (least significant difference-based analysis of variance) showed that there were no significant (P > 0.05) differences in APC among control, water at 25 degrees C, and 5% acetic acid at 25 degrees C.
  • Thermal treatments with water at 95 degrees C, and 5% acetic acid at 95 degrees C, were both significantly (P < 0.05) more effective in APC reduction than were nonthermal treatments, but were not significantly different from each other.
  • Results indicated that a thermal water immersion intervention in primary processing of fresh melons can result in a 3-log reduction of natural microflora surface contamination, but 5% acetic acid will not significantly augment this reduction.

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  • (PMID = 20501053.001).
  • [ISSN] 0362-028X
  • [Journal-full-title] Journal of food protection
  • [ISO-abbreviation] J. Food Prot.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents, Local; Q40Q9N063P / Acetic Acid
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17. Hosseini BH, Louban I, Djandji D, Wabnitz GH, Deeg J, Bulbuc N, Samstag Y, Gunzer M, Spatz JP, Hämmerling GJ: Immune synapse formation determines interaction forces between T cells and antigen-presenting cells measured by atomic force microscopy. Proc Natl Acad Sci U S A; 2009 Oct 20;106(42):17852-7
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  • This recognition results in the formation of a so-called immune synapse (IS) at the T-cell/APC interface, which is crucial for T-cell activation.
  • Dynamic analysis of T-cell/APC interaction by AFM revealed that in the presence of antigen interaction forces increased from 1 to 2 nN at early time-points to a maximum of approximately 14 nN after 30 min and decreased again after 60 min.
  • Because the integrin lymphocyte function antigen-1 (LFA-1) and its counterpart intercellular adhesion molecule-1 (ICAM-1) are prominent members of a mature IS, the effect of a small molecular inhibitor for LFA-1, BIRT377, was investigated.
  • BIRT377 almost completely abolish the interaction forces, emphasizing the importance of LFA-1/ICAM-1-interactions for firm T-cell/APC adhesion.

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  • (PMID = 19822763.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / PN2 EY016586
  • [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 / BIRT 377; 0 / Imidazolidines; 0 / Lymphocyte Function-Associated Antigen-1; 0 / Peptide Fragments; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 3.2.1.- / hen egg lysozyme; EC 3.2.1.17 / Muramidase
  • [Other-IDs] NLM/ PMC2764924
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18. Lyons LC, Collado MS, Khabour O, Green CL, Eskin A: The circadian clock modulates core steps in long-term memory formation in Aplysia. J Neurosci; 2006 Aug 23;26(34):8662-71
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  • We investigated whether the circadian clock modulated core molecular processes necessary for memory formation in vivo by analyzing circadian regulation of basal and LTS-induced levels of phosphorylated mitogen-activated protein kinase (P-MAPK) and Aplysia CCAAT/enhancer binding protein (ApC/EBP).
  • In contrast, the circadian clock regulated basal levels of ApC/EBP protein with peak levels at night, antiphase to the rhythm in LTS.
  • Importantly, LTS training during the (subjective) day produced greater increases in P-MAPK and ApC/EBP than training at night.
  • Thus, circadian modulation of LTS occurs, at least in part, by suppressing changes in key proteins at night.
  • Rescue of long-term memory formation at night required both facilitation of MAPK and transcription in conjunction with LTS training, confirming that the circadian clock at night actively suppresses MAPK activation and transcription involved in memory formation.
  • The circadian clock appears to modulate LTS at multiple levels.
  • Together, our studies suggest that the circadian clock modulates LTS at multiple steps and locations during the formation of long-term memory.
  • [MeSH-minor] Animals. CCAAT-Enhancer-Binding Proteins / metabolism. Electric Stimulation / methods. Enzyme Activation / physiology. Ganglia, Invertebrate / enzymology. Hemolymph / metabolism. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Serotonin / metabolism

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  • (PMID = 16928854.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS050589
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 333DO1RDJY / Serotonin; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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19. Favory R, Lancel S, Maréchal X, Tissier S, Neviere R: Cardiovascular protective role for activated protein C during endotoxemia in rats. Intensive Care Med; 2006 Jun;32(6):899-905
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  • [Title] Cardiovascular protective role for activated protein C during endotoxemia in rats.
  • OBJECTIVE: We examined whether activated protein C (APC) treatment improves cardiovascular inflammation and dysfunction in endotoxemic rats.
  • DESIGN AND SETTING: Randomized, controlled trial in an experimental laboratory of a university physiology department SUBJECTS: Male Sprague Dawley rats.
  • INTERVENTIONS: Internal carotid artery and external jugular vein were catheterized under sterile conditions in rats.
  • Instrumented rats infused or not with APC (240 microg/kg per hour) were challenged with E. coli endotoxin (10 mg/kg).
  • MEASUREMENTS AND RESULTS: Endotoxin administration induced systemic hypotension, depression of myocardial systolic performance and reduction in capillary density of the small intestine muscularis layer.
  • Plasma levels of nitrite/nitrate, tumor necrosis factor alpha and macrophage migration inhibitory factor, mesentery venule leukocyte-endothelium interactions, heart and small intestine myeloperoxidase activities were increased in endotoxin-treated rats.
  • APC largely prevented endotoxin-induced cardiovascular dysfunction with improved systemic hemodynamics, functional capillary density, and myocardial contractile performance.
  • Beneficial cardiovascular effects of APC were associated with attenuation of entotoxin-induced inflammatory response in terms of plasma levels of nitrite/nitrate, tumor necrosis factor alpha, macrophage migration inhibitory factor, and endothelial cell-leukocyte activation.
  • CONCLUSION: APC reduces systemic and tissue inflammation and preserves cardiovascular function during experimental endotoxemia.
  • [MeSH-major] Cardiovascular System / drug effects. Endotoxemia. Protein C Inhibitor / pharmacology. Serine Proteinase Inhibitors / pharmacology

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  • (PMID = 16601957.001).
  • [ISSN] 0342-4642
  • [Journal-full-title] Intensive care medicine
  • [ISO-abbreviation] Intensive Care Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein C Inhibitor; 0 / Serine Proteinase Inhibitors
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20. Kalchayanand N, Arthur TM, Bosilevac JM, Brichta-Harhay DM, Guerini MN, Shackelford SD, Wheeler TL, Koohmaraie M: Microbiological characterization of lamb carcasses at commercial processing plants in the United States. J Food Prot; 2007 Aug;70(8):1811-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To address this missing information, a total of 2,548 sponge samples from pelts, preevisceration carcasses, and postintervention carcasses were collected from multiple large commercial lamb processing plants to determine aerobic plate counts, the prevalences of Escherichia coli O157:H7, non-O157 Shiga toxin-producing E. coli (STEC), and Salmonella.
  • The prevalences of E. coli O157:H7 from the pelts, the preevisceration carcasses, and the postintervention carcasses were 12.8, 1.6, and 2.9%, respectively.
  • The average Salmonella prevalences were 14.4, 4.3, and 1.8% for pelts, preevisceration carcasses, and postintervention carcasses, respectively.
  • A small number of STEC serotypes associated with severe human illness were isolated from postintervention carcasses.
  • The results of this study establish a baseline for microbiological quality and prevalences of Salmonella, E. coli O157:H7, and STEC in U.S. lamb processing plants.
  • [MeSH-major] Escherichia coli / isolation & purification. Food Contamination / analysis. Food-Processing Industry / standards. Salmonella / isolation & purification. Sheep / microbiology
  • [MeSH-minor] Abattoirs. Animals. Colony Count, Microbial. Consumer Product Safety. Escherichia coli O157 / isolation & purification. Food Microbiology. Humans. Meat / microbiology. Prevalence. Serotyping. United States

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  • (PMID = 17803136.001).
  • [ISSN] 0362-028X
  • [Journal-full-title] Journal of food protection
  • [ISO-abbreviation] J. Food Prot.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Holler E, Landfried K, Meier J, Hausmann M, Rogler G: The role of bacteria and pattern recognition receptors in GVHD. Int J Inflam; 2010;2010:814326
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  • Graft-versus-Host Disease (GvHD) is the most serious complication of allogeneic stem cell transplantation (SCT) and results from an activation of donor lymphocytes by recipient antigen-presenting cells (APCs).
  • For a long time, it has been postulated that the intestinal microflora and endotoxin exert a crucial step in this APC activation, as there is early and severe gastrointestinal damage induced by pretransplant conditioning.
  • With the detailed description of pathogen-associated molecular patterns and pathogen recognition receptors single nucleotide polymorphisms of TLRs and especially NOD2 have been identified as potential risk factors of GvHD and transplant related complications thus further supporting the crucial role of innate immunity in SCT, related complications.
  • Gastrointestinal decontamination and neutralization of endotoxin have been used to interfere with this early axis of activation with some success but more specific approaches of modulation of innate immunity are needed for further improvement of clinical outcome.

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  • (PMID = 21188220.001).
  • [ISSN] 2042-0099
  • [Journal-full-title] International journal of inflammation
  • [ISO-abbreviation] Int J Inflam
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3003997
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22. Marrocco K, Bergdoll M, Achard P, Criqui MC, Genschik P: Selective proteolysis sets the tempo of the cell cycle. Curr Opin Plant Biol; 2010 Dec;13(6):631-9
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  • This is achieved by the action of ubiquitin ligases (E3s), which remove both negative and positive regulators of the cell cycle.
  • Though our current understanding of the plant cell cycle has improved a lot these recent years, the identity of the E3s regulating it and their mode of action is still in its infancy.
  • Thus the anaphase promoting complex/cyclosome (APC/C) not only controls mitotic events, but is also important in post-mitotic cells for normal plant development and cell differentiation.
  • [MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Models, Biological. Plant Growth Regulators / metabolism. Ubiquitin-Protein Ligase Complexes / genetics. Ubiquitin-Protein Ligase Complexes / metabolism. Ubiquitin-Protein Ligases / genetics. Ubiquitin-Protein Ligases / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20810305.001).
  • [ISSN] 1879-0356
  • [Journal-full-title] Current opinion in plant biology
  • [ISO-abbreviation] Curr. Opin. Plant Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Plant Growth Regulators; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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23. Yoshida K: Cell-cycle-dependent regulation of the human and mouse Tome-1 promoters. FEBS Lett; 2005 Feb 28;579(6):1488-92
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  • In turn, Tome-1 itself is targeted for degradation by APC in the G1 phase of the cell cycle.
  • [MeSH-major] Cell Cycle / genetics. Cell Cycle Proteins / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] 5' Flanking Region / genetics. Animals. Base Sequence. Cell Division. Down-Regulation / genetics. G2 Phase. Humans. Mice. Molecular Sequence Data. Mutation / genetics. NIH 3T3 Cells. Sequence Alignment. Transcriptional Activation / genetics

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  • (PMID = 15733861.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CDCA3 protein, human; 0 / Cell Cycle Proteins; 0 / Tome-1 protein, mouse
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24. Koester MP, Müller O, Pollerberg GE: Adenomatous polyposis coli is differentially distributed in growth cones and modulates their steering. J Neurosci; 2007 Nov 14;27(46):12590-600
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  • [Title] Adenomatous polyposis coli is differentially distributed in growth cones and modulates their steering.
  • Axonal steering reactions depend on the transformation of environmental information into internal, directed structures, which is achieved by differential modulation of the growth cone cytoskeleton; key elements are the microtubules, which are regulated in their dynamics by microtubule-associated proteins (MAPs).
  • We investigated a potential role of the MAP adenomatous polyposis coli (APC) for growing axons, employing embryonic visual system as a model system.
  • APC is concentrated in the distalmost (i.e., growing) region of retinal ganglion cell axons in vivo and in vitro.
  • Within the growth cone, APC is enriched in the central domain; it only partially colocalizes with microtubules.
  • When axons are induced to turn toward a cell or away from a substrate border, APC is present in the protruding and absent from the collapsing growth cone regions, thus indicating the future growth direction of the axon.
  • To assess the functional role of the differential distribution of APC in navigating growth cones, the protein was inactivated via micro-scale chromophore-assisted laser inactivation in one half of the growth cone.
  • If the N-terminal APC region (crucial for its oligomerization) is locally inactivated, the treated growth cone side collapses and the axon turns away.
  • In contrast, if the 20 aa repeats in the middle region of APC (which can negatively regulate its microtubule association) are inactivated, protrusions are formed and the growth cone turns toward.
  • Our data thus demonstrate a crucial role of APC for axon steering attributable to its multifunctional domain structure and differential distribution in the growth cone.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Cell Differentiation / physiology. Central Nervous System / embryology. Central Nervous System / metabolism. Growth Cones / metabolism
  • [MeSH-minor] Animals. Body Patterning / physiology. Body Patterning / radiation effects. Cell Communication / physiology. Chick Embryo. Chickens. Humans. Lasers. Microtubules / metabolism. Microtubules / ultrastructure. Protein Structure, Tertiary / physiology. Protein Structure, Tertiary / radiation effects. Retinal Ganglion Cells / cytology. Retinal Ganglion Cells / metabolism. Retinal Ganglion Cells / radiation effects. Visual Pathways / cytology. Visual Pathways / embryology. Visual Pathways / metabolism

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  • (PMID = 18003838.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
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25. Chambers WM, McC Mortensen NJ: Should ileal pouch-anal anastomosis include mucosectomy? Colorectal Dis; 2007 Jun;9(5):384-92
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  • OBJECTIVE: Debate exists as to the benefits of performing mucosectomy as part of pouch surgery for ulcerative colitis (UC) and familial adenomatous polyposis (FAP).
  • Potential reasons for functional problems were investigated, as were rates of 'cuffitis', dysplasia, polyposis and cancer in the ileal pouch and anal canal.
  • Meta-analysis suggested that nighttime seepage of stool and resting and squeeze pressure were worse after mucosectomy.
  • Mucosectomy does seem to confer benefit in terms of disease control but this benefit does not reach statistical significance.
  • Performing mucosectomy results in some clinical benefits in terms of lower rates of inflammation and dysplasia in the retained mucosa in UC patients and lower rates of cuff polyposis in FAP patients.
  • However, on the basis of available evidence mucosectomy is only indicated in those cases where the patient is at a high risk of disease in the retained rectal cuff.
  • [MeSH-major] Colonic Pouches / adverse effects. Intestinal Mucosa / surgery. Proctocolectomy, Restorative / adverse effects
  • [MeSH-minor] Adenocarcinoma / prevention & control. Adenomatous Polyposis Coli / surgery. Anastomosis, Surgical / adverse effects. Anastomosis, Surgical / methods. Anus Neoplasms / prevention & control. Arsenates. Colitis, Ulcerative / surgery. Humans. Ileal Neoplasms / prevention & control. Randomized Controlled Trials as Topic

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  • (PMID = 17504334.001).
  • [ISSN] 1462-8910
  • [Journal-full-title] Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland
  • [ISO-abbreviation] Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenates; N7CIZ75ZPN / arsenic acid
  • [Number-of-references] 70
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26. Mozaffarian N, Wiedeman AE, Stevens AM: Active systemic lupus erythematosus is associated with failure of antigen-presenting cells to express programmed death ligand-1. Rheumatology (Oxford); 2008 Sep;47(9):1335-41
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  • [Title] Active systemic lupus erythematosus is associated with failure of antigen-presenting cells to express programmed death ligand-1.
  • OBJECTIVE: Antigen-presenting cells (APC) play critical roles in establishing and maintaining peripheral tolerance.
  • This is accomplished in part via expression of negative co-stimulatory molecules such as programmed death ligand-1 (PD-L1) on tolerogenic APC, such as immature myeloid dendritic cells (mDC).
  • Several studies have strongly linked dysfunction of APC, including mDC, to the pathogenesis of SLE.
  • The objective of this study was to determine whether APC expressed PD-L1 protein at normal levels during active lupus.
  • In contrast, both mDC and Mo from patients with active SLE failed to up-regulate PD-L1 over a 5 day time course, expressing this protein only during disease remissions.
  • CONCLUSIONS: These data are the first to link active lupus with reversibly decreased PD-L1 expression on professional APC, suggesting a novel mechanism for loss of peripheral tolerance in SLE.

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  • (PMID = 18650228.001).
  • [ISSN] 1462-0332
  • [Journal-full-title] Rheumatology (Oxford, England)
  • [ISO-abbreviation] Rheumatology (Oxford)
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000037; United States / NIAMS NIH HHS / AR / T32 AR007108; United States / NCRR NIH HHS / RR / M01-RR-00037
  • [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, CD; 0 / Antigens, CD274; 0 / CD274 protein, human
  • [Other-IDs] NLM/ PMC2722808
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27. Alferez DG, Ryan AJ, Goodlad RA, Wright NA, Wilkinson RW: Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model. Int J Oncol; 2010 Oct;37(4):767-72
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  • [Title] Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.
  • The Apc(MIN/+) mouse is a well-characterised model of intestinal tumourigenesis in which animals develop macroscopically detectable adenomas.
  • However, most of the adenomas are formed in the small intestine and resolution of events in the colon, the most relevant site for human disease, is limited.
  • Inducing colitis with dextran sodium sulphate (DSS) can selectively enhance the development of lesions in the colon.
  • We demonstrated that a DSS pre-treatment is well tolerated and effective at inducing colon adenomas in an Apc(MIN/+) mouse model.
  • We then investigated the effect of inhibiting vascular endothelial growth factor (VEGFR)- and epidermal growth factor receptor (EGFR)-dependent signalling pathways on the development of adenomas induced in DSS-pretreated (DSS/Apc(MIN/+)) or non-DSS-pretreated (Apc(MIN/+)) mice using vandetanib (ZD6474), a potent and selective inhibitor of VEGFR and EGFR tyrosine kinase activity.
  • Eight-week old Apc(MIN/+) mice were given either drinking water or 1.8% DSS and then vandetanib (ZD6474) (50 mg/kg/day) or vehicle by oral gavage for 28 days and sacrificed 24 h after the last dose and assessed for adenoma formation in the intestines.
  • DSS pre-treatment was well tolerated and significantly enhanced formation of adenomas in the colon of control Apc(MIN/+) mice.
  • Vandetanib treatment significantly reduced adenoma formation in the small intestine by 68% (P=0.001) and the colon by 77% (from 13.8 to 3.1, P=0.01) of DSS-pretreated Apc(MIN/+) mice.
  • In the Apc(MIN/+) group, vandetanib also reduced the mean number of adenomas in the small intestine by 76% (P<0.001) and in the colon by 60% (from 3.9 to 1.5, P=0.1).
  • DSS-pre-treatment increased the resolution of the model, allowing us to confirm statistically significant effects of vandetanib on the development and growth of colon adenomas in the Apc(MIN/+) mouse.
  • Moreover these preclinical data provide a rationale for studying the effects of vandetanib in early stages of intestinal cancer in the clinic.
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / pharmacology. Colitis / chemically induced. Colonic Neoplasms / prevention & control. Dextran Sulfate. Genes, APC. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Intestine, Small / drug effects. Intestine, Small / enzymology. Intestine, Small / pathology. Mice. Mice, Inbred C57BL. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / metabolism. beta Catenin / metabolism

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  • (PMID = 20811697.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 2.7.10.1 / EGFR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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28. Heng W, Huang JA, Shen WH, Dai L, Bai X, Wang ZY: [Expression of endothelial protein C receptor in tumor cell lines and It's significance]. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2010 Aug;26(8):761-3
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  • [Title] [Expression of endothelial protein C receptor in tumor cell lines and It's significance].
  • AIM: To detect the role of activated protein C(APC) on proliferation of endothelial cell and investigate the expression of endothelial protein C receptor( EPCR) in variety of tumor cell lines.
  • METHODS: The effect of APC on endotheliocyte proliferation was determined by MTT colorimetry.
  • RESULTS: APC can increase the proliferation of EC significantly.
  • CONCLUSION: APC can stimulate the proliferation of endothelial cell.
  • High expression of EPCR in tumor cell lines provides a potential biological marker for malignancies.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Interleukin-6 / metabolism. Interleukin-8 / metabolism. Protein C / metabolism

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  • (PMID = 20619102.001).
  • [ISSN] 1007-8738
  • [Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
  • [ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Interleukin-6; 0 / Interleukin-8; 0 / PROCR protein, human; 0 / Protein C; 0 / Receptors, Cell Surface
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29. Kryczek I, Wei S, Gong W, Shu X, Szeliga W, Vatan L, Chen L, Wang G, Zou W: Cutting edge: IFN-gamma enables APC to promote memory Th17 and abate Th1 cell development. J Immunol; 2008 Nov 1;181(9):5842-6
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  • [Title] Cutting edge: IFN-gamma enables APC to promote memory Th17 and abate Th1 cell development.
  • However, Th1, Th17, and memory but not naive T cells are colocalized in an inflammatory environment.
  • We show that IFN-gamma stimulates B7-H1 expression on APC subsets and abates their Th1 polarization capacity in a B7-H1-dependent manner.
  • Interestingly, IFN-gamma triggers APCs to produce IL-1 and IL-23 and enables them to induce memory Th17 expansion via IL-1 and IL-23 in a B7-H1-independent manner.
  • We propose a novel dynamic between Th1 and Th17 in the course of inflammation as follows: Th1-mediated inflammation is attenuated by IFN-gamma-induced B7-H1 on APCs and is evolved toward Th17-mediated chronic inflammation by IFN-gamma-induced, APC-derived IL-1 and IL-23.

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  • (PMID = 18941172.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099985; United States / NCI NIH HHS / CA / CA123088
  • [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 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human; 0 / Growth Inhibitors; 0 / Interleukin-1; 0 / Interleukin-17; 0 / Interleukin-23; 82115-62-6 / Interferon-gamma
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30. Walker A, Acquaviva C, Matsusaka T, Koop L, Pines J: UbcH10 has a rate-limiting role in G1 phase but might not act in the spindle checkpoint or as part of an autonomous oscillator. J Cell Sci; 2008 Jul 15;121(Pt 14):2319-26
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  • [Title] UbcH10 has a rate-limiting role in G1 phase but might not act in the spindle checkpoint or as part of an autonomous oscillator.
  • Ubiquitin-dependent proteolysis mediated by the anaphase-promoting complex/cyclosome (APC/C) ubiquitin ligase lies at the heart of the cell cycle.
  • The APC/C targets mitotic cyclins for destruction in mitosis and G1 phase and is then inactivated at S phase, thereby generating the alternating states of high and low cyclin-Cdk activity required for the alternation of mitosis and DNA replication.
  • Two key questions are how the APC/C is held in check by the spindle-assembly checkpoint to delay cells in mitosis in the presence of improperly attached chromosomes, and how the APC/C is inactivated once cells exit mitosis.
  • The ubiquitin-conjugating protein UbcH10 has been proposed to be crucial in the answers to both questions.
  • However, here we show that the behaviour of UbcH10 is inconsistent with both a crucial role in the spindle checkpoint and in inactivating the APC/C as part of an autonomous oscillator.

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  • (PMID = 18559889.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin A; EC 6.3.2.19 / UBE2C protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
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31. Tojo K, Sekijima Y, Kelly JW, Ikeda S: Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis. Neurosci Res; 2006 Dec;56(4):441-9
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  • [Title] Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis.
  • Transthyretin (TTR) tetramer dissociation, misfolding and misassembly are required for the process of amyloid fibril formation associated with familial amyloid polyneuropathy (FAP).
  • Here, we investigated the feasibility of using these molecules for the treatment of FAP utilizing serum samples from 37 FAP patients with 10 different mutations.
  • We demonstrated that the TTR heterotetramer structures in FAP patients serum are significantly less stable than that in normal subjects, indicating the instability of the variant TTR structure is a fundamental cause of TTR amyloidosis.
  • Trivalent chromium at levels obtained by oral supplementation did not stabilize TTR in a statistically significant fashion.
  • Importantly, diflunisal increased serum TTR stability in FAP patients beyond the level of normal controls.
  • [MeSH-major] Amyloid Neuropathies, Familial / metabolism. Amyloid beta-Peptides / biosynthesis. Amyloid beta-Peptides / genetics. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Diflunisal / pharmacology. Prealbumin / biosynthesis. Prealbumin / genetics
  • [MeSH-minor] Adult. Aged. Chromium / pharmacology. Female. Flufenamic Acid / pharmacology. Humans. Hydrogen-Ion Concentration. Iron / physiology. Male. Middle Aged. Mutation / physiology. Protein Denaturation

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  • (PMID = 17028027.001).
  • [ISSN] 0168-0102
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK046335
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Prealbumin; 0R0008Q3JB / Chromium; 60GCX7Y6BH / Flufenamic Acid; 7C546U4DEN / Diflunisal; E1UOL152H7 / Iron
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32. Langelaar MF, Hope JC, Rutten VP, Noordhuizen JP, van Eden W, Koets AP: Mycobacterium avium ssp. paratuberculosis recombinant heat shock protein 70 interaction with different bovine antigen-presenting cells. Scand J Immunol; 2005 Mar;61(3):242-50
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  • [Title] Mycobacterium avium ssp. paratuberculosis recombinant heat shock protein 70 interaction with different bovine antigen-presenting cells.
  • Abstract Heat shock proteins (Hsp) can deliver antigen into the major histocompatibility complex class I presentation pathway of antigen-presenting cells (APC), a process called cross priming, thus stimulating antigen-specific CD8+ T-cell reactions.
  • Hsp were shown to elicit proinflammatory responses in APC.
  • Both processes require interaction of Hsp with APC via specific receptors.
  • Characterized monocyte-derived macrophages, monocyte-derived dendritic cells (DC) and BoMac, an immortalized bovine macrophage cell line, were used to investigate the interaction of rHsp70 with different bovine APC.
  • Involvement of CD91 as a cellular receptor for rHsp70 was demonstrated; however, competition studies with immature DC demonstrated that other receptors exist on bovine APC.
  • [MeSH-major] Antigen-Presenting Cells / immunology. Bacterial Proteins / immunology. HSP70 Heat-Shock Proteins / immunology. Mycobacterium avium subsp. paratuberculosis / immunology

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  • (PMID = 15787741.001).
  • [ISSN] 0300-9475
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Bacterial Proteins; 0 / Bacterial Vaccines; 0 / HSP70 Heat-Shock Proteins; 0 / alpha-Macroglobulins
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33. Yamashita T, Ando Y, Ueda M, Okamoto S, Misumi Y, Nakamura M, Takashi O, Uchino M: A rapid and sensitive prenatal diagnosis of familial amyloidotic polyneuropathy ATTR Val30Met by mass spectrometry. Prenat Diagn; 2009 Oct;29(10):930-3
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  • [Title] A rapid and sensitive prenatal diagnosis of familial amyloidotic polyneuropathy ATTR Val30Met by mass spectrometry.
  • OBJECTIVE: To make a prenatal diagnosis of familial amyloidotic polyneuropathy (FAP) by mass spectrometry with the amniotic fluid.
  • METHODS: Amniotic-fluid samples of three non-FAP pregnant women and six amniotic-fluid samples of fetal mice whose mother was a heterozygotic FAP amyloidgenic transthyretin (ATTR) Val30Met gene carrier were collected.
  • CONCLUSION: Mass spectrometry analysis of the amniotic fluid might be a useful tool to make a prenatal diagnosis of FAP ATTR Val30Met.
  • [MeSH-major] Amyloid Neuropathies, Familial / diagnosis. Mass Spectrometry / methods. Prealbumin / analysis. Prenatal Diagnosis / methods

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  • (PMID = 19609897.001).
  • [ISSN] 1097-0223
  • [Journal-full-title] Prenatal diagnosis
  • [ISO-abbreviation] Prenat. Diagn.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Prealbumin; AE28F7PNPL / Methionine; HG18B9YRS7 / Valine
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34. Dalby M, Kharbanda R, Ghimire G, Spiro J, Moore P, Roughton M, Lane R, Al-Obaidi M, Teoh M, Hutchison E, Whitbread M, Fountain D, Grocott-Mason R, Mitchell A, Mason M, Ilsley C: Achieving routine sub 30 minute door-to-balloon times in a high volume 24/7 primary angioplasty center with autonomous ambulance diagnosis and immediate catheter laboratory access. Am Heart J; 2009 Nov;158(5):829-35
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  • [Title] Achieving routine sub 30 minute door-to-balloon times in a high volume 24/7 primary angioplasty center with autonomous ambulance diagnosis and immediate catheter laboratory access.
  • Using autonomous ambulance diagnosis with open access to the myocardial infarction center catheter laboratory, we compared reperfusion times and clinical outcomes for the final 2 years of TL with the first 3 years of PPCI.
  • RESULTS: Comparison was made between TL (2002-2004, n = 185) and PPCI (2004-2007, n = 704); all times are medians in minutes (interquartile range): for TL, symptom to needle 153 (85-225), call to needle 58 (49-73), first professional contact (FPC) to needle 47 (39-63), door to needle 18 (12-30) (mortality: 7.6% at 30 days, 9.2% at 1 year); for interhospital transfer PPCI (n = 227), symptom to balloon 226 (175-350), call to balloon 135 (117-188), FPC to balloon 121 (102-166), first door-to-balloon 100 (80-142) (mortality: 7.0% at 30 days, 12.3% at 1 year); for direct-access PPCI (n = 477), symptom to balloon 142 (101-238), call to balloon 79 (70-93), FPC to balloon 69 (59-82), door to balloon 20 (16-29) (mortality: 4.6% at 30 days, 8.6% at 1 year).
  • With autonomous ambulance diagnosis and open access direct to the catheter laboratory, a median door-to-balloon time of <30 minutes day and night was achieved, and >95% of patients were reperfused within 1 hour.

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  • [ErratumIn] Am Heart J. 2010 Feb;159(2):330
  • (PMID = 19853705.001).
  • [ISSN] 1097-6744
  • [Journal-full-title] American heart journal
  • [ISO-abbreviation] Am. Heart J.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibrinolytic Agents
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35. Wen K, Azevedo MS, Gonzalez A, Zhang W, Saif LJ, Li G, Yousef A, Yuan L: Toll-like receptor and innate cytokine responses induced by lactobacilli colonization and human rotavirus infection in gnotobiotic pigs. Vet Immunol Immunopathol; 2009 Feb 15;127(3-4):304-15
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  • We demonstrated that LAB induced strong TLR2-expressing APC responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood).
  • LAB and HRV have an additive effect on TLR2- and TLR9-expressing APC responses, consistent with the adjuvant effect of LAB.
  • LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14- APC responses in spleen and the serum IFN-alpha response induced by HRV.

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  • (PMID = 19054578.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI033561-11; United States / NIAID NIH HHS / AI / R01 AI033561; United States / NCCIH NIH HHS / AT / R21 AT002524-02; United States / NCCIH NIH HHS / AT / R21 AT002524; United States / NIAID NIH HHS / AI / AI033561-11; United States / NCCIH NIH HHS / AT / 1R21AT002524; United States / NIAID NIH HHS / AI / R01AI033561
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Toll-Like Receptors
  • [Other-IDs] NLM/ NIHMS89734; NLM/ PMC2653198
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36. Zurbuchen U, Kroesen AJ, Buhr HJ: [Continent ileoanal reservoir--a surgical challenge]. Urologe A; 2008 Jan;47(1):18-24
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  • Nowadays, patients with ulcerative colitis or familial adenomatous polyposis of the colon undergo proctocolectomy as the definitive treatment for their underlying disease.
  • This contribution describes the surgical indications and pathophysiological changes for the colon J-pouch and ileoanal reservoir.
  • In addition, explanations of the surgical techniques for both procedures are presented.

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  • (PMID = 18210064.001).
  • [ISSN] 1433-0563
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 40
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37. Terazaki H, Ando Y, Fernandes R, Yamamura K, Maeda S, Saraiva MJ: Immunization in familial amyloidotic polyneuropathy: counteracting deposition by immunization with a Y78F TTR mutant. Lab Invest; 2006 Jan;86(1):23-31
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  • [Title] Immunization in familial amyloidotic polyneuropathy: counteracting deposition by immunization with a Y78F TTR mutant.
  • The mechanism of amyloid formation in familial amyloidotic polyneuropathy (FAP), a hereditary disorder associated with mutant transthyretin (TTR), is still unknown.
  • To test whether TTR deposition in FAP can be counteracted by antibodies for cryptic epitopes, we immunized with TTR Y78F, transgenic mice carrying the most common FAP-associated TTR mutant--V30M (transthyretin mutant with methionine replacing valine at position 30)--at selected ages that present normally with either nonfibrillar or TTR amyloid deposition.
  • Compared to age-matched control nonimmunized mice, Y78F-immunized mice had a significant reduction in TTR deposition usually found in this strain, in particular in stomach and intestine; by contrast, animals immunized with V30M did not show differences in deposition in comparison with nonimmunized mice.
  • Immunohistochemical analyses of tissues revealed that immunization with Y78F lead to infiltration by lymphocytes and macrophages at common deposition sites, but not in tissues such as liver, choroid plexus, and Langerhans islets, in which TTR is produced.
  • Therefore, TTR immunization with selected TTR mutants has potential application in immune therapy for FAP.
  • [MeSH-major] Amyloid Neuropathies, Familial / prevention & control. Mutation. Prealbumin / administration & dosage

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  • (PMID = 16357867.001).
  • [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 / Prealbumin
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38. Dietrich KA, Schwarz R, Liska M, Grass S, Menke A, Meister M, Kierschke G, Längle C, Genze F, Giehl K: Specific induction of migration and invasion of pancreatic carcinoma cells by RhoC, which differs from RhoA in its localisation and activity. Biol Chem; 2009 Oct;390(10):1063-77
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  • These differences are not mediated by a different interaction with RhoGDIs.
  • [MeSH-major] Cell Movement. Neoplasm Invasiveness. Pancreatic Neoplasms / pathology. rho GTP-Binding Proteins / metabolism. rhoA GTP-Binding Protein / metabolism
  • [MeSH-minor] Cell Line, Tumor. Deep Brain Stimulation. Humans. Protein Isoforms / chemistry. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. rap GTP-Binding Proteins / chemistry. rap GTP-Binding Proteins / genetics. rap GTP-Binding Proteins / metabolism

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  • (PMID = 19642867.001).
  • [ISSN] 1437-4315
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RHOC protein, human; 0 / RNA, Messenger; EC 3.6.5.2 / rap GTP-Binding Proteins; EC 3.6.5.2 / rho GTP-Binding Proteins; EC 3.6.5.2 / rhoA GTP-Binding Protein
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39. Chen D, Kennedy A, Wang JY, Zeng W, Zhao Q, Pearl M, Zhang M, Suo Z, Nesland JM, Qiao Y, Ng AK, Hirashima N, Yamane T, Mori Y, Mitsumata M, Ghersi G, Chen WT: Activation of EDTA-resistant gelatinases in malignant human tumors. Cancer Res; 2006 Oct 15;66(20):9977-85
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  • [Title] Activation of EDTA-resistant gelatinases in malignant human tumors.
  • Among the many proteases associated with human cancer, seprase or fibroblast activation protein alpha, a type II transmembrane glycoprotein, has two types of EDTA-resistant protease activities: dipeptidyl peptidase and a 170-kDa gelatinase activity.
  • To test if activation of gelatinases associated with seprase could be involved in malignant tumors, we used a mammalian expression system to generate a soluble recombinant seprase (r-seprase).
  • Proteins purified from experimental xenografts and malignant tumors using antibody- or lectin-affinity columns in the presence of 5 mmol/L EDTA were assayed for seprase activation in vivo.
  • Seprase expression and activation occur most prevalently in ovarian carcinoma but were also detected in four other malignant tumor types, including adenocarcinoma of the colon and stomach, invasive ductal carcinoma of the breast, and malignant melanoma.

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  • (PMID = 17047060.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA039077; United States / NIBIB NIH HHS / EB / R01EB002065; United States / NIBIB NIH HHS / EB / R01 EB002065; United States / NCRR NIH HHS / RR / M01 RR010710; United States / NCRR NIH HHS / RR / M01RR10710; United States / NCI NIH HHS / CA / R01CA0039077
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / Recombinant Proteins; 9G34HU7RV0 / Edetic Acid; EC 3.4.14.- / Dipeptidyl-Peptidases and Tripeptidyl-Peptidases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ NIHMS11890; NLM/ PMC1626657
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40. Morais-de-Sá E, Neto-Silva RM, Pereira PJ, Saraiva MJ, Damas AM: The binding of 2,4-dinitrophenol to wild-type and amyloidogenic transthyretin. Acta Crystallogr D Biol Crystallogr; 2006 May;62(Pt 5):512-9
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  • [Title] The binding of 2,4-dinitrophenol to wild-type and amyloidogenic transthyretin.
  • Systemic deposition of transthyretin (TTR) amyloid fibrils is always observed in familial amyloidotic polyneuropathy, senile systemic amyloidosis and familial amyloidotic cardiomyopathy patients.
  • The destabilization of a native protein with consequent conformational changes appears to be a common link in several human amyloid diseases.
  • Intensive research has been directed towards finding small molecules that could work as therapeutic agents for the prevention/inhibition of amyloid diseases through stabilization of the native fold of the potentially amyloidogenic protein.
  • This work provides insight into the structural determinants of the highly stabilizing effects of 2,4-dinitrophenol on wild-type TTR.
  • As a result of 2,4-dinitrophenol binding, the two dimers in the TTR tetramer become closer, increasing the stability of the protein.
  • The three-dimensional structures now determined allow a comprehensive description of key interactions between transthyretin and 2,4-dinitrophenol, a small compound that holds promise as a template for the design of a therapeutical drug for amyloid diseases.

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  • (PMID = 16627944.001).
  • [ISSN] 0907-4449
  • [Journal-full-title] Acta crystallographica. Section D, Biological crystallography
  • [ISO-abbreviation] Acta Crystallogr. D Biol. Crystallogr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Peptides; 0 / Prealbumin; Q13SKS21MN / 2,4-Dinitrophenol
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41. Inoue K, Hiraoka T, Kanemitsu K, Takamori H, Tsuji T, Kawasuji M: Onset of liver metastasis after histologically curative resection of pancreatic cancer. Surg Today; 2006;36(3):252-6
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  • [Title] Onset of liver metastasis after histologically curative resection of pancreatic cancer.
  • PURPOSE: We assessed the possibility of predicting the time of onset of liver metastases by measuring the postoperative changes in serum carbohydrate antigen (CA)19-9 after curative resection of pancreatic cancers.
  • METHODS: Among 28 patients who underwent histologically defined curative resection of pancreatic cancer between 1984 and 1999, liver metastasis developed in 11 patients with elevated serum CA19-9 levels.
  • We plotted the serum CA19-9 levels against time on a semilogarithmic graph.
  • Over the linear part of the curve, the time when log[CA19-9] equaled zero was defined as the time of onset of liver metastases.
  • The log[CA19-9] level doubling time was then calculated and evaluated in relation to the survival period.
  • RESULTS: The serum CA19-9 levels increased linearly in 10 of the 11 patients.
  • The predicted time of onset of liver metastasis ranged from preoperative day 163.0 to postoperative day 27.1, being preoperative in eight patients.
  • The doubling time until death correlated strongly with survival in the eight patients with maintained log[CA19-9] linearity.
  • CONCLUSION: The onset of liver metastases might be preoperative in patients with advanced pancreatic cancer.
  • Therefore, neoadjuvant chemotherapy should be mandatory even if there is no sign of liver metastases.
  • [MeSH-major] Biomarkers, Tumor / blood. CA-19-9 Antigen / blood. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Prognosis. Time Factors

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  • (PMID = 16493535.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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42. Cai H, Hua B, Fan L, Wang Q, Wang S, Zhao Y: A novel mutation (g2172--&gt;c) in the factor V gene in a Chinese family with hereditary activated protein C resistance. Thromb Res; 2010 Jun;125(6):545-8
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  • [Title] A novel mutation (g2172-->c) in the factor V gene in a Chinese family with hereditary activated protein C resistance.
  • BACKGROUND: Activated protein C resistance (APC-R) was a major risk factor for venous thromboembolism(VTE) in Caucasians, and at least 90% of APC-R were associated with the point mutation of factor V (FV) gene (Arg506-->Gln, FV Leiden).
  • OBJECTIVE: To identify the genetic defect of FV in a Chinese family with APC-R associated with VTE.
  • Blood samples were obtained from five family members (including the proband) for screening APC-R by coagulation assay and the genetic defect of FV using direct sequencing.
  • RESULTS: Four out of five members had APC-R.
  • We identified a novel mutation (G2172-->C) in exon 13 of the FV gene, which was present in all the individuals with APC-R but was absent in the individual without APC-R.
  • This mutation is predicted to result in the replacement of glutamate by aspartate at position 666, close to one of the APC cleavage sites.
  • CONCLUSIONS: We have identified, for the first time, a novel mutation (G2172-->C) of FV that was associated with APC-R in a Chinese family with VTE.
  • We speculate that this mutation interferes with cleavage at Arg679 by APC.
  • [MeSH-major] Activated Protein C Resistance / genetics. Factor V / genetics. Point Mutation

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20304467.001).
  • [ISSN] 1879-2472
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9001-24-5 / Factor V
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43. Sangha S, Yao M, Wolfe MM: Non-steroidal anti-inflammatory drugs and colorectal cancer prevention. Postgrad Med J; 2005 Apr;81(954):223-7
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  • Currently, the most effective strategy available for colon cancer prevention is endoscopic screening, with polypectomy or surgical resection for advanced lesions.
  • Data obtained from animal and epidemiological studies and most recently from randomised, placebo controlled trials, suggest that non-steroidal anti-inflammatory drugs may prove effective chemopreventive agents in different groups of people, from patients with familial adenomatous polyposis to those with sporadic adenomas.
  • [MeSH-minor] Colorectal Neoplasms, Hereditary Nonpolyposis / prevention & control. Humans. Randomized Controlled Trials as Topic. Treatment Outcome

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  • (PMID = 15811884.001).
  • [ISSN] 0032-5473
  • [Journal-full-title] Postgraduate medical journal
  • [ISO-abbreviation] Postgrad Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents
  • [Other-IDs] NLM/ PMC1743256
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44. Wick EC, Sears CL: Bacteroides spp. and diarrhea. Curr Opin Infect Dis; 2010 Oct;23(5):470-4
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  • RECENT FINDINGS: Bacteroides fragilis is the only strain of Bacteroides spp. associated with diarrheal disease.
  • Toxin-producing strains of B. fragilis, termed enterotoxigenic Bacteroides fragilis (ETBF), are an established cause of diarrheal disease in people.
  • The clinical syndrome associated with ETBF diarrheal disease encompasses abdominal pain, tenesmus and inflammatory diarrhea.
  • Two new studies conducted in mice have further defined the chronic inflammatory response associated with ETBF infection and observed that in the multiple intestinal neoplasia mouse strain, heterozygotes for the adenomatous polyposis coli gene, ETBF infection enhances development of colonic tumors.
  • SUMMARY: B. fragilis remains the leading anaerobe in human disease.
  • ETBF is emerging as an important cause of human diarrheal disease but additional epidemiologic studies are needed to better understand the role of ETBF human disease.

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  • (PMID = 20697287.001).
  • [ISSN] 1473-6527
  • [Journal-full-title] Current opinion in infectious diseases
  • [ISO-abbreviation] Curr. Opin. Infect. Dis.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK045496-16; United States / NIDDK NIH HHS / DK / DK059655-01; United States / NIDDK NIH HHS / DK / R01 DK059655-03; United States / NIDDK NIH HHS / DK / R01 DK045496-13; United States / NIDDK NIH HHS / DK / DK045496-15; United States / NIDDK NIH HHS / DK / DK059655-02; United States / NIDDK NIH HHS / DK / R01 DK080817-01; United States / NIDDK NIH HHS / DK / DK080817-04; United States / NIDDK NIH HHS / DK / DK080817-01; United States / NIDDK NIH HHS / DK / R01 DK045496; United States / NIDDK NIH HHS / DK / R01 DK059655-02; United States / NIDDK NIH HHS / DK / R01 DK045496-17; United States / NIDDK NIH HHS / DK / R01 DK080817-02; United States / NIDDK NIH HHS / DK / DK045496-16; United States / NIDDK NIH HHS / DK / DK059655-03; United States / NIDDK NIH HHS / DK / DK045496-18; United States / NIDDK NIH HHS / DK / DK080817-02; United States / NIDDK NIH HHS / DK / DK045496-14; United States / NIDDK NIH HHS / DK / R01 DK080817-03; United States / NIDDK NIH HHS / DK / R01 DK059655; United States / NIDDK NIH HHS / DK / R01 DK045496-14; United States / NIDDK NIH HHS / DK / R01 DK045496-15; United States / NIDDK NIH HHS / DK / DK045496-13; United States / NIDDK NIH HHS / DK / R01 DK080817; United States / NIDDK NIH HHS / DK / R01 DK059655-01; United States / NIDDK NIH HHS / DK / DK080817-03; United States / NIDDK NIH HHS / DK / DK045496-17; United States / NIDDK NIH HHS / DK / R01 DK045496-18; United States / NIDDK NIH HHS / DK / R01 DK080817-04
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Bacterial Toxins; 0 / Virulence Factors
  • [Other-IDs] NLM/ NIHMS262792; NLM/ PMC3079340
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45. Winship IM, Dudding TE: Lessons from the skin--cutaneous features of familial cancer. Lancet Oncol; 2008 May;9(5):462-72
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  • [Title] Lessons from the skin--cutaneous features of familial cancer.
  • As the molecular basis of disease continues to be elucidated, familial cancer syndromes, which consist of a range of neoplastic and non-neoplastic features, are emerging.
  • The usual pathway of referral to a genetics clinic or familial cancer centre is via an oncologist, when high-risk features that suggest a possible hereditary basis for the presenting cancer are recognised.
  • These features are effective in ascertaining a substantial proportion of families with hereditary breast and ovarian cancer due to a BRCA mutation, or the more common bowel-cancer predisposition syndromes, such as hereditary non-polyposis colon cancer and familial adenomatous polyposis.
  • However, there are a range of familial cancer syndromes that are not easily detected and that can remain undiagnosed when history and examination are not extended to include non-malignant features.
  • The identification of cutaneous signs associated with rare familial-cancer syndromes provides individuals and their families with the opportunity to undertake early surveillance for malignant and non-malignant complications that might in time be shown to improve outcomes.
  • [MeSH-major] Colonic Neoplasms / pathology. Endocrine Gland Neoplasms / pathology. Kidney Neoplasms / pathology. Neoplastic Syndromes, Hereditary / pathology. Skin / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adenomatous Polyposis Coli / pathology. Basal Cell Nevus Syndrome / pathology. Carcinoma, Renal Cell / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology. Disease Progression. Gene Expression Regulation, Neoplastic. Genetic Testing. Hamartoma Syndrome, Multiple / pathology. Humans. Leiomyomatosis / pathology. Multiple Endocrine Neoplasia / pathology. Multiple Endocrine Neoplasia Type 2a / pathology. Multiple Endocrine Neoplasia Type 2b / pathology. Mutation. Neurofibromatosis 1 / pathology. Neurofibromatosis 2 / pathology. Pedigree. Peutz-Jeghers Syndrome / pathology. Tuberous Sclerosis / pathology

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  • (PMID = 18452857.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 75
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46. Giles RH, Lolkema MP, Snijckers CM, Belderbos M, van der Groep P, Mans DA, van Beest M, van Noort M, Goldschmeding R, van Diest PJ, Clevers H, Voest EE: Interplay between VHL/HIF1alpha and Wnt/beta-catenin pathways during colorectal tumorigenesis. Oncogene; 2006 May 18;25(21):3065-70
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  • Activation of the Wnt signaling pathway initiates the transformation of colorectal epithelial cells, although the transition to metastatic cancer requires angiogenesis.
  • Here, we show that VHL expression is regulated by TCF4 and is restricted to the proliferative compartment at the bottom of intestinal crypts.
  • Accordingly, VHL is completely absent from the proliferative intestinal pockets of Tcf4(-/-) perinatal mice.
  • We observed complementary staining of the hypoxia-inducible factor (HIF) 1alpha to VHL in normal intestinal epithelium as well as in all stages of colorectal cancer (CRC).
  • Although we observed upregulated levels of VHL in very early CRC lesions from sporadic and familial adenomatous polyposis patients - presumably due to activated Wnt signaling - a clear reduction of VHL expression is observed in later stages of CRC progression, coinciding with stabilization of HIF1alpha.
  • [MeSH-major] Adenocarcinoma / etiology. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / etiology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Nerve Tissue Proteins / physiology. TCF Transcription Factors / physiology. Von Hippel-Lindau Tumor Suppressor Protein / physiology. Wnt Proteins / physiology. beta Catenin / physiology
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli / pathology. Animals. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Line. Colon / cytology. Colon / metabolism. Colon / pathology. Colonic Polyps / genetics. Colonic Polyps / metabolism. Colonic Polyps / pathology. Disease Progression. Epithelial Cells / metabolism. Erythropoietin / genetics. Gene Expression Regulation, Neoplastic. Genes, Reporter. Humans. Intestinal Mucosa / cytology. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Kidney. L Cells (Cell Line). Mice. Mice, Knockout. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Promoter Regions, Genetic. Recombinant Fusion Proteins / biosynthesis. Recombinant Fusion Proteins / genetics. Signal Transduction / physiology. Transcription Factor 7-Like 2 Protein. Wnt3 Protein

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  • (PMID = 16407833.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / CTNNB1 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf4 protein, mouse; 0 / Tcf7l2 protein, mouse; 0 / Transcription Factor 7-Like 2 Protein; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / beta Catenin; 11096-26-7 / Erythropoietin; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Vhlh protein, mouse; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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47. Li JM, Southerland LT, Lu Y, Darlak KA, Giver CR, McMillin DW, Harris WA, Jaye DL, Waller EK: Activation, immune polarization, and graft-versus-leukemia activity of donor T cells are regulated by specific subsets of donor bone marrow antigen-presenting cells in allogeneic hemopoietic stem cell transplantation. J Immunol; 2009 Dec 15;183(12):7799-809
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  • [Title] Activation, immune polarization, and graft-versus-leukemia activity of donor T cells are regulated by specific subsets of donor bone marrow antigen-presenting cells in allogeneic hemopoietic stem cell transplantation.
  • We investigated the roles of specific subsets of donor APCs purified from bone marrow in donor T cell activation and graft-vs-leukemia (GvL) activity in murine models of hemopoietic stem cell transplantation.
  • Lineage(-)CD11c(+) APC precursors were separated from donor bone marrow based on expression of CD11b.
  • Transplanting lineage(-)CD11c(+)CD11b(-) APC (CD11b(-) APC) in combination with c-kit(+)Sca-1(+)lineage(-) hemopoietic stem cells (HSC) and congenic donor T cells led to increased donor CD4(+) and CD8(+) T cell proliferation and higher donor T cell chimerism than with transplanting grafts containing HSC, T cells, and lineage(-)CD11c(+)CD11b(+) APCs (CD11b(+) APC), or grafts containing only HSC and T cells.
  • Transplanting CD11b(-) APCs induced Th1/type 1 cytotoxic T lymphocyte donor T cell immune polarization and enhanced GvL activity of donor T cells without increased graft-vs-host disease in both MHC- and minor histocompatibility Ag-mismatched murine hemopoietic stem cell transplantation models, whereas CD11b(+) APCs led to Th2/type 2 cytotoxic T lymphocyte donor T cell immune polarization.
  • Donor CD11b(-) APCs were plasmacytoid dendritic cell progenitors (>90% CD317; PDCA-1(+)) and up-regulated CD80, CD86, and IL-12 during alloantigen presentation, whereas CD11b(+) APCs expressed Gr-1 and up-regulated expression of programmed death ligands-1 and 2 after activation.
  • These results are the first to show that manipulation of the content of donor APCs in allogeneic HSC grafts can regulate donor T cell immunity and enhance GvL without increasing graft-vs-host disease activity.

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  • (PMID = 19933853.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL086773; United States / NCI NIH HHS / CA / R01 CA074364; United States / PHS HHS / / NHLBI P01HL086773; United States / NCI NIH HHS / CA / R01 CA-74364-03
  • [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 / Isoantigens
  • [Other-IDs] NLM/ NIHMS549152; NLM/ PMC3908652
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48. Bauer S, Adrian N, Siebenborn U, Fadle N, Plesko M, Fischer E, Wüest T, Stenner F, Mertens JC, Knuth A, Ritter G, Old LJ, Renner C: Sequential cancer immunotherapy: targeted activity of dimeric TNF and IL-8. Cancer Immun; 2009;9:2
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  • Polymorphonuclear neutrophils (PMNs) are potent effectors of inflammation and their attempts to respond to cancer are suggested by their systemic, regional and intratumoral activation.
  • We previously reported on the recruitment of CD11b+ leukocytes due to tumor site-specific enrichment of TNF activity after intravenous administration of a dimeric TNF immunokine with specificity for fibroblast activation protein (FAP).
  • With the aim to amplify the TNF-induced and IL-8-mediated chemotactic response, we generated immunocytokines by N-terminal fusion of a human anti-FAP scFv fragment with human IL-8 (IL-8(72)) and its N-terminally truncated form IL-8(3-72).
  • Due to the dramatic difference in chemotaxis induction in vitro, we favored the mature chemokine fused to the anti-FAP scFv for further investigation in vivo.
  • BALB/c nu/nu mice were simultaneously xenografted with FAP-positive or -negative tumors and extended chemo-attraction of PMNs was only detectable in FAP-expressing tissue after intravenous administration of the anti-FAP scFv-IL-8(72) construct.
  • As TNF-activated PMNs are likewise producers and primary targets for IL-8, we investigated the therapeutic efficacy of co-administration of both effectors: Sequential application of scFv-IL-8(72) and dimeric IgG1-TNF fusion proteins significantly enhanced anti-tumor activity when compared either to a single effector treatment regimen or sequential application of non-targeted cytokines, indicating that the tumor-restricted sequential application of IL-8(72) and TNF is a promising approach for cancer therapy.
  • [MeSH-major] Immunotherapy. Interleukin-8 / therapeutic use. Neoplasms / drug therapy. Neoplasms / immunology. Protein Multimerization. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Animals. Antigens. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Chemotaxis / drug effects. Gelatinases. Humans. Kinetics. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / metabolism. Membrane Proteins. Mice. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / therapeutic use. Serine Endopeptidases / metabolism. Transfection. Treatment Outcome. Xenograft Model Antitumor Assays

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  • (PMID = 19267427.001).
  • [ISSN] 1424-9634
  • [Journal-full-title] Cancer immunity
  • [ISO-abbreviation] Cancer Immun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Interleukin-8; 0 / Membrane Proteins; 0 / Recombinant Fusion Proteins; 0 / Tumor Necrosis Factor-alpha; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ PMC2935764
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49. Crane CH, Winter K, Regine WF, Safran H, Rich TA, Curran W, Wolff RA, Willett CG: Phase II study of bevacizumab with concurrent capecitabine and radiation followed by maintenance gemcitabine and bevacizumab for locally advanced pancreatic cancer: Radiation Therapy Oncology Group RTOG 0411. J Clin Oncol; 2009 Sep 01;27(25):4096-102
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  • PURPOSE: The primary objective of this study was to assess the 1-year survival of patients with locally advanced, unresectable pancreatic cancer treated with the combination of bevacizumab, capecitabine, and radiation.
  • The median and 1-year survival rates were 11.9 months (95% CI, 9.9 to 14.0 months) and 47% (95% CI, 36% to 57%).
  • Median PFS was 8.6 months (95% CI, 6.9 to 10.5), and RR was 26%.
  • Unacceptable radiotherapy protocol deviations (ie, inappropriately generous volume contoured) correlated with grade 3 or greater gastrointestinal toxicity during chemoradiotherapy (45% v 18%; adjusted odds ratio, 3.7; 95% CI, 0.98 to 14.1; P = .05).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Angiogenesis Inhibitors / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antimetabolites, Antineoplastic / administration & dosage. Bevacizumab. Capecitabine. Chemotherapy, Adjuvant. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Disease-Free Survival. Female. Fluorouracil / administration & dosage. Fluorouracil / analogs & derivatives. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Pancreatectomy. Pancreaticoduodenectomy. Radiotherapy, Adjuvant. Time Factors. Treatment Outcome

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  • (PMID = 19636002.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00114179
  • [Grant] United States / NCI NIH HHS / CA / U10 CA32115; United States / NCI NIH HHS / CA / U10 CA21661; United States / NCI NIH HHS / CA / U10 CA37422; United States / NCI NIH HHS / CA / U10 CA037422; United States / NCI NIH HHS / CA / U10 CA021661; United States / NCI NIH HHS / CA / U10 CA032115
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 2S9ZZM9Q9V / Bevacizumab; 6804DJ8Z9U / Capecitabine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2734421
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50. Lee EJ, Park CK, Kim JW, Chang DK, Kim KM: Deletion mutation of BRAF in a serrated adenoma from a patient with familial adenomatous polyposis. APMIS; 2007 Aug;115(8):982-6
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  • [Title] Deletion mutation of BRAF in a serrated adenoma from a patient with familial adenomatous polyposis.
  • BRAF gene mutations in the colorectum have been associated with serrated adenomas and less frequently with hyperplastic polyps, villous adenomas, tubular adenomas, and carcinomas.
  • Most BRAF mutations in the colon have been reported as a V600E substitution.
  • We report a case with a very rare deletion mutation of BRAF (c.1799-1801delTGA, p.Val600_Lys601delinsGlu) in a serrated adenoma; the patient has familial adenomatous polyposis with a germline mutation of the APC gene (c.3578delA, p.Gln1193ArgfsX1264).
  • This case is the first reported with a deletion mutation of BRAF found in the colon.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Gene Deletion. Proto-Oncogene Proteins B-raf / genetics
  • [MeSH-minor] Female. Genes, APC. Humans. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 17696956.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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51. Langford KJ, Askham JM, Lee T, Adams M, Morrison EE: Examination of actin and microtubule dependent APC localisations in living mammalian cells. BMC Cell Biol; 2006;7:3
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  • [Title] Examination of actin and microtubule dependent APC localisations in living mammalian cells.
  • BACKGROUND: The trafficking of the adenomatous polyposis coli (APC) tumour suppressor protein in mammalian cells is a perennially controversial topic.
  • Immunostaining evidence for an actin-associated APC localisation at intercellular junctions has been previously presented, though live imaging of mammalian junctional APC has not been documented.
  • RESULTS: Using live imaging of transfected COS-7 cells we observed intercellular junction-associated pools of GFP-APC in addition to previously documented microtubule-associated GFP-APC and a variety of minor localisations.
  • Although both microtubule and junction-associated populations could co-exist within individual cells, they differed in their subcellular location, dynamic behaviour and sensitivity to cytoskeletal poisons.
  • GFP-APC deletion mutant analysis indicated that a protein truncated immediately after the APC armadillo repeat domain retained the ability to localise to adhesive membranes in transfected cells.
  • Supporting this, we also observed junctional APC immunostaining in cultures of human colorectal cancer cell line that express truncated forms of APC.
  • CONCLUSION: Our data indicate that APC can be found in two spatially separate populations at the cell periphery and these populations can co-exist in the same cell.
  • The first localisation is highly dynamic and associated with microtubules near free edges and in cell vertices, while the second is comparatively static and is closely associated with actin at sites of cell-cell contact.
  • Our imaging confirms that human GFP-APC possesses many of the localisations and behaviours previously seen by live imaging of Xenopus GFP-APC.
  • However, we report the novel finding that GFP-APC puncta can remain associated with the ends of shrinking microtubules.
  • Deletion analysis indicated that the N-terminal region of the APC protein mediated its junctional localisation, consistent with our observation that truncated APC proteins in colon cancer cell lines are still capable of localising to the cell cortex.
  • [MeSH-major] Actins / metabolism. Adenomatous Polyposis Coli Protein / metabolism. Microtubules / metabolism
  • [MeSH-minor] Animals. Armadillo Domain Proteins / genetics. Armadillo Domain Proteins / metabolism. COS Cells. Cell Line, Tumor. Cercopithecus aethiops. Colorectal Neoplasms / pathology. Green Fluorescent Proteins. Humans. Intercellular Junctions / chemistry. Microscopy, Fluorescence. Mutation. Protein Binding. Transfection. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism

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  • (PMID = 16423286.001).
  • [ISSN] 1471-2121
  • [Journal-full-title] BMC cell biology
  • [ISO-abbreviation] BMC Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Adenomatous Polyposis Coli Protein; 0 / Armadillo Domain Proteins; 0 / Tumor Suppressor Proteins; 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ PMC1386658
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52. Supić G, Kozomara R, Branković-Magić M, Jović N, Magić Z: Gene hypermethylation in tumor tissue of advanced oral squamous cell carcinoma patients. Oral Oncol; 2009 Dec;45(12):1051-7
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  • The genes selected for our investigation are involved in key cellular processes of malignant transformation, including cell cycle control (p16), apoptosis (Death Associated Protein Kinase, DAPK), Wnt signaling (Adenomatous Polyposis Coli, APC), cell-cell adhesion (E-cadherin, E-cad), and DNA repair (O(6)-methylguanine-DNA methyltransferase, MGMT, Werner syndrome gene, WRN).
  • Methylation of p16 gene promoter was detected in 58.4% of samples, E-cad in 42.9%, DAPK in 36.8%, MGMT in 33.8%, WRN in 23.8%, and APC in 18.2% of OSCC samples.
  • Patients with E-cad promoter methylation had significantly worse overall survival (p=0.039, log-rank test), while hypermethylation of other genes did not have prognostic significance.
  • Stratified analysis by the lymph node involvement and tumor stage showed that E-cad promoter methylation is associated to poor survival in N positive (p=0.024), and stage III tumors (p=0.027), as an opposite to N0 and stage II tumors, where E-cad methylation did not have prognostic significance (p=0.849, p=0.794, respectively).
  • Our findings indicate that multiple genes are frequently aberrantly methylated in OSCC, and that E-cad promoter methylation should be considered as a potential molecular marker for the poor survival in advanced OSCC.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis / genetics. Biomarkers, Tumor / genetics. Cell Adhesion / genetics. Cell Cycle / genetics. DNA Repair / genetics. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. Serbia. Survival Analysis. Wnt Proteins / genetics


53. Al-Sukhni W, Aronson M, Gallinger S: Hereditary colorectal cancer syndromes: familial adenomatous polyposis and lynch syndrome. Surg Clin North Am; 2008 Aug;88(4):819-44, vii
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  • [Title] Hereditary colorectal cancer syndromes: familial adenomatous polyposis and lynch syndrome.
  • Familial colorectal cancer (CRC) accounts for 10% to 20% of all cases of CRC.
  • Two major autosomal dominant forms of heritable CRC are familial adenomatous polyposis (FAP) and Lynch syndrome (also known as hereditary nonpolyposis colorectal cancer).
  • Along with the risk for CRC, both syndromes are associated with elevated risk for other tumors.
  • Improved understanding of the genetic basis of these diseases has not only facilitated the identification and screening of at-risk individuals and the development of prophylactic or early-stage intervention strategies but also provided better insight into sporadic CRC.
  • This article reviews the clinical and genetic characteristics of FAP and Lynch syndrome, recommended screening and surveillance practices, and appropriate surgical and nonsurgical interventions.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Genetic Predisposition to Disease
  • [MeSH-minor] Diagnosis, Differential. Humans


54. Kastritis E, Murray S, Kyriakou F, Horti M, Tamvakis N, Kavantzas N, Patsouris ES, Noni A, Legaki S, Dimopoulos MA, Bamias A: Somatic mutations of adenomatous polyposis coli gene and nuclear b-catenin accumulation have prognostic significance in invasive urothelial carcinomas: evidence for Wnt pathway implication. Int J Cancer; 2009 Jan 1;124(1):103-8
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  • [Title] Somatic mutations of adenomatous polyposis coli gene and nuclear b-catenin accumulation have prognostic significance in invasive urothelial carcinomas: evidence for Wnt pathway implication.
  • Wnt pathway signaling is crucial in many cancers and data indicate crosstalk with other key cancer pathways, however in urothelial carcinogenesis it has not been extensively studied.
  • We searched for mutations in adenomatous polyposis coli (APC), a key regulator of the pathway, and studied b-catenin expression and interactions with the expression of other markers of apoptosis, angiogenesis, and proliferation in patients with invasive urothelial cancer.
  • The mutation cluster region of APC was directly sequenced in 70 patients with muscle invasive disease who were treated with surgery and adjuvant chemotherapy.
  • Patients having either APC missense mutations or b-catenin nuclear accumulation had less frequent COX-2 overexpression (24% vs. 76%, p = 0.043) and more frequent lymph node involvement (75% vs. 38%, p = 0.023).
  • Patients with either APC mutations or b-catenin accumulation had shorter disease-free interval (13.4 vs. 28 months, p = 0.07), whereas in multivariate analysis they had shorter disease-specific survival (60.5 vs. 20.6 months, p = 0.048).
  • Somatic APC missense mutations are not rare in advanced urothelial neoplasms.
  • Either APC mutations and/or aberrant expression of b-catenin are associated with worse outcome.
  • Further study of the role of the Wnt pathway, potential crosstalk with other pathways and potential candidate therapeutic targets in urothelial cancer is needed.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Carcinoma / genetics. Cell Nucleus / metabolism. Mutation. Urinary Bladder Neoplasms / genetics. Urothelium / pathology. Wnt Proteins / metabolism. beta Catenin / biosynthesis

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  • (PMID = 18844223.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents; 0 / Wnt Proteins; 0 / beta Catenin; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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55. Mirabella D, Spena R, Scognamiglio G, Luca L, Gracco A, Siciliani G: LED vs halogen light-curing of adhesive-precoated brackets. Angle Orthod; 2008 Sep;78(5):935-40
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  • OBJECTIVE: To test the hypothesis that bonding with a blue light-emitting diode (LED) curing unit produces no more failures in adhesive-precoated (APC) orthodontic brackets than bonding carried out by a conventional halogen lamp.
  • MATERIALS AND METHODS: Sixty-five patients were selected for this randomized clinical trial, in which a total of 1152 stainless steel APC brackets were employed.
  • In order to carry out a valid comparison of the bracket failure rate following use of each type of curing unit, each patient's mouth was divided into four quadrants.
  • In 34 of the randomly selected patients, designated group A, the APC brackets of the right maxillary and left mandibular quadrants were bonded using a halogen light, while the remaining quadrants were treated with an LED curing unit.
  • In the other 31 patients, designated group B, halogen light was used to cure the left maxillary and right mandibular quadrants, whereas the APC brackets in the remaining quadrants were bonded using an LED dental curing light.
  • The bonding date, the type of light used for curing, and the date of any bracket failures over a mean period of 8.9 months were recorded for each bracket and, subsequently, the chi-square test, the Yates-corrected chi-square test, the Fisher exact test, Kaplan-Meier survival estimates, and the log-rank test were employed in statistical analyses of the results.
  • RESULTS: No statistically significant difference in bond failure rate was found between APC brackets bonded with the halogen light-curing unit and those cured with LED light.
  • CONCLUSIONS: The hypothesis cannot be rejected since use of an LED curing unit produces similar APC bracket failure rates to use of conventional halogen light, with the advantage of a far shorter curing time (10 seconds).

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  • (PMID = 18298197.001).
  • [ISSN] 0003-3219
  • [Journal-full-title] The Angle orthodontist
  • [ISO-abbreviation] Angle Orthod
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Composite Resins; 0 / Resin Cements; 0 / Transbond XT; 12597-68-1 / Stainless Steel
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56. Baum P, Müller D, Rüger R, Kontermann RE: Single-chain Fv immunoliposomes for the targeting of fibroblast activation protein-expressing tumor stromal cells. J Drug Target; 2007 Jul;15(6):399-406
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  • [Title] Single-chain Fv immunoliposomes for the targeting of fibroblast activation protein-expressing tumor stromal cells.
  • Fibroblast activation protein (FAP) represents a cell surface antigen selectively expressed by reactive tumor stromal fibroblasts of various cancers.
  • Here, we describe anti-FAP immunoliposomes as carrier systems for active targeting of FAP-expressing cells.
  • As targeting ligand we used single-chain Fv (scFv) molecules cross-reacting with human and mouse FAP.
  • These scFv molecules were genetically modified to express an additional cysteine residue at the C-terminus allowing a defined and site-directed conjugation.
  • Coupling to Mal-PEG(2000)-DSPE containing liposomes resulted in sterically stabilized scFv immunoliposomes showing strong and specific binding to FAP-expressing cells.
  • In addition, we could show that binding to FAP-expressing cells leads to internalization of intact liposomes into the endosomal compartment.
  • Thus, these anti-FAP scFv immunoliposomes should be suitable for target cell-specific delivery and uptake of encapsulated drugs.
  • [MeSH-major] Antigens, Neoplasm / immunology. Biomarkers, Tumor / immunology. Immunoglobulin Fragments / chemistry. Immunoglobulin Variable Region / chemistry. Liposomes / chemistry. Membrane Proteins / immunology. Serine Endopeptidases / immunology. Stromal Cells / metabolism

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  • (PMID = 17613658.001).
  • [ISSN] 1061-186X
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Drug Carriers; 0 / Immunoglobulin Fragments; 0 / Immunoglobulin Variable Region; 0 / Liposomes; 0 / Membrane Proteins; 0 / Phosphatidylethanolamines; 0 / immunoglobulin Fv; 1G4B5265CQ / 1,2-distearoylphosphatidylethanolamine; 30IQX730WE / Polyethylene Glycols; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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57. Imanaka H, Tanaka S, Feng B, Imamura K, Nakanishi K: Cultivation characteristics and gene expression profiles of Aspergillus oryzae by membrane-surface liquid culture, shaking-flask culture, and agar-plate culture. J Biosci Bioeng; 2010 Mar;109(3):267-73
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  • We cultivated a filamentous fungus, Aspergillus oryzae IAM 2706 by three different cultivation methods, i.e., shaking-flask culture (SFC), agar-plate culture (APC), and membrane-surface liquid culture (MSLC), to elucidate the differences of its behaviors by different cultivation methods under the same media, by measuring the growth, secretion of proteases and alpha-amylase, secreted protein level, and gene transcriptional profile by the DNA microarray analysis.
  • The protease activities detected by MSLC and APC were much higher than that by SFC, using both modified Czapek-Dox (mCD) and dextrin-peptone-yeast extract (DPY) media.
  • The alpha-amylase activity was detected in MSLC and APC in a much larger extent than that in SFC when DPY medium was used.
  • On the basis of SDS-PAGE analyses and N-terminal amino acid sequences, 6 proteins were identified in the supernatants of the culture broths using DPY medium, among which oryzin (alkaline protease) and alpha-amylase were detected at a much higher extent for APC and MSLC than those for SFC while only oryzin was detected in mCD medium, in accordance with the activity measurements.
  • A microarray analysis for the fungi cultivated by SFC, APC, and MSLC using mCD medium was carried out to elucidate the differences in the gene transcriptional profile by the cultivation methods.
  • The gene transcriptional profile obtained for the MSLC sample showed a similar tendency to the APC sample while it was quite different from that for the SFC sample.
  • Most of the genes specifically transcribed in the MSLC sample versus those in the SFC sample with a 10-fold up-regulation or higher were unknown or predicted proteins.
  • [MeSH-major] Agar / metabolism. Aspergillus oryzae / metabolism. Bioreactors / microbiology. Cell Culture Techniques / methods. Cell Membrane / metabolism. Culture Media / metabolism. Fungal Proteins / metabolism. Gene Expression Regulation, Fungal / physiology

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  • [Copyright] Copyright 2009 The Society for Biotechnology, Japan. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20159576.001).
  • [ISSN] 1347-4421
  • [Journal-full-title] Journal of bioscience and bioengineering
  • [ISO-abbreviation] J. Biosci. Bioeng.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Culture Media; 0 / Fungal Proteins; 0 / Solutions; 9002-18-0 / Agar
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58. Kretschmer B, Lüthje K, Ehrlich S, Osterloh A, Piedavent M, Fleischer B, Breloer M: CD83 on murine APC does not function as a costimulatory receptor for T cells. Immunol Lett; 2008 Oct 30;120(1-2):87-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD83 on murine APC does not function as a costimulatory receptor for T cells.
  • The transmembrane glycoprotein CD83 is rapidly upregulated on murine and human DC upon maturation and therefore a costimulatory function for T cell activation has been suggested.
  • Studies employing human APC indeed showed that CD83 expression was positively correlated to the stimulatory capacity of the APC.
  • Murine APC that were CD83 deficient however, did not display a reduced capacity to activate T cells.
  • To elucidate this contradiction, we thoroughly compared the stimulatory capacity of CD83-overexpressing and CD83-deficient APC.
  • Here we show that CD83 expression levels on APC did not affect the capacity of the APC to activate CD8(+) T cells.
  • CD83 expression levels did not significantly affect CD4(+) T cell activation in vivo, but a weak positive correlation of CD83 expression with CD4(+) T cell activation was observed in vitro under suboptimal stimulation conditions.
  • As CD83 expression also positively correlated with MHC-II but not with MHC-I expression, this differential stimulation specifically of CD4(+) T cells could be explained by a higher density of MHC-II peptide complexes on the APC surface.
  • Taken together, our results strongly suggest that CD83 does not deliver crucial costimulatory signals to murine T cells.

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  • (PMID = 18675848.001).
  • [ISSN] 0165-2478
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD86; 0 / CD83 antigen; 0 / Cd86 protein, mouse; 0 / Histocompatibility Antigens Class II; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Receptors, Antigen, T-Cell
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59. Clarke DJ, Bachant J: Kinetochore structure and spindle assembly checkpoint signaling in the budding yeast, Saccharomyces cerevisiae. Front Biosci; 2008;13:6787-819
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  • Here we review recent developments in our understanding of SAC control with particular emphasis on the role of the kinetochore, the nature of the tension sensing mechanism and the possibility that the SAC encompasses more than just stabilization of securin and/or cyclin-B via inhibition of the APC/C to delay anaphase initiation.
  • [MeSH-minor] Cell Cycle. Chromatids / physiology. Chromosomes, Fungal / genetics. Chromosomes, Fungal / physiology. DNA Topoisomerases, Type II / metabolism. Saccharomyces cerevisiae Proteins / metabolism. Stress, Mechanical

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  • (PMID = 18508695.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099033; United States / NIGMS NIH HHS / GM / GM-66190
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin; 0 / Saccharomyces cerevisiae Proteins; EC 5.99.1.3 / DNA Topoisomerases, Type II
  • [Number-of-references] 326
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60. Lin H, Yamada Y, Nguyen S, Linhart H, Jackson-Grusby L, Meissner A, Meletis K, Lo G, Jaenisch R: Suppression of intestinal neoplasia by deletion of Dnmt3b. Mol Cell Biol; 2006 Apr;26(8):2976-83
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  • [Title] Suppression of intestinal neoplasia by deletion of Dnmt3b.
  • Aberrant gene silencing accompanied by DNA methylation is associated with neoplastic progression in many tumors that also show global loss of DNA methylation.
  • Using conditional inactivation of de novo methyltransferase Dnmt3b in Apc(Min/+) mice, we demonstrate that the loss of Dnmt3b has no impact on microadenoma formation, which is considered the earliest stage of intestinal tumor formation.
  • Interestingly, many large adenomas showed regions with Dnmt3b inactivation, indicating that Dnmt3b is required for initial outgrowth of macroscopic adenomas but is not required for their maintenance.
  • These results support a role for Dnmt3b in the transition stage between microadenoma formation and macroscopic colonic tumor growth and further suggest that Dnmt3b, and by extension de novo methylation, is not required for maintaining tumor growth after this transition stage has occurred.

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  • (PMID = 16581773.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R37 CA 84198; United States / NICHD NIH HHS / HD / R01 HD050760; United States / NCI NIH HHS / CA / R01 CA 87869; United States / NCI NIH HHS / CA / R37 CA084198; United States / NICHD NIH HHS / HD / R01 HD 0445022; United States / NCI NIH HHS / CA / R01 CA087869
  • [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 / DNA, Neoplasm; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3B
  • [Other-IDs] NLM/ PMC1446955
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61. Chen WT, Khazaie K, Zhang G, Weissleder R, Tung CH: Detection of dysplastic intestinal adenomas using a fluorescent folate imaging probe. Mol Imaging; 2005 Jan-Mar;4(1):67-74
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  • [Title] Detection of dysplastic intestinal adenomas using a fluorescent folate imaging probe.
  • Activated macrophages overexpress folate receptors and we used this phenomenon to image inflammatory reactions in colon dysplasia using a fluorescent folate probe (FFP).
  • APC(Delta468) mice injected with FFP showed fluorescent adenomas (target-to-background ratio, adenoma vs. adjacent normal mucosa, of 2.46 +/- 0.41), significantly higher (p < .001) than adenomas in animals injected with a non-folate-containing control probe.
  • Taken together, these results indicate that probe potentially can be used to image dysplastic intestinal adenomas in vivo.
  • [MeSH-major] Adenoma / pathology. Flow Cytometry / methods. Folic Acid / analysis. Intestinal Neoplasms / pathology
  • [MeSH-minor] Animals. Antigens, Differentiation / metabolism. Carrier Proteins / metabolism. Fluorescent Dyes. Folate Receptors, GPI-Anchored. Genes, APC. Macrophage-1 Antigen / metabolism. Macrophages / metabolism. Macrophages / pathology. Mice. Mice, Mutant Strains. Receptors, Cell Surface / metabolism

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  • (PMID = 15967128.001).
  • [ISSN] 1535-3508
  • [Journal-full-title] Molecular imaging
  • [ISO-abbreviation] Mol Imaging
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA 86355; United States / NCI NIH HHS / CA / R01 CA 104547-01A1; United States / NCI NIH HHS / CA / R01 CA 99385; United States / NCI NIH HHS / CA / R33 CA 88365
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Carrier Proteins; 0 / Fluorescent Dyes; 0 / Folate Receptors, GPI-Anchored; 0 / Macrophage-1 Antigen; 0 / Receptors, Cell Surface; 0 / monocyte-macrophage differentiation antigen; 935E97BOY8 / Folic Acid
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62. Loeffler M, Krüger JA, Niethammer AG, Reisfeld RA: Targeting tumor-associated fibroblasts improves cancer chemotherapy by increasing intratumoral drug uptake. J Clin Invest; 2006 Jul;116(7):1955-62
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  • [Title] Targeting tumor-associated fibroblasts improves cancer chemotherapy by increasing intratumoral drug uptake.
  • Tumor-associated fibroblasts are key regulators of tumorigenesis.
  • These cells are also the primary source of collagen type I, which contributes to decreased chemotherapeutic drug uptake in tumors and plays a significant role in regulating tumor sensitivity to a variety of chemotherapies.
  • To specifically kill tumor-associated fibroblasts, we constructed an oral DNA vaccine targeting fibroblast activation protein (FAP), which is specifically overexpressed by fibroblasts in the tumor stroma.
  • Through CD8+ T cell-mediated killing of tumor-associated fibroblasts, our vaccine successfully suppressed primary tumor cell growth and metastasis of multidrug-resistant murine colon and breast carcinoma.
  • Furthermore, tumor tissue of FAP-vaccinated mice revealed markedly decreased collagen type I expression and up to 70% greater uptake of chemotherapeutic drugs.

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  • (PMID = 16794736.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA083856; United States / NCI NIH HHS / CA / CA83856
  • [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 / Cancer Vaccines; 0 / Collagen Type I; 0 / Membrane Proteins; 0 / Recombinant Fusion Proteins; 0 / Vaccines, DNA; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ PMC1481657
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63. Saito T, Oda Y, Yamamoto H, Kawaguchi K, Tanaka K, Matsuda S, Iwamoto Y, Tsuneyoshi M: Nuclear beta-catenin correlates with cyclin D1 expression in spindle and pleomorphic sarcomas but not in synovial sarcoma. Hum Pathol; 2006 Jun;37(6):689-97
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  • [Title] Nuclear beta-catenin correlates with cyclin D1 expression in spindle and pleomorphic sarcomas but not in synovial sarcoma.
  • Frequent activation of Wnt signaling pathway has been also shown in synovial sarcoma (SS), suggesting a specific role of this pathway in SS.
  • Immunohistochemical detection of nuclear beta-catenin accumulation correlated with cyclin D1 overexpression in spindle cell and pleomorphic sarcomas (P = .037), and the expression of these proteins evenly distributed throughout each section.
  • Cyclin D1 mRNA expression levels were statistically higher in tumors with cyclin D1 overexpression than in tumors without (P = .037), suggesting that cyclin D1 overexpression is due to transcriptional activation.
  • However, these correlations could not be detected in SS.
  • Mutations in exon 3 of the beta-catenin gene and in the mutation cluster region of adenomatous polyposis coli gene were absent in this series of cases.


64. Juhlin CC, Kiss NB, Villablanca A, Haglund F, Nordenström J, Höög A, Larsson C: Frequent promoter hypermethylation of the APC and RASSF1A tumour suppressors in parathyroid tumours. PLoS One; 2010;5(3):e9472
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent promoter hypermethylation of the APC and RASSF1A tumour suppressors in parathyroid tumours.
  • BACKGROUND: Parathyroid adenomas constitute the most common entity in primary hyperparathyroidism, and although recent advances have been made regarding the underlying genetic cause of these lesions, very little data on epigenetic alterations in this tumour type exists.
  • In this study, we have determined the levels of promoter methylation regarding the four tumour suppressor genes APC, RASSF1A, p16(INK4A) and RAR-beta in parathyroid adenomas.
  • Using Pyrosequencing analysis, we demonstrate APC promoter 1A and RASSF1A promoter hypermethylation in the majority of parathyroid tumours (71% and 98%, respectively).
  • Using TaqMan qRT-PCR, all tumours analyzed displayed lower RASSF1A mRNA expression and higher levels of total APC mRNA than normal parathyroid, the latter of which was largely conferred by augmented APC 1B transcription levels.
  • Hypermethylation of p16(INK4A) was demonstrated in a single adenoma, whereas RAR-beta hypermethylation was not observed in any sample.
  • CONCLUSIONS/SIGNIFICANCE: The results demonstrate that APC and RASSF1A promoter hypermethylation are common events in parathyroid tumours.
  • While RASSF1A mRNA levels were found downregulated in all tumours investigated, APC gene expression was retained through APC 1B mRNA levels.
  • Additionally, in contrast to most other human cancers, parathyroid tumours were not characterized by global hypomethylation, as parathyroid tumours exhibited LINE-1 methylation levels similar to that of normal parathyroid tissues.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Genes, APC. Parathyroid Neoplasms / genetics. Promoter Regions, Genetic. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adenoma / metabolism. CpG Islands. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Epigenesis, Genetic. Gene Expression Profiling. Genotype. Humans. Long Interspersed Nucleotide Elements. Parathyroid Glands / metabolism. Receptors, Retinoic Acid / metabolism

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  • (PMID = 20208994.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RASSF1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor beta
  • [Other-IDs] NLM/ PMC2830427
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65. Walker LR, Bülow S: [Restorative proctocolectomy with an ileoanal pouch. Postoperative course and long-term functional results]. Ugeskr Laeger; 2008 May 12;170(20):1721-5
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  • INTRODUCTION: Over the last 25 years restorative proctocolectomy with an ileoanal pouch has been the gold standard in the surgical treatment of ulcerative colitis and in selected patients with familial adenomatous polyposis.
  • MATERIALS AND METHODS: A prospective cohort analysis and a questionnaire in 178 consecutive patients operated since 1987 in Hvidovre Hospital.
  • The late complications comprised reoperation for intestinal bowel obstruction in 10 (6%), pouch fistula in 6 (3%), pouchitis in 22 (12%), and anastomotic stricture in 8 (5%).
  • In our opinion restorative proctocolectomy with an ileoanal pouch is still the gold standard for patients with ulcerative colitis and for selected patients with familial adenomatous polyposis.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Colitis, Ulcerative / surgery. Colonic Pouches. Proctocolectomy, Restorative

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  • (PMID = 18489884.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Denmark
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66. Wang D, Wang H, Guo Y, Ning W, Katkuri S, Wahli W, Desvergne B, Dey SK, DuBois RN: Crosstalk between peroxisome proliferator-activated receptor delta and VEGF stimulates cancer progression. Proc Natl Acad Sci U S A; 2006 Dec 12;103(50):19069-74
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  • Here, we present genetic and pharmacologic evidence demonstrating that deletion of PPARdelta decreases intestinal adenoma growth in Apc(Min/+) mice and inhibits tumor-promoting effects of a PPARdelta agonist GW501516.
  • More importantly, we found that activation of PPARdelta up-regulated VEGF in colon carcinoma cells.
  • VEGF directly promotes colon tumor epithelial cell survival through activation of PI3K-Akt signaling.
  • These results not only highlight concerns about the use of PPARdelta agonists for treatment of metabolic disorders in patients who are at high risk for colorectal cancer, but also support the rationale for developing PPARdelta antagonists for prevention and/or treatment of cancer.

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  • (PMID = 17148604.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 77839; United States / NIDDK NIH HHS / DK / R01 DK 62112; United States / NICHD NIH HHS / HD / R37 HD 12304; United States / NIDDK NIH HHS / DK / R37 DK 47297; United States / NICHD NIH HHS / HD / P30 HD033994; United States / NICHD NIH HHS / HD / R37 HD012304; United States / NCI NIH HHS / CA / P01 CA077839; United States / NCI NIH HHS / CA / P30 CA 068485; United States / NCI NIH HHS / CA / P30 CA068485; United States / NIDDK NIH HHS / DK / R37 DK047297; United States / NIDDK NIH HHS / DK / R01 DK062112; United States / NICHD NIH HHS / HD / U54 HD033994
  • [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 / GW 501516; 0 / PPAR delta; 0 / Thiazoles; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC1748178
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67. Schönthal AH, Chen TC, Hofman FM, Louie SG, Petasis NA: Celecoxib analogs that lack COX-2 inhibitory function: preclinical development of novel anticancer drugs. Expert Opin Investig Drugs; 2008 Feb;17(2):197-208
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  • In addition, it was more recently approved as an oral adjunct to prevent colon cancer development in patients with familial adenomatous polyposis and is presently being investigated for its chemotherapeutic potential in the therapy of advanced cancers.
  • However, in laboratory studies it was discovered that celecoxib was able to suppress tumor growth in the absence of any apparent involvement of COX-2, and additional pharmacologic activities associated with this drug were found.

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  • (PMID = 18230053.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2,5-dimethylcelecoxib; 0 / Antineoplastic Agents; 0 / OSU 03012; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
  • [Number-of-references] 91
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68. Saif MW, Podoltsev NA, Rubin MS, Figueroa JA, Lee MY, Kwon J, Rowen E, Yu J, Kerr RO: Phase II clinical trial of paclitaxel loaded polymeric micelle in patients with advanced pancreatic cancer. Cancer Invest; 2010 Feb;28(2):186-94
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  • PURPOSE: To determine in patients, with locally advanced or metastatic pancreatic cancer (APC), efficacy and safety of treatment with intravenous paclitaxel loaded polymeric micelle (GPM).
  • Patients with APC, ECOG performance status < or = 2, no prior chemotherapy and adequate organ function were treated with 3-hour GPM infusions every 3 weeks.
  • Median TTP for patients treated with 300 or 350 mg/m(2) doses was 3.2 months (95% CI, 2.6-4.2).
  • Median progression free survival (PFS) was 2.8 months (95% CI, 1.4-4.0).
  • Median overall survival (OS) was 6.5 months (95% CI, 5.1-7.9).
  • Disease control rate (CR + PR + stable disease) was 60.0%.
  • CONCLUSIONS: Treatment of APC with GPM at a dose of 300 mg/m(2) q 3 weeks was well tolerated and common toxicities were qualitatively similar to Cremophor-based paclitaxel.
  • Future studies of GPM in combination with other agents for treatment of APC are warranted.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Neoplasm Metastasis

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  • (PMID = 19968498.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Micelles; P88XT4IS4D / Paclitaxel
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69. Rajakannu M, Ananthakrishnan N, Madhavan M: Isolated mesenteric fibromatosis. Trop Gastroenterol; 2008 Jul-Sep;29(3):179-80
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  • Fibromatosis is a rare, locally aggressive but non-metastasising fibrous mass often associated with familial adenomatous polyposis in Gardner's Syndrome (GS).
  • We report the case of a 40-year-old lady who underwent laparotomy for a large isolated abdominal mass three years after a Whipple's procedure for adenocarcinoma of the distal common bile duct.
  • This case is peculiar in that mesenteric fibromatosis occurred in a patient with prior history of periampullary carcinoma and without history of familial adenomatous polyposis.
  • [MeSH-major] Fibroma / diagnosis. Jejunal Neoplasms / diagnosis

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  • (PMID = 19115615.001).
  • [ISSN] 0250-636X
  • [Journal-full-title] Tropical gastroenterology : official journal of the Digestive Diseases Foundation
  • [ISO-abbreviation] Trop Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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70. Szczepański M, Stelmachowska M, Stryczyński L, Golusiński W, Samara H, Mozer-Lisewska I, Zeromski J: Assessment of expression of toll-like receptors 2, 3 and 4 in laryngeal carcinoma. Eur Arch Otorhinolaryngol; 2007 May;264(5):525-30
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  • Toll-like receptors 1-13 (TLRs) are crucial for activation of innate immunity and secondarily for the induction of acquired response.
  • Ligand binding to TLR leads to the activation of several genes, predominantly proinflammatory ones such as IL-1 and TNF-alpha and maturation of professional antigen presenting cells (APC) i.e., dendritic cells.
  • It can cause better tumor antigen presentation by APC.
  • Immunohistochemistry and indirect immunoflourescence on frozen tissue sections.
  • It is of interest that TLRs tested were expressed not only on cells of inflammatory infiltrate, but also on tumor cells.

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  • (PMID = 17165086.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD11; 0 / Antigens, CD3; 0 / HLA-DR Antigens; 0 / Interleukin-1; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 3; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha
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71. Cai SR, Yu JK, Jiang WZ, Zhang SZ, Zheng S: [Application of serum protein markers to distinguish familial adenomatous polyposis (FAP) and sporadic colorectal adenomas]. Zhonghua Zhong Liu Za Zhi; 2009 Mar;31(3):192-5
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  • [Title] [Application of serum protein markers to distinguish familial adenomatous polyposis (FAP) and sporadic colorectal adenomas].
  • OBJECTIVE: To screen out specifically-expressed serum protein markers in familial adenomatous polyposis (FAP) and to establish a serum protein fingerprint diagnostic model for distinguishing FAP from sporadic colorectal adenomas.
  • METHODS: Serum samples were collected from 19 FAP cases and 16 sporadic colorectal adenomas with informed consent.
  • Serum protein fingerprint profiles were detected by SELDI-TOF-MS with CM 10 protein chip to screen out FAP adenoma-related serum protein markers, and support vector machine (SVG) technique was used to establish the diagnostic model to distinguish FAP from sporadic colorectal adenomas.
  • RESULTS: Six differently-expressed protein peaks (P < 0.01) were detected.
  • Among them proteins of 5640, 3160, 4180 and 4290 m/z were highly expressed in FAP adenomas, and proteins of 3940 and 3400 m/z were highly expressed in sporadic colorectal adenomas.
  • The accuracy of diagnostic model established with SVG to distinguish FAP adenomas and sporadic colorectal adenomas was 94.7% and 93.7%, respectively.
  • CONCLUSION: SELDI-TOF-MS can be effectively used to screen out the differentially expressed serum protein markers in FAP adenomas and sporadic colorectal adenomas, and a diagnostic model build by SVG to distinguish them has been successfully established.
  • Therefore, a useful breakthrough point for research on molecular mechanisms of FAP pathogenesis is provided.
  • [MeSH-major] Adenoma / metabolism. Adenomatous Polyposis Coli / metabolism. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / metabolism. Gene Expression Profiling
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Protein Array Analysis. Proteomics. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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  • (PMID = 19615258.001).
  • [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] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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72. Lee SH, Ahn BK, Chang HK, Baek SU: Adenocarcinoma in ileal pouch after proctocolectomy for familial adenomatous polyposis: report of a case. J Korean Med Sci; 2009 Oct;24(5):985-8
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  • [Title] Adenocarcinoma in ileal pouch after proctocolectomy for familial adenomatous polyposis: report of a case.
  • Restorative proctocolectomy with ileal pouch-anal anastomosis is one of the surgical treatments of choice for patients with familial adenomatous polyposis.
  • Although the risk of cancer developing in an ileal pouch is not yet clear, a few cases of adenocarcinoma arising in an ileal pouch have been reported.
  • A 56-yr-old woman was diagnosed as having familial adenomatous polyposis.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenomatous Polyposis Coli / surgery. Colonic Pouches / pathology. Colorectal Neoplasms / diagnosis. Proctocolectomy, Restorative

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  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2752792
  • [Keywords] NOTNLM ; Adenocarcinoma / Adenomatous Polyposis Coli / Ileal Pouches
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73. Mahalingam D, Kelly KR, Swords RT, Carew J, Nawrocki ST, Giles FJ: Emerging drugs in the treatment of pancreatic cancer. Expert Opin Emerg Drugs; 2009 Jun;14(2):311-28
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  • [Title] Emerging drugs in the treatment of pancreatic cancer.
  • BACKGROUND: Pancreatic cancer is the fourth leading cause of cancer-related death in the US.
  • However, there is a growing belief that novel biological agents could improve survival of patients with this cancer.
  • Gemcitabine-based chemotherapy remains the cornerstone treatment for advanced pancreatic cancers.
  • So far, the current targeted agents that have been used in combination with gemcitabine have failed to improve clinical outcomes.
  • This failure may stem from the heterogeneous molecular pathogenesis of pancreatic cancers, which involves several oncogenic pathways and defined genetic mutations.
  • OBJECTIVE: The aims of this review are: i) to define the existing treatments available at present for patients with pancreatic cancers in the neo-adjuvant, adjuvant, locally advanced and metastatic settings;.
  • ii) to highlight the molecular heterogeneity of the cancers and the rationale for targeting specific oncogenic pathways;.
  • iii) to give an overview of targeted agents that may potentially have an impact in the treatment of pancreatic cancers.
  • CONCLUSIONS: Molecular pathogenesis of pancreatic cancer involves several pathways and defined genetic mutations.
  • Targeting these complex molecular pathways with a combination of novel biological and chemotherapeutic agents could potentially improve patient outcome.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drugs, Investigational / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Chemotherapy, Adjuvant / trends. Drug Delivery Systems. Humans. Mutation. Oncogenes / physiology. Signal Transduction / drug effects. Signal Transduction / physiology


74. Ma JG, Yasue H, Eyer KE, Hiraiwa H, Shimogiri T, Meyers SN, Beever JE, Schook LB, Beattie CW, Liu WS: An integrated RH map of porcine chromosome 10. BMC Genomics; 2009;10:211
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  • [Title] An integrated RH map of porcine chromosome 10.
  • BACKGROUND: Whole genome radiation hybrid (WG-RH) maps serve as "scaffolds" to significantly improve the orientation of small bacterial artificial chromosome (BAC) contigs, order genes within the contigs and assist assembly of a sequence-ready map for virtually any species.
  • Here, we report the construction of a porcine: human comparative map for pig (Sus scrofa) chromosome 10 (SSC10) using the IMNpRH2(12,000-rad) porcine WG-RH panel, integrated with the IMpRH(7000-rad) WG-RH, genetic and BAC fingerprinted contig (FPC) maps.
  • RESULTS: Map vectors from the IMNpRH2(12,000-rad) and IMpRH(7,000-rad) panels were merged to construct parallel framework (FW) maps, within which FW markers common to both panels have an identical order.
  • This strategy reduced map discrepancies between the two panels and significantly improved map accuracy.
  • One linkage group covers SSC10p with accumulated map distances of 738.2 cR(7,000) and 1814.5 cR(12,000), respectively.
  • The second group covers SSC10q at map distances of 1336.9 cR(7,000) and 3353.6 cR(12,000), yielding an overall average map resolution of 16.4 kb/cR(12,000) or 393.5 kb per marker on SSC10.
  • This represents an approximately 2.5-fold increase in map resolution over the IMpRH(7,000-rad) panel.
  • Based on 127 porcine markers that have homologous sequences in the human genome, a detailed comparative map between SSC10 and human (Homo sapiens) chromosome (HSA) 1, 9 and 10 was built.
  • CONCLUSION: This initial comparative RH map of SSC10 refines the syntenic regions between SSC10 and HSA1, 9 and 10.
  • It integrates the IMNpRH2(12,000-rad) and IMpRH(7,000-rad), genetic and BAC FPC maps and provides a scaffold to close potential gaps between contigs prior to genome sequencing and assembly.
  • This map is also useful in fine mapping of QTLs on SSC10.

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  • (PMID = 19426492.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Other-IDs] NLM/ PMC2689272
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75. Hara T, Nagata M, Yamashita Y, Fujimoto K, Muraki Y, Yasuda Y, Kurahashi T: [Usefulness of S-1/gemcitabine combination therapy for advanced pancreatic cancer]. Gan To Kagaku Ryoho; 2008 Jul;35(7):1233-7
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  • [Title] [Usefulness of S-1/gemcitabine combination therapy for advanced pancreatic cancer].
  • Combination chemotherapy with S-1 and gemcitabine(GEM)was given to patients with advanced pancreatic cancer and favorable results were obtained.
  • They were administered S-1 at a dose of 80-100 mg/day for 2 weeks and GEM at a dose of 1,000-1,200 mg/body on days 8 and 15 followed by a 2-week recovery period.
  • One course consisted of a 2-week treatment period and a recovery period; this course was repeated in all of these patients.
  • The 3 types of patients have survived for a year and five months, a year and three months, and nine months, respectively, after diagnosis.
  • Combination therapy with S-1 and GEM can be provided for a long-term treatment with few adverse reactions on an outpatient basis.

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  • (PMID = 18633271.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Drug Combinations; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine
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76. Moschos J, Tzilves D, Paikos D, Tagarakis G, Pilpilidis I, Antonopoulos Z, Kadis S, Katsos I, Tarpagos A: Large mesenteric gastrointestinal stromal tumor in a patient with familial adenomatous polyposis syndrome. Wien Klin Wochenschr; 2006 Jun;118(11-12):355-7
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  • [Title] Large mesenteric gastrointestinal stromal tumor in a patient with familial adenomatous polyposis syndrome.
  • We report a case of a 30-year-old man who presented with severe debilitation, anemia and diarrhea over two months.
  • Colonoscopy revealed many (>100) polyps (familial adenomatous polyposis syndrome).
  • Abdominal CT scan showed a large mass at the left upper abdomen in conjunction with the splenic flexure.
  • We describe for the first time in medical literature the coexistence of familial adenomatous polyposis syndrome and GIST in a 30-year-old man.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / diagnosis. Gastrointestinal Stromal Tumors / complications. Gastrointestinal Stromal Tumors / diagnosis. Mesentery / pathology
  • [MeSH-minor] Adult. Humans. Male. Rare Diseases / diagnosis. Syndrome

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  • (PMID = 16855925.001).
  • [ISSN] 0043-5325
  • [Journal-full-title] Wiener klinische Wochenschrift
  • [ISO-abbreviation] Wien. Klin. Wochenschr.
  • [Language] eng
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77. Buckman SA, Heise CP: Nutrition considerations surrounding restorative proctocolectomy. Nutr Clin Pract; 2010 Jun;25(3):250-6
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  • Restorative proctocolectomy with ileal pouch-anal anastomosis has become the surgical treatment of choice for patients with ulcerative colitis and familial polyposis coli syndromes.
  • Pouch construction uses the distal 30-40 cm of ileum, and there exists a potential for postoperative nutrition consequences.
  • Patients who have undergone an ileal pouch-anal anastomosis procedure often describe specific food sensitivities that may require diet alteration, even more so than do patients with permanent ileostomy.
  • [MeSH-minor] Adenomatous Polyposis Coli / surgery. Anal Canal / surgery. Anemia, Iron-Deficiency / etiology. Colitis, Ulcerative / surgery. Diet. Dietary Supplements. Electrolytes / pharmacokinetics. Humans. Ileostomy. Intestinal Absorption. Pouchitis / etiology. Pouchitis / prevention & control. Probiotics. Trace Elements / pharmacokinetics. Vitamin B 12 Deficiency / etiology

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  • (PMID = 20581318.001).
  • [ISSN] 1941-2452
  • [Journal-full-title] Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition
  • [ISO-abbreviation] Nutr Clin Pract
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Electrolytes; 0 / Trace Elements
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78. Abdelrazeq AS, Scott N, Thorn C, Verbeke CS, Ambrose NS, Botterill ID, Jayne DG: The impact of spontaneous tumour perforation on outcome following colon cancer surgery. Colorectal Dis; 2008 Oct;10(8):775-80
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  • [Title] The impact of spontaneous tumour perforation on outcome following colon cancer surgery.
  • OBJECTIVE: The impact of spontaneous tumour perforation on survival following surgery for colon cancer is unclear.
  • METHOD: A prospective histological database was searched for all patients undergoing resection for adenocarcinoma of the colon between 1996 and 2002.
  • Patients with synchronous colonic and rectal cancers, familial polyposis, inflammatory bowel disease, iatrogenic or remote colonic perforation were excluded.
  • Data were analysed for differences in demographics, histological variables, operative mortality, disease-free and overall survival.
  • Patients with perforated cancers were more likely to present with metastatic disease and undergo emergency surgery with a higher 30-day mortality.
  • There was a trend towards reduced overall survival in the perforated group (P = 0.06), but no difference in disease-free survival (P = 0.43).
  • CONCLUSION: Both perforated and nonperforated T4 colon cancers have a poor prognosis.
  • Spontaneous perforation of the cancer is associated with reduced overall survival, due to higher 30-day mortality, but in itself does not appear to significantly impact on disease-free survival.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / surgery. Cause of Death. Colonic Neoplasms / mortality. Colonic Neoplasms / surgery. Intestinal Perforation / mortality
  • [MeSH-minor] Adult. Age Factors. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Colectomy / adverse effects. Colectomy / methods. Disease-Free Survival. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Postoperative Complications / diagnosis. Postoperative Complications / mortality. Probability. Prognosis. Proportional Hazards Models. Prospective Studies. Registries. Risk Assessment. Sex Factors. Statistics, Nonparametric. Survival Analysis

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  • (PMID = 18266887.001).
  • [ISSN] 1463-1318
  • [Journal-full-title] Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland
  • [ISO-abbreviation] Colorectal Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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79. Chung CS, Jiang Y, Cheng D, Birt DF: Impact of adenomatous polyposis coli (APC) tumor supressor gene in human colon cancer cell lines on cell cycle arrest by apigenin. Mol Carcinog; 2007 Sep;46(9):773-82
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  • [Title] Impact of adenomatous polyposis coli (APC) tumor supressor gene in human colon cancer cell lines on cell cycle arrest by apigenin.
  • This research assessed the importance of the adenomatous polyposis coli (APC) tumor suppressor mutation in the ability of apigenin to induce cell cycle arrest using HT29-APC cells, which contain inducible wild-type APC under the metallothionein promoter.
  • Treatment with apigenin (0, 20, 40, 60, and 80 microM) for 48 h resulted in reduction in the cell number (P < 0.05) concurrent with flow cytometry results showing a dose-dependent accumulation of cells in the G2/M phase in both HT29-APC and HT29-GAL cells without ZnCl(2) treatment.
  • Flow cytometric analysis showed an increase (P < 0.05) in the percentage of cells in G2/M when HT29-APC cells were treated with 80 microM apigenin for 120 h.
  • This increase was not present in HT29-APC cells when treated with both 80 microM apigenin and 100 microM ZnCl(2) for 120 h.
  • Western blot analysis verified the induction of APC protein expression in ZnCl(2)-treated HT29-APC cells but not in ZnCl(2)-treated HT29-GAL cells.
  • Apigenin plus ZnCl(2) treatment increased the expression of APC protein in HT29-APC cells by 50 fold above expression observed with ZnCl(2) alone.
  • Upon induction of the APC gene with ZnCl(2) in HT29-APC cells, the percentage of apoptotic cells increased significantly (P < 0.05) after 120-h treatment.
  • Additionally, apigenin treatment (80 microM) further increased the percentage of apopototic HT29-APC following ZnCl(2) treatment to induce wild-type APC expression.
  • These results suggest that APC dysfunction may be critical for apigenin to induce cell cycle arrest in human colon cancer cell lines and furthermore, apigenin enhances APC expression and apoptosis in cells with wild-type APC.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Apigenin / pharmacology. Cell Cycle / drug effects. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology

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  • Hazardous Substances Data Bank. ZINC COMPOUNDS .
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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17620292.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Chlorides; 0 / Zinc Compounds; 7V515PI7F6 / Apigenin; 86Q357L16B / zinc chloride
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80. Scott EN, Garcea G, Doucas H, Steward WP, Dennison AR, Berry DP: Surgical bypass vs. endoscopic stenting for pancreatic ductal adenocarcinoma. HPB (Oxford); 2009 Mar;11(2):118-24
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  • Methods of palliation in such patients with locally advanced disease comprise endoscopic placement of a biliary endoprosthesis or surgical bypass.
  • RESULTS: We identified a total of 56 patients, of whom 33 underwent endoscopic stenting and 23 underwent a surgical bypass consisting of a hepaticojejunostomy-en-Y and a gastrojejunostomy.

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  • (PMID = 19590634.001).
  • [ISSN] 1365-182X
  • [Journal-full-title] HPB : the official journal of the International Hepato Pancreato Biliary Association
  • [ISO-abbreviation] HPB (Oxford)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2697879
  • [Keywords] NOTNLM ; biliary bypass / biliary stent / pancreatic cancer / surgical bypass / survival
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81. González MA, Menéndez R, Ayala JM, Herrero M, Cuesta J, Domínguez A, Martínez M, Graña JL, Pozo F: [Intra-abdominal desmoid tumor]. Cir Esp; 2005 Jun;77(6):362-4
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  • Aggressive fibromatosis (desmoid tumor) are rare connective tissue tumors that occur sporadically or in association with familial adenomatous polyposis.
  • Biopsy is required to establish the diagnosis.

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  • (PMID = 16420952.001).
  • [ISSN] 0009-739X
  • [Journal-full-title] Cirugía española
  • [ISO-abbreviation] Cir Esp
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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82. Mahjoub T, Mtiraoui N, Tamim H, Hizem S, Finan RR, Nsiri B, Almawi WY: Association between adverse pregnancy outcomes and maternal factor V G1691A (Leiden) and prothrombin G20210A genotypes in women with a history of recurrent idiopathic miscarriages. Am J Hematol; 2005 Sep;80(1):12-9
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  • APC resistance (APCR) was detected functionally (measuring the activated clotting time triggered by activated factor X in presence of a fixed amount of purified APC), and FV-Leiden and PRT G20210A genotypes were assessed by PCR.
  • The frequency of the mutant FV (0.1400 vs. 0.0276; P < 0.001) but not PRT 20210 (0.0100 vs. 0.0225; P = 0.159) allele was higher in patients than controls, respectively.
  • APC resistance with factor V Leiden was seen in 27% of patients compared to 11.5% of controls, while APC resistance without factor V Leiden was seen in 12.5% of patients compared to 9.5% of controls.
  • APC resistance and FV Leiden, as well as combination of both, are common thrombotic defects seen in women with idiopathic recurrent pregnancy loss, thus testing for these is recommended in women who have experienced recurrent miscarriages.

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16138341.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / factor V Leiden; 9001-24-5 / Factor V; 9001-26-7 / Prothrombin
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83. Deriy L, Ogawa H, Gao GP, Galili U: In vivo targeting of vaccinating tumor cells to antigen-presenting cells by a gene therapy method with adenovirus containing the alpha1,3galactosyltransferase gene. Cancer Gene Ther; 2005 Jun;12(6):528-39
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  • Poor uptake by antigen-presenting cells (APC) is a major reason for low immunogenicity of autologous tumor vaccines.
  • Anti-Gal binds to alpha-gal epitopes (Galalpha1-3Galbeta1-4GlcNAc-R) on vaccinating tumor cells and opsonizes them for effective uptake by APC.
  • Immunization with AdalphaGT transduced autologous tumor cells may serve as adjuvant immunotherapy delivered after completion of standard therapy.
  • This method may complement another gene therapy method in which GM-CSF-secreting vaccinating tumor cells recruit APC to vaccination sites.
  • Anti-Gal-opsonized vaccinating tumor cells will be effectively internalized by GM-CSF recruited APC and transported to draining lymph nodes for processing and presentation of tumor antigens.
  • The subsequent uptake of anti-Gal-opsonized tumor membranes by APC results in their effective transportation to lymph nodes where processed tumor antigens may elicit a protective antitumor immune response.

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  • (PMID = 15818383.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 85868
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Immunodominant Epitopes; EC 2.4.1.- / Galactosyltransferases; EC 2.4.1.133 / alpha 1,3 galactosyltransferase, mouse
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84. Nojima J, Kuratsune H, Suehisa E, Iwatani Y, Kanakura Y: Acquired activated protein C resistance associated with IgG antibodies against beta2-glycoprotein I and prothrombin as a strong risk factor for venous thromboembolism. Clin Chem; 2005 Mar;51(3):545-52
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  • [Title] Acquired activated protein C resistance associated with IgG antibodies against beta2-glycoprotein I and prothrombin as a strong risk factor for venous thromboembolism.
  • BACKGROUND: Venous thromboembolic events such as deep vein thrombosis and pulmonary embolism are common manifestations of antiphospholipid syndrome.
  • We therefore studied the in vitro effects of IgG fractions containing anti-CL/beta2-GPI or anti-PS/PT antibodies on the anticoagulant activity of activated protein C (APC) and found that purified IgG containing anti-CL/beta2-GPI or anti-PS/PT antibodies significantly hampered the anticoagulant activity of APC.
  • We also studied the ability of IgG fractions to impede the anticoagulant activity of APC before and after complete removal of anti-CL/beta2-GPI or anti-PS/PT antibodies by adsorption.
  • Removal of anti-CL/beta2-GPI or anti-PS/PT antibodies from all positive IgG samples clearly decreased the inhibitory effect of those samples on APC anticoagulant activity.
  • CONCLUSIONS: Anti-CL/beta2-GPI and anti-PS/PT antibodies independently cause APC resistance, which may contribute to risk of VTE in patients with SLE.
  • [MeSH-major] Activated Protein C Resistance / immunology. Antibodies, Antiphospholipid / blood. Glycoproteins / immunology. Immunoglobulin G / blood. Prothrombin / immunology. Thromboembolism / immunology. Venous Thrombosis / immunology
  • [MeSH-minor] Adult. Antiphospholipid Syndrome / etiology. Antiphospholipid Syndrome / immunology. Cardiolipins / immunology. Enzyme-Linked Immunosorbent Assay. Female. Humans. In Vitro Techniques. Lupus Erythematosus, Systemic / complications. Male. Middle Aged. Multivariate Analysis. Partial Thromboplastin Time. Phosphatidylserines / immunology. Protein C / analysis. Risk Factors. beta 2-Glycoprotein I

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  • (PMID = 15637132.001).
  • [ISSN] 0009-9147
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Cardiolipins; 0 / Glycoproteins; 0 / Immunoglobulin G; 0 / Phosphatidylserines; 0 / Protein C; 0 / beta 2-Glycoprotein I; 9001-26-7 / Prothrombin
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85. Haddad F, Zeeni C, El Rassi I, Yazigi A, Madi-Jebara S, Hayeck G, Jebara V, Yazbeck P: Can femoral artery pressure monitoring be used routinely in cardiac surgery? J Cardiothorac Vasc Anesth; 2008 Jun;22(3):418-22
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  • [Title] Can femoral artery pressure monitoring be used routinely in cardiac surgery?
  • OBJECTIVE: The purpose of this study was to evaluate the safety of femoral arterial pressure monitoring in cardiac surgery.
  • PARTICIPANTS: Of a total of 2,350 consecutive patients scheduled for elective cardiac surgery with cardiopulmonary bypass, 2,264 patients with femoral artery pressure monitoring were included.
  • INTERVENTIONS: A femoral arterial catheter was inserted percutaneously before the induction of anesthesia.
  • It was replaced by a radial artery catheter in patients staying for more than 4 days in the CSU or in case of pulse loss or lower limb ischemia.
  • Complications related to femoral artery cannulation were recorded.
  • No cases of femoral artery thrombosis, lower extremity ischemia, or hematoma requiring surgery were noted.
  • CONCLUSIONS: Femoral artery pressure monitoring was associated with a low complication rate and, therefore, it can be used routinely in cardiac surgery.
  • [MeSH-major] Blood Pressure / physiology. Blood Pressure Monitors. Cardiopulmonary Bypass / methods. Femoral Artery / physiology. Monitoring, Intraoperative / methods

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  • [CommentIn] J Cardiothorac Vasc Anesth. 2009 Dec;23(6):932-3 [19217313.001]
  • (PMID = 18503931.001).
  • [ISSN] 1532-8422
  • [Journal-full-title] Journal of cardiothoracic and vascular anesthesia
  • [ISO-abbreviation] J. Cardiothorac. Vasc. Anesth.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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86. El-Rayes BF, Zalupski MM, Shields AF, Ferris AM, Vaishampayan U, Heilbrun LK, Venkatramanamoorthy R, Adsay V, Philip PA: A phase II study of celecoxib, gemcitabine, and cisplatin in advanced pancreatic cancer. Invest New Drugs; 2005 Dec;23(6):583-90
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  • A Phase II study was undertaken to determine the effect of gemcitabine by fixed-dose rate infusion (FDR), cisplatin and the COX-2 inhibitor, celecoxib, on the 6-month survival rate in patients with metastatic pancreatic cancer.
  • METHODS: The eligibility criteria included a pathologically or cytologically confirmed diagnosis of adenocarcinoma of the pancreas.
  • Patients received a combination of gemcitabine 1,000 mg/m(2) over 100 minutes, cisplatin 35 mg/m(2) I.V. on days 1 and 8, and celecoxib continuously at a daily dose of 800 mg.
  • The median survival time was 5.8 months (90% CI, 3.6-7.6 months).
  • The probability of survival at 6 months was 46% (90% CI, 27-62%).
  • CONCLUSIONS: The addition of celecoxib to gemcitabine (by FDR) and cisplatin did not appear to increase activity of the chemotherapy doublet in patients with advanced pancreatic cancer.
  • Celecoxib alone may not be sufficient to sensitize pancreatic cancer to the effects of conventional cytotoxic therapy.

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  • (PMID = 16034525.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; JCX84Q7J1L / Celecoxib; Q20Q21Q62J / Cisplatin
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87. Bommareddy A, Zhang X, Schrader D, Kaushik RS, Zeman D, Matthees DP, Dwivedi C: Effects of dietary flaxseed on intestinal tumorigenesis in Apc(Min) mouse. Nutr Cancer; 2009;61(2):276-83
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  • [Title] Effects of dietary flaxseed on intestinal tumorigenesis in Apc(Min) mouse.
  • The present study was designed to investigate the chemopreventive effects of dietary flaxseed on the development of intestinal tumors in Apc(Min) mice.
  • Apc(Min) mice were divided into five different groups, fed with control (AIN-93M meal), corn meal, flaxseed meal, corn oil, and flaxseed oil supplemented diets.
  • Results showed that dietary flaxseed significantly decreased (P < 0.05) tumor multiplicity and size in the small intestine and colon as compared to control, corn-treated groups.
  • Intestine, colon, and serum samples of corn-treated groups showed higher levels of omega -6 fatty acids, whereas the flaxseed treated groups exhibited higher levels of omega -3 fatty acids.
  • Lignans were detected in the serum, intestine, and colon samples for flaxseed meal group.
  • COX-1 and COX-2 expression in the colon samples from the flaxseed meal group were significantly lower (P < 0.05) as compared to the corn meal group.
  • Dietary flaxseed may be chemopreventive for intestinal tumor development in Apc(Min) mice possibly by increasing omega -3 fatty acid levels, lignans, and decreasing COX-1 and COX-2 levels.
  • [MeSH-major] Diet. Flax. Intestinal Neoplasms / prevention & control
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Animals. Anticarcinogenic Agents / administration & dosage. Apoptosis. Azoxymethane. Colon / chemistry. Colon / pathology. Colonic Neoplasms / chemically induced. Colonic Neoplasms / pathology. Colonic Neoplasms / prevention & control. Corn Oil / administration & dosage. Corn Oil / chemistry. Cyclooxygenase 1 / analysis. Cyclooxygenase 2 / analysis. Fatty Acids / analysis. Fatty Acids / blood. Fatty Acids, Omega-3 / administration & dosage. Intestine, Small / chemistry. Intestine, Small / pathology. Lignans / administration & dosage. Lignans / analysis. Linseed Oil / administration & dosage. Linseed Oil / chemistry. Mice. Phytotherapy. Zea mays. alpha-Linolenic Acid / administration & dosage

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  • (PMID = 19235044.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Fatty Acids; 0 / Fatty Acids, Omega-3; 0 / Lignans; 0RBV727H71 / alpha-Linolenic Acid; 8001-26-1 / Linseed Oil; 8001-30-7 / Corn Oil; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; MO0N1J0SEN / Azoxymethane
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88. Gadish T, Tulchinsky H, Deutsch AA, Rabau M: Pinealoblastoma in a patient with familial adenomatous polyposis: variant of Turcot syndrome type 2? Report of a case and review of the literature. Dis Colon Rectum; 2005 Dec;48(12):2343-6
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  • [Title] Pinealoblastoma in a patient with familial adenomatous polyposis: variant of Turcot syndrome type 2? Report of a case and review of the literature.
  • We report a case of a 23-year-old Turcot female patient who was first diagnosed as having a pinealoblastoma.
  • Thyroid papillary carcinoma was diagnosed a few months later, and multiple colonic polyps were detected three years after that.
  • A genetic workup revealed an APC gene mutation in her family.
  • Restorative proctocolectomy may itself cause major morbidity but is currently the only way to prevent colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Brain Neoplasms / genetics. Pineal Gland. Pinealoma / genetics
  • [MeSH-minor] Adult. Carcinoma, Papillary / genetics. Carcinoma, Papillary / pathology. DNA Mutational Analysis. Female. Genes, APC. Humans. Syndrome. Thyroid Neoplasms / genetics. Thyroid Neoplasms / pathology


89. Bibbo C, Bono CM, Lin SS: Union rates using autologous platelet concentrate alone and with bone graft in high-risk foot and ankle surgery patients. J Surg Orthop Adv; 2005;14(1):17-22
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  • [Title] Union rates using autologous platelet concentrate alone and with bone graft in high-risk foot and ankle surgery patients.
  • Adjuvant use of autologous platelet concentrate (APC) to assist bone healing in foot and ankle surgery has not been reported.
  • This study examined the clinical results and complications after the adjuvant use of APC in high-risk patients undergoing elective foot and ankle surgery.
  • Patients at risk for bone-healing complications were prospectively enrolled over a 6-month period for the intraoperative application of APC.
  • Sixty-two high-risk patients were enrolled, totaling 123 procedures.
  • For APC alone, the mean time to union was 40 days; when APC was used with autograft, the mean time to union was 45 days (p = .173, two-tailed t test).
  • These data suggest that adjuvant APC results in an acceptable time to union and may be a useful adjunct to promote osseous healing in high-risk patients undergoing elective foot and ankle surgery.
  • [MeSH-major] Ankle Injuries / surgery. Bone Transplantation. Foot Injuries / surgery. Fractures, Bone / surgery. Platelet Transfusion
  • [MeSH-minor] Adolescent. Adult. Aged. Comorbidity. Elective Surgical Procedures. Female. Fracture Healing. Humans. Immunocompromised Host. Male. Middle Aged. Prospective Studies. Risk Factors. Smoking / epidemiology. Surgical Wound Infection. Transplantation, Autologous. Transplantation, Homologous


90. Tao H, Shinmura K, Yamada H, Maekawa M, Osawa S, Takayanagi Y, Okamoto K, Terai T, Mori H, Nakamura T, Sugimura H: Identification of 5 novel germline APC mutations and characterization of clinical phenotypes in Japanese patients with classical and attenuated familial adenomatous polyposis. BMC Res Notes; 2010;3:305
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  • [Title] Identification of 5 novel germline APC mutations and characterization of clinical phenotypes in Japanese patients with classical and attenuated familial adenomatous polyposis.
  • BACKGROUND: Familial adenomatous polyposis (FAP) is an autosomal dominant hereditary disease characterized by multiple colorectal adenomatous polyps and frequent extracolonic manifestations.
  • An attenuated form of FAP (AFAP) is diagnosed based on a milder colorectal phenotype, and the colorectal phenotype of (A)FAP has been linked to germline APC mutations.
  • FINDINGS: Nine germline APC mutations, but no large deletions, were identified in the APC locus of 8 (A)FAP patients, and 5 of the mutations, c.446A > T (p.Asp149Val), c.448A > T (p.Lys150X), c.454_457insAGAA (p.Glu152ArgfsX17), c.497insA (p.Thr166AsnfsX2), and c.1958G > C (p.Arg653Ser), were novel mutations.
  • In one patient the p.Asp149Val mutation and p.Lys150X mutation were detected in the same APC allele.
  • The c.1958G > C mutation was located in the last nucleotide of exon 14, and RT-PCR analysis revealed that the mutation resulted in abnormal splicing.
  • The following phenotypes, especially extracolonic manifestations, were observed in our (A)FAP patients:.
  • (1) multiple gastroduodenal adenomas and early-onset gastric carcinoma in AFAP patients with an exon 4 mutation;.
  • (2) a desmoid tumor in two FAP patients with a germline APC mutation outside the region between codons 1403 and 1578, which was previously reported to be associated with the development of desmoid tumors in FAP patients;.
  • (3) multiple myeloma in an AFAP patient with an exon 4 mutation.
  • CONCLUSIONS: Nine germline APC mutations, 5 of them were novel, were identified in 8 Japanese (A)FAP patients, and some associations between germline APC mutations and extracolonic manifestations were demonstrated.
  • These findings should contribute to establishing relationships between germline APC mutations and the extracolonic manifestations of (A)FAP patients in the future.

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  • (PMID = 21078199.001).
  • [ISSN] 1756-0500
  • [Journal-full-title] BMC research notes
  • [ISO-abbreviation] BMC Res Notes
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2994888
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91. Diegel CR, Cho KR, El-Naggar AK, Williams BO, Lindvall C: Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma. Cancer Res; 2010 Nov 15;70(22):9143-52
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  • [Title] Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma.
  • Cross-talk between the canonical Wnt and mammalian target of rapamycin (mTOR) signaling pathways occurs at multiple levels in the cell and likely contributes to the oncogenic effects of these pathways in human cancer.
  • To gain more insight into the interplay between Wnt and mTOR signaling in salivary gland tumorigenesis, we developed a mouse model in which both pathways are constitutively activated by the conditional inactivation of the Apc and Pten tumor suppressor genes.
  • Loss of either Apc or Pten alone did not cause tumor development.
  • However, deletion of both genes resulted in the formation of salivary gland tumors with 100% penetrance and short latency that showed a remarkable morphologic similarity to human acinic cell carcinoma.
  • Together, these results suggest that aberrant activation of mTOR signaling plays a pivotal role in acinar cell neoplasia of the salivary gland.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / deficiency. Carcinoma, Acinar Cell / metabolism. PTEN Phosphohydrolase / deficiency. Salivary Glands / metabolism. TOR Serine-Threonine Kinases / metabolism


92. Valderrama MJ, Ocaña FA, Aguilera AM, Ocaña-Peinado FM: Forecasting pollen concentration by a two-step functional model. Biometrics; 2010 Jun;66(2):578-85
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  • A functional regression model to forecast the cypress pollen concentration during a given time interval, considering the air temperature in a previous interval as the input, is derived by means of a two-step procedure.
  • This estimation is carried out by functional principal component (FPC) analysis and the residual noise is also modeled by FPC regression, taking as the explicative process the pollen concentration during the earlier interval.

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  • (PMID = 19645702.001).
  • [ISSN] 1541-0420
  • [Journal-full-title] Biometrics
  • [ISO-abbreviation] Biometrics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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93. Benmaamar R, Pagano M: Involvement of the SCF complex in the control of Cdh1 degradation in S-phase. Cell Cycle; 2005 Sep;4(9):1230-2
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  • The anaphase promoting complex/cyclosome (APC/C) is a multisubunit ubiquitin ligase that acts as a key regulator in the progression through mitosis (when mostly in complex with Cdc20) and as a stabilizer of the G1 phase (when in complex with Cdh1).
  • Cdh1 is an activator of APC/C, and it has previously been reported that it is capable of mediating its own degradation during Go and G1.
  • Herein, we show that the SCF complex (Skp1/Cul1/F-box protein/Roc1) intervenes in the surveillance of Cdh1 cellular abundance in S-phase.
  • [MeSH-major] Cell Cycle Proteins / chemistry. Ubiquitin-Protein Ligase Complexes / physiology
  • [MeSH-minor] Amino Acid Motifs. Anaphase-Promoting Complex-Cyclosome. Cdh1 Proteins. Cell Cycle. Cell Line. Doxycycline / pharmacology. G0 Phase. G1 Phase. Gene Deletion. Genes, Dominant. HeLa Cells. Humans. Immunoblotting. Mitosis. Protein Conformation. RNA Interference. S Phase. Time Factors. Transfection. Ubiquitins / chemistry

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  • (PMID = 16123585.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdh1 Proteins; 0 / Cell Cycle Proteins; 0 / FZR1 protein, human; 0 / Ubiquitins; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes; N12000U13O / Doxycycline
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94. Warnecke G, Feng G, Goto R, Nadig SN, Francis R, Wood KJ, Bushell A: CD4+ regulatory T cells generated in vitro with IFN-{gamma} and allogeneic APC inhibit transplant arteriosclerosis. Am J Pathol; 2010 Jul;177(1):464-72
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  • [Title] CD4+ regulatory T cells generated in vitro with IFN-{gamma} and allogeneic APC inhibit transplant arteriosclerosis.
  • We hypothesized that these IFN-gamma-conditioned T cells (Tcon) would reduce transplantation-associated arteriosclerosis.
  • These cultures were pulsed with bone marrow-derived B6 (H-2(b)) APC.
  • In addition, the CD31(-) donor endothelium was fully repopulated by CD31(+) recipient endothelial cells in the absence of Tcon, but not in the presence of Tcon.
  • These data illustrate the potential of ex vivo generated regulatory T cells for the inhibition of transplant-associated vasculopathy.

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  • (PMID = 20472892.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2893688
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95. Bria E, Milella M, Gelibter A, Cuppone F, Pino MS, Ruggeri EM, Carlini P, Nisticò C, Terzoli E, Cognetti F, Giannarelli D: Gemcitabine-based combinations for inoperable pancreatic cancer: have we made real progress? A meta-analysis of 20 phase 3 trials. Cancer; 2007 Aug 1;110(3):525-33
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  • A literature-based meta-analysis was performed, event-based relative risk ratios with 95% confidence intervals were derived through both a fixed-effect model approach and a random-effect model approach, and overall survival (OS) was explored as the primary endpoint.
  • A sensitivity analysis for OS was performed according to the type of agent used in combination with gemcitabine.
  • Platinum combinations led to the greatest absolute benefits for PFS and ORR compared with single-agent gemcitabine (10% and 6.5%, respectively), but this did not result in an OS benefit.
  • Improvement in PFS, but not in the ORR, was correlated with an improvement in OS.
  • [MeSH-minor] Clinical Trials, Phase III as Topic. Disease Progression. Dose-Response Relationship, Drug. Humans. Prospective Studies. Randomized Controlled Trials as Topic. Survival Rate. Treatment Outcome

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  • [Copyright] (c) 2007 American Cancer Society.
  • (PMID = 17577216.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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96. Mitsunaga S, Kinoshita T, Hasebe T, Nakagohri T, Konishi M, Takahashi S, Gotohda N, Ochiai A: Low serum level of cholinesterase at recurrence of pancreatic cancer is a poor prognostic factor and relates to systemic disorder and nerve plexus invasion. Pancreas; 2008 Apr;36(3):241-8
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  • [Title] Low serum level of cholinesterase at recurrence of pancreatic cancer is a poor prognostic factor and relates to systemic disorder and nerve plexus invasion.
  • OBJECTIVES: Systemic disorder is a characteristic of advanced pancreatic cancer.
  • Clinical prognostic factors in earlier disease state than terminal stage are expected to be sensitive markers for the foresight of systemic disorder.
  • This study aimed to find the associations between these sensitive markers and morphological factors of primary tumor that may indicate finding a way of pathogenesis of systemic disorder.
  • Patients with low cholinesterase levels show systemic disorder, including poor performance status, anemia, and hypoalbuminemia.
  • CONCLUSIONS: Nerve invasion may thus result in low functional state of the liver followed by systemic disorder.

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  • (PMID = 18362836.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.1.8 / Cholinesterases
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97. Kurata T, Hayashi T, Yoshikawa T, Okamoto T, Yoshida K, Iino T, Uchida A, Suzuki K: Activated protein C stimulates osteoblast proliferation via endothelial protein C receptor. Thromb Res; 2010 Feb;125(2):184-91
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  • [Title] Activated protein C stimulates osteoblast proliferation via endothelial protein C receptor.
  • INTRODUCTION: Bone is continually remodeled by the action of osteoblasts, osteocytes, and osteoclasts.
  • Activated protein C (APC) is a serine protease that functions in anticoagulation, anti-inflammation, anti-apoptosis, cell proliferation, and wound repair.
  • In this study, we examined the effect of APC on osteoblast proliferation and differentiation.
  • MATERIALS AND METHODS: We examined the presence of protein C in human fracture hematoma by immunohistochemical staining.
  • We then evaluated the effect of APC, diisopropyl fluorophosphate-inactivated APC (DIP-APC) or protein C zymogen on normal human osteoblast (NHOst) proliferation using tetrazolium salt assay in the presence or absence of aprotinin, hirudin, protein C, antibody against protein C, endothelial protein C receptor (EPCR) or protease-activated receptor (PAR)-1.
  • Finally, activation of p44/42 MAP kinase was evaluated by Western blot analysis.
  • RESULTS: Both APC and DIP-APC increased osteoblast proliferation in a dose-dependent manner, while protein C did not.
  • The APC-induced increased proliferation of osteoblast was not affected by aprotinin, hirudin, and anti-protein C antibody which inhibits the protease activity of APC.
  • Treatment with protein C or anti-EPCR antibody which inhibits APC binding to EPCR inhibited APC-mediated osteoblast proliferation, while treatment with anti-PAR-1 antibody did not.
  • APC promoted the phosphorylation of p44/42 MAP kinase within osteoblasts; this effect was inhibited by the anti-EPCR antibody.
  • CONCLUSIONS: APC stimulates osteoblast proliferation by activating p44/42 MAP kinase through a mechanism that requires EPCR but not PAR-1 or the proteolytic activity of APC.
  • APC generated at fracture sites may contribute to fracture healing by promoting osteoblast proliferation.
  • [MeSH-major] Cell Proliferation / drug effects. Osteoblasts / drug effects. Protein C / metabolism. Protein C / pharmacology. Receptors, Cell Surface

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19804899.001).
  • [ISSN] 1879-2472
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / PROCR protein, human; 0 / Protein C; 0 / Receptors, Cell Surface
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98. Yegneswaran S, Nguyen PM, Gale AJ, Griffin JH: Prothrombin amino terminal region helps protect coagulation factor Va from proteolytic inactivation by activated protein C. Thromb Haemost; 2009 Jan;101(1):55-61
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  • [Title] Prothrombin amino terminal region helps protect coagulation factor Va from proteolytic inactivation by activated protein C.
  • The hypothesis that prothrombin (FII) protects coagulation factor Va (FVa) from proteolytic inactivation by activated protein C (APC) was tested using purified proteins.
  • FII dose-dependently protected FVa from APC proteolysis under conditions where competition of proteins for binding to negatively-charged phospholipid surface was not relevant (i.e. either at high phospholipid vesicle concentrations or using soluble dicaproylphosphatidylserine at levels below its critical micellar concentration).
  • Cleavages in FVa at both Arg(506) and Arg(306) by APC were inhibited by FII.
  • FII did not alter the amidolytic activity of APC towards chromogenic oligopeptide substrates or inhibit FVIIIa inactivation by APC, implying that the FII-mediated protection of FVa from APC proteolysis was due to the ability of FII to inhibit protein-protein interactions between FVa and APC.
  • FII also protected FVa from inactivation by Gla-domainless APC, ruling out a role for the APC Gla domain for these observations.
  • Biotin-Phe-ProArg-CMK-inhibited meizothrombin and fII-fragment 1*2 protected FVa from proteolysis by APC.
  • In contrast, no significant protection of FVa from APC cleavage was observed for Gladomainless-FII, prethrombin-1, prethrombin-2, FII fragment 1 or active site inhibited-thrombin (DEGR-thrombin).
  • Overall, these data demonstrate that the Gla domain of FII linked to kringle 1 and 2 is necessary for the ability of FII to protect FVa from APC cleavage and support the general concept that assembly of the FII activation complex (FXa*FVa*FII*lipid surface) protects FVa from APC inactivation so that the procoagulant, thrombin generating pathway can act unhindered by APC.
  • Only following FII activation and dissociation of the FII Gla domain fragments from the FII-ase complex, can APC inactivate FVa and down-regulate thrombin generation.

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  • (PMID = 19132189.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R37 HL052246; United States / NHLBI NIH HHS / HL / R01 HL082588; United States / NHLBI NIH HHS / HL / R01 HL082588-04; United States / NHLBI NIH HHS / HL / R01 HL052246-15; United States / NHLBI NIH HHS / HL / HL082588-04; United States / NHLBI NIH HHS / HL / R01 HL052246; United States / NHLBI NIH HHS / HL / R01 HL021544; United States / NHLBI NIH HHS / HL / HL021544-32; United States / NHLBI NIH HHS / HL / R01 HL021544-32; United States / NHLBI NIH HHS / HL / HL052246-15
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Enzyme Precursors; 0 / Peptide Fragments; 0 / Phospholipids; 0 / Protein C; 0 / Recombinant Proteins; 0 / prothrombin fragment 1.2; 65522-14-7 / Factor Va; 72175-66-7 / Factor VIIIa; 9001-26-7 / Prothrombin; 9070-19-3 / prethrombins; EC 3.4.21.- / meizothrombin; EC 3.4.21.5 / Thrombin; EC 3.4.21.6 / Factor Xa
  • [Other-IDs] NLM/ NIHMS104707; NLM/ PMC2730196
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99. Looney MR, Matthay MA: Bench-to-bedside review: the role of activated protein C in maintaining endothelial tight junction function and its relationship to organ injury. Crit Care; 2006;10(6):239
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  • [Title] Bench-to-bedside review: the role of activated protein C in maintaining endothelial tight junction function and its relationship to organ injury.
  • Activated protein C (APC) has emerged as a novel therapeutic agent for use in selected patients with severe sepsis, even though the mechanism of its benefit is not well established.
  • APC has anticoagulant, anti-inflammatory, antiapoptotic, and profibrinolytic properties, but it is not clear through which of these mechanisms APC exerts its benefit in severe sepsis.
  • Focus has recently turned to the role of APC in maintaining endothelial barrier function, and in vitro and in vivo studies have examined this relationship.
  • This article critically reviews these studies, with a focus on potential mechanisms of action.
  • [MeSH-major] Protein C / pharmacology. Protein C / physiology. Sepsis / complications. Tight Junctions / physiology
  • [MeSH-minor] Endothelium / physiology. Humans. Multiple Organ Failure / etiology. Multiple Organ Failure / physiopathology

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  • [CommentIn] Crit Care. 2007;11(1):407; author reply 407 [17328792.001]
  • (PMID = 17169139.001).
  • [ISSN] 1466-609X
  • [Journal-full-title] Critical care (London, England)
  • [ISO-abbreviation] Crit Care
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein C
  • [Number-of-references] 38
  • [Other-IDs] NLM/ PMC1794467
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100. Baron TH: Ampullary adenoma. Curr Treat Options Gastroenterol; 2008 Apr;11(2):96-102
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ampullary adenoma.
  • Ampullary adenoma is a premalignant lesion involving the major papilla and surrounding mucosa of the second duodenum.
  • These lesions may arise sporadically or in the setting of familial adenomatous polyposis syndrome.
  • Ampullary adenoma may be found because of symptoms, at the time of adenomatous polyposis syndrome surveillance, or incidentally when upper endoscopy is performed for other reasons.

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  • (PMID = 18321436.001).
  • [ISSN] 1092-8472
  • [Journal-full-title] Current treatment options in gastroenterology
  • [ISO-abbreviation] Curr Treat Options Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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