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1. Mehrotra S, Zaidi N, Chakraborty NG, Mukherji B: Macrophages as stimulators of MART-1 27-35 epitope-specific human cytolytic T lymphocytes in vitro. Pathobiology; 2006;73(5):238-43
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  • BACKGROUND: Activation and expansion of antigen-specific cytolytic T lymphocytes (CTL) require epitope presented by antigen-presenting cells (APC).
  • Presently, dendritic cells (DC) are viewed as the most efficient APC.
  • Since the recognition of DCs as the professional APC, the paradigm has emerged that macrophage (MPhi) are scavengers and are incapable of activating T cells.
  • METHOD: The melanoma-associated MART-1(27-35) peptide-loaded MPhi from HLA-A2-positive donors were used to activate MART-1(27-35) epitope-specific CTL in vitro.
  • We also show that upon restimulation with the peptide pulsed MPhi, a fraction of the epitope-specific CTLs undergoes activation-induced cell death.
  • The activation-induced cell death is induced in an epitope-specific manner and through apoptosis.
  • CONCLUSION: MPhi can function as APC and are also capable of modulating expansion and contraction of CTL response in vitro.
  • [MeSH-major] Antigen Presentation / immunology. Epitopes / immunology. Lymphocyte Activation / immunology. Macrophages / immunology. Neoplasm Proteins / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 17314494.001).
  • [ISSN] 1015-2008
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Epitopes; 0 / Epitopes, T-Lymphocyte; 0 / MART-1-Melan-A(27-35) epitope; 0 / Neoplasm Proteins
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2. Feine O, Zur A, Mahbubani H, Brandeis M: Human Kid is degraded by the APC/C(Cdh1) but not by the APC/C(Cdc20). Cell Cycle; 2007 Oct 15;6(20):2516-23
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  • [Title] Human Kid is degraded by the APC/C(Cdh1) but not by the APC/C(Cdc20).
  • The APC/C(Cdh1) (anaphase promoting complex/cyclosome) targets numerous cell cycle proteins for ubiquitin mediated degradation in late mitosis and G1.
  • The KEN box is one of two major recognition motifs of APC/C(Cdh1) substrates.
  • This motif is however very common and shared by a tenth of the human proteome, the vast majority of which are obviously not APC/C substrates.
  • We have observed that most known functional KEN boxes are followed by a proline residue and show that this proline plays a role in APC/C(Cdh1) specific degradation.
  • This insight can be instrumental for identifying novel APC/C(Cdh1) substrates.
  • We used this KENxP motif to identify human Aurora B and Kid as APC/C(Cdh1) substrates.
  • The degradation of Xenopus XKid at metaphase by APC/C(Cdc20) is essential for chromatid segregation.
  • Human Kid in contrast is degraded later and its APC/C(Cdh1) specific degradation is not required for mitotic progress.
  • It is thus likely that Kid inactivation in G1 takes place both by nuclear sequestration and degradation by the APC/C(Cdh1).
  • [MeSH-major] DNA-Binding Proteins / metabolism. Kinesin / metabolism. Protein Processing, Post-Translational. Ubiquitin-Protein Ligase Complexes / metabolism
  • [MeSH-minor] Amino Acid Motifs. Anaphase-Promoting Complex-Cyclosome. Animals. Aurora Kinase B. Aurora Kinases. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Line. Humans. Mice. Proline / genetics. Proline / metabolism. Protein-Serine-Threonine Kinases / metabolism. Substrate Specificity. Xenopus laevis

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  • (PMID = 17726374.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / KIF22 protein, human; 9DLQ4CIU6V / Proline; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.6.1.- / Kinesin; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
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3. Guadagni S, Clementi M, Valenti M, Fiorentini G, Cantore M, Kanavos E, Caterino GP, Di Giuro G, Amicucci G: Hypoxic abdominal stop-flow perfusion in the treatment of advanced pancreatic cancer: a phase II evaluation/trial. Eur J Surg Oncol; 2007 Feb;33(1):72-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, these promising results have not been confirmed by others, making it difficult to define the effectiveness of this loco-regional chemotherapy.
  • The aim of this study, therefore, was to evaluate the response rate, time to disease progression and overall survival following HAP treatment of 22 consecutive patients with advanced pancreatic tumors.
  • Within the period from 1999 to 2003, 22 patients with histological diagnosis of unresectable stage III/IV pancreatic cancer, not responsive to systemic chemotherapy, were treated with mitomycin C 30mg/m(2) and cisplatin 60mg/m(2) by HAP (stop flow technique).
  • Following 26 treatment cycles no death or technical complications were recorded; four patients (18.2%) achieved a partial response, 2 (9.1%) a minimal response and 13 (59.1%) stable disease.
  • The remaining 3 patients (13.6%) showed progression of the disease.
  • The median time to disease progression was 3 months (range 1-10).
  • The median survival time from the start of regional chemotherapy was 6 months (range 1.9-16), with a 1-year survival rate of 9%.
  • We do not concur with the opinion of others that HAP is an inactive treatment approach.
  • However, taking into account the invasiveness of this procedure, and associated morbidity and cost, HAP would not appear to be preferable to less invasive loco-regional chemotherapeutic alternatives.

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  • (PMID = 17166688.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 50SG953SK6 / Mitomycin; Q20Q21Q62J / Cisplatin
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4. Wilkins JA, Sansom OJ: C-Myc is a critical mediator of the phenotypes of Apc loss in the intestine. Cancer Res; 2008 Jul 1;68(13):4963-6
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  • [Title] C-Myc is a critical mediator of the phenotypes of Apc loss in the intestine.
  • The Adenomatous polyposis coli (Apc) gene is mutated in up to 80% of sporadic colorectal cancers.
  • After Apc loss, there is deregulation of the Wnt signaling pathway and transactivation of T-cell factor/leukemia enhancing factor target genes such as C-Myc.
  • This review focuses on recent data highlighting the importance of the C-Myc oncogene and its transcriptional targets in establishing all of the phenotypes caused by the deletion of the Apc tumor suppressor gene within the intestinal epithelium.
  • The importance of investigating Apc and C-Myc gene function in the correct tissue context is also discussed.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Genes, APC. Intestines / metabolism. Loss of Heterozygosity. Proto-Oncogene Proteins c-myc / physiology
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / metabolism. Animals. Cell Proliferation. Humans. Models, Biological. Phenotype. Precancerous Conditions / genetics

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  • (PMID = 18593890.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc
  • [Number-of-references] 31
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5. Liu Y, Zhang CG, Zhou CY: [Dual-role regulations of canonical Wnt/beta-catenin signaling pathway]. Beijing Da Xue Xue Bao; 2010 Apr 18;42(2):238-42
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  • Canonical Wnt signaling pathway is controlled by a variety of classic molecules like Wnt, beta-catenin, Axin, APC, GSK-3beta and CK1, which interact and coordinate to regulate the expressions of cell signaling molecules.
  • The latest evidences suggest that some components of the Wnt/beta-catenin signaling, like APC, GSK-3beta, CK1, Dkk2 and WISE, play dual roles different from what they have been thought previously.
  • [MeSH-major] Signal Transduction / physiology. Wnt Proteins / physiology. beta Catenin / physiology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Adaptor Proteins, Signal Transducing / physiology. Adenomatous Polyposis Coli Protein / metabolism. Adenomatous Polyposis Coli Protein / physiology. Animals. Axin Protein. Gene Expression Regulation. Humans. Repressor Proteins / metabolism. Repressor Proteins / physiology

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  • (PMID = 20396373.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Axin Protein; 0 / Repressor Proteins; 0 / Wnt Proteins; 0 / beta Catenin
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6. Casadei R, Ricci C, Pezzilli R, Serra C, Calculli L, Morselli-Labate AM, Santini D, Minni F: A prospective study on radiofrequency ablation locally advanced pancreatic cancer. Hepatobiliary Pancreat Dis Int; 2010 Jun;9(3):306-11
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  • METHODS: RFA was the first step of the surgical procedure and was carried out on the mobilized pancreatic head followed by biliary by-pass and gastrojejunal-anastomosis.
  • The RFA procedure was carried out in 3 of the 4 patients; in one patient it was not carried out because of the upstaging of the neoplasm.
  • A biliary fistula developed 7 days after the procedure in one patient; all 3 patients developed ascites 8.6 days (range 7-9 days) on average after RFA.
  • CONCLUSIONS: In our experience, RFA is a feasible procedure, but it presents a very high rate of postoperative complications.

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  • (PMID = 20525559.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
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7. Marciniak A, Wlazło M: Activity coefficients at infinite dilution measurements for organic solutes and water in the ionic liquid 1-(3-hydroxypropyl)pyridinium trifluorotris(perfluoroethyl)phosphate. J Phys Chem B; 2010 May 27;114(20):6990-4
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  • The activity coefficients at infinite dilution, gamma(13)(infinity), for 37 solutes, alkanes, alkenes, alkynes, cycloalkanes, aromatic hydrocarbons, alcohols, thiophene, ethers, ketones, and water, in the ionic liquid 1-(3-hydroxypropyl)pyridinium trifluorotris(perfluoroethyl)phosphate [N-C(3)OHPY][FAP] were determined by gas-liquid chromatography at the temperatures from 308.15 to 358.15 K.
  • It was found that the investigated [N-C(3)OHPY][FAP] ionic liquid shows much higher selectivity and capacity at infinite dilution than the generally used organic solvents such as NMP, sulfolane, and other ionic liquids.

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  • (PMID = 20429540.001).
  • [ISSN] 1520-5207
  • [Journal-full-title] The journal of physical chemistry. B
  • [ISO-abbreviation] J Phys Chem B
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Kitamura T, Biyajima K, Aoki M, Oshima M, Taketo MM: Matrix metalloproteinase 7 is required for tumor formation, but dispensable for invasion and fibrosis in SMAD4-deficient intestinal adenocarcinomas. Lab Invest; 2009 Jan;89(1):98-105
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Matrix metalloproteinase 7 is required for tumor formation, but dispensable for invasion and fibrosis in SMAD4-deficient intestinal adenocarcinomas.
  • However, its contribution to colon cancer pathogenesis is not understood thoroughly.
  • To investigate the roles of MMP7 in colon cancer progression, we introduced an Mmp7 knockout mutation into the cis-Apc/Smad4 mutant mouse, a model of invasive colon cancer in which SMAD4-dependent TGF-beta family signaling is inactivated.
  • We demonstrate here that lack of MMP7 reduces the number and size of tumors in the cis-Apc/Smad4 mice.
  • On the other hand, MMP7-deficiency does not affect the depth of tumor invasion, number of stromal fibroblasts or levels of extracellular matrix components in the tumors.
  • These results indicate that MMP7 is required for tumor formation, but not for the invasion or fibrosis of the colon cancer whose SMAD4-dependent TGF-beta family signaling is blocked.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Colonic Neoplasms / etiology. Colonic Neoplasms / pathology. Matrix Metalloproteinase 7 / metabolism. Smad4 Protein / deficiency
  • [MeSH-minor] Animals. Cell Count. Collagen Type I / metabolism. Disease Progression. Female. Fibroblasts / pathology. Fibrosis. Genes, APC. Male. Mice. Mice, Knockout. Neoplasm Invasiveness. Signal Transduction. Transforming Growth Factor beta / antagonists & inhibitors. Transforming Growth Factor beta / metabolism

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  • (PMID = 19002110.001).
  • [ISSN] 1530-0307
  • [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 / Collagen Type I; 0 / Smad4 Protein; 0 / Transforming Growth Factor beta; EC 3.4.24.23 / Matrix Metalloproteinase 7
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9. Gerth HU, Dammaschke T, Schäfer E, Züchner H: A three layer structure model of fluoridated enamel containing CaF2, Ca(OH)2 and FAp. Dent Mater; 2007 Dec;23(12):1521-8
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  • [Title] A three layer structure model of fluoridated enamel containing CaF2, Ca(OH)2 and FAp.
  • However, up to now Ca(OH)(2) has not been described as a reaction product after topical fluoridation.
  • Below the Ca(OH)(2) layer an acid resistant apatite species (FAp) was detected which reached directly into the bulk enamel HAp species.

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  • (PMID = 17353046.001).
  • [ISSN] 0109-5641
  • [Journal-full-title] Dental materials : official publication of the Academy of Dental Materials
  • [ISO-abbreviation] Dent Mater
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amines; 0 / Apatites; 0 / Cariostatic Agents; 0 / Diamines; 0 / Fluorides, Topical; 8NY9L8837D / Olaflur; 91D9GV0Z28 / Durapatite; M4CM1H238J / fluorapatite; O3B55K4YKI / Calcium Fluoride; PF5DZW74VN / Calcium Hydroxide; Q80VPU408O / Fluorides
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10. Wasmuth HH, Svinsås M, Tranø G, Rydning A, Endreseth BH, Wibe A, Myrvold HE: Surgical load and long-term outcome for patients with Kock continent ileostomy. Colorectal Dis; 2007 Oct;9(8):713-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The aim of the study was to evaluate the results of Kock continent ileostomy (CI) during the same period when ileal pouch-anal anastomosis was the preferred operation for patients with ulcerative colitis (UC) or familial adenomatous polyposis (FAP).
  • METHOD: During the period 1983-2002, 50 patients underwent CI.
  • Forty-eight patients had UC, two of these had the diagnosis later changed to Crohn's disease and two had FAP.
  • Seventeen (45%) underwent a revision of the nipple valve and the pouch and nine (24%) a local procedure.
  • The reoperation rate was higher among patients having a conventional ileostomy converted to CI than among those having CI.
  • As a primary procedure (P = 0.016).
  • The risk of a second reoperation was higher for those reoperated within the first year after having a CI, than for those reoperated later (P = 0.007).
  • CONCLUSIONS: The reoperation rate of patients with CI is high but the removal rate of the pouch is low and is not associated with a high rate of revision.
  • CI is a good alternative to conventional ileostomy in patients not suitable for restorative proctocolectomy or where this procedure has failed.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Colitis, Ulcerative / surgery. Colonic Pouches. Treatment Outcome

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  • (PMID = 17784871.001).
  • [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
  • [Publication-country] England
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11. Alonso A, Moreno S, Valiente A, Artigas M, Pérez-Juana A, Ramos Arroyo MA: [Genetic mechanisms in the hereditary predisposition to colorectal cancer]. An Sist Sanit Navar; 2006 Jan-Apr;29(1):59-76
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  • [Title] [Genetic mechanisms in the hereditary predisposition to colorectal cancer].
  • [Transliterated title] Mecanismos genéticos en la predisposición hereditaria al cáncer colorrectal.
  • A proportion of colorectal cancers shows some type of genetic predisposition that can be recognised in clinical practice.
  • From the classical dominant inheritance pattern of familial adenomatous polyposis or hereditary non-polyposis colorectal cancer, through the recessive transmission of the MYH associated polyposis, to the new syndromes of the "serrated pathway" or low-penetrance alleles, the discovery of new genes and a deeper understanding of the mechanisms of action of already-known ones are enabling us to understand new aspects of the colorectal carcinogenesis.
  • This is throwing a new light on some of the observed familial aggregation patterns which had remained unexplained.
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Alleles. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Genes, Recessive. Genetic Predisposition to Disease. Genotype. Humans. Immunohistochemistry. Middle Aged. Mutation. Phenotype

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  • (PMID = 16670730.001).
  • [ISSN] 1137-6627
  • [Journal-full-title] Anales del sistema sanitario de Navarra
  • [ISO-abbreviation] An Sist Sanit Navar
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 91
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12. Nagel R, le Sage C, Diosdado B, van der Waal M, Oude Vrielink JA, Bolijn A, Meijer GA, Agami R: Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer. Cancer Res; 2008 Jul 15;68(14):5795-802
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer.
  • Inactivation of the adenomatous polyposis coli (APC) gene is a major initiating event in colorectal tumorigenesis.
  • Most of the mutations in APC generate premature stop codons leading to truncated proteins that have lost beta-catenin binding sites.
  • APC-free beta-catenin stimulates the Wnt signaling pathway, leading to active transcription of target genes.
  • In the current study, we describe a novel mechanism for APC regulation.
  • We show that miR-135a&b target the 3' untranslated region of APC, suppress its expression, and induce downstream Wnt pathway activity.
  • Interestingly, we find a considerable up-regulation of miR-135a&b in colorectal adenomas and carcinomas, which significantly correlated with low APC mRNA levels.
  • This genetic interaction is also preserved in full-blown cancer cell lines expressing miR-135a&b, regardless of the mutational status of APC.
  • Thus, our results uncover a miRNA-mediated mechanism for the control of APC expression and Wnt pathway activity, and suggest its contribution to colorectal cancer pathogenesis.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / physiology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. MicroRNAs / genetics
  • [MeSH-minor] 3' Untranslated Regions. Cell Line. Cell Line, Tumor. DNA Mutational Analysis. Gene Expression Profiling. HeLa Cells. Humans. Models, Biological. Promoter Regions, Genetic. Signal Transduction. Wnt Proteins / metabolism


13. Sinha A, Tekkis PP, Rashid S, Phillips RK, Clark SK: Risk factors for secondary proctectomy in patients with familial adenomatous polyposis. Br J Surg; 2010 Nov;97(11):1710-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk factors for secondary proctectomy in patients with familial adenomatous polyposis.
  • BACKGROUND: Colectomy and ileorectal anastomosis (IRA) or restorative proctocolectomy are performed for prophylaxis in familial adenomatous polyposis (FAP).
  • After IRA patients may require secondary proctectomy for worsening polyposis or rectal cancer.
  • Outcomes after IRA were evaluated and risk factors predictive of progressive rectal disease identified.
  • METHODS: Parametric survival analysis was used to identify predictors of progressive rectal disease in all patients undergoing an IRA for FAP at a single centre.
  • RESULTS: Of 427 patients who underwent IRA, 48 (11.2 per cent) developed rectal cancer and 77 (18.0 per cent) required proctectomy for worsening polyposis over a median follow-up of 15 (range 7-25) years.
  • Rectal polyp count exceeding 20 (HR 30.99, 95 per cent confidence interval 9.57 to 100.32; P < 0.001), APC mutation codon 1250-1450 (HR 3.91, 1.45 to 10.51; P = 0.007), colonic polyp count 500 or more (HR 2.18, 1.24 to 3.82; P = 0.006) and age less than 25 years at the time of surgery (HR 1.99, 1.17 to 3.37; P = 0.011) were independent predictors of progressive rectal disease.
  • CONCLUSION: The risk of proctectomy after IRA for FAP is based on patient genotype, phenotype and age at surgery.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Neoplasm Recurrence, Local / surgery. Proctocolectomy, Restorative. Rectal Neoplasms / surgery

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  • [Copyright] Copyright © 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
  • (PMID = 20665483.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
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14. Planté-Bordeneuve V, Ferreira A, Lalu T, Zaros C, Lacroix C, Adams D, Said G: Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP). Neurology; 2007 Aug 14;69(7):693-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP).
  • Transthyretin familial amyloid polyneuropathies (TTR-FAPs) are autosomal dominant neuropathies of fatal outcome within 10 years after inaugural symptoms.
  • Late diagnosis in patients who present as nonfamilial cases delays adequate management and genetic counseling.
  • Clinical data of the 90 patients who presented as nonfamilial cases of the 300 patients of our cohort of patients with TTR-FAP were reviewed.
  • Mean interval to diagnosis was 4 years (range 1 to 10 years); 18 cases were mistaken for chronic inflammatory demyelinating polyneuropathy, which was the most common diagnostic error.
  • Decreased nerve conduction velocity, increased CSF protein, negative biopsy findings, and false immunolabeling of amyloid deposits were the main causes of diagnostic errors.
  • We conclude that DNA testing, which is the most reliable test for TTR-FAP, should be performed in patients with a progressive length-dependent small fiber polyneuropathy of unknown origin, especially when associated with autonomic dysfunction.
  • [MeSH-major] Amyloid Neuropathies, Familial / diagnosis. Amyloid Neuropathies, Familial / genetics. Prealbumin / genetics
  • [MeSH-minor] Adult. Aged. Demyelinating Diseases / diagnosis. Demyelinating Diseases / genetics. Demyelinating Diseases / pathology. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Molecular Diagnostic Techniques


15. Kimata Y, Yamano H: Structural analysis sheds light on APC/C-mediated ubiquitylation. Dev Cell; 2006 Jan;10(1):4-5
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  • [Title] Structural analysis sheds light on APC/C-mediated ubiquitylation.
  • In the December 22nd issue of Molecular Cell, two groups report refined cryo-electron microscopic structures of the APC/C at approximately 20 A resolution.
  • They also reveal important new features including multiple copies of subunits, dimerization and structural flexibility of the APC/C, which give a hint to solve the mechanisms of the APC/C-dependent ubiquitylation.
  • [MeSH-major] Polyubiquitin / metabolism. Protein Structure, Quaternary. Ubiquitin-Protein Ligase Complexes / chemistry

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  • [CommentOn] Mol Cell. 2005 Dec 22;20(6):867-79 [16364912.001]
  • [CommentOn] Mol Cell. 2005 Dec 22;20(6):855-66 [16364911.001]
  • (PMID = 16399071.001).
  • [ISSN] 1534-5807
  • [Journal-full-title] Developmental cell
  • [ISO-abbreviation] Dev. Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 120904-94-1 / Polyubiquitin; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
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16. Borad MJ, Saadati H, Lakshmipathy A, Campbell E, Hopper P, Jameson G, Von Hoff DD, Saif MW: Skeletal metastases in pancreatic cancer: a retrospective study and review of the literature. Yale J Biol Med; 2009 Mar;82(1):1-6
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  • All patients had advanced disease and had received prior systemic therapy (range: 1-4 lines, median: 2 lines).

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  • (PMID = 19325940.001).
  • [ISSN] 1551-4056
  • [Journal-full-title] The Yale journal of biology and medicine
  • [ISO-abbreviation] Yale J Biol Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 28
  • [Other-IDs] NLM/ PMC2660584
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17. Basdanis G, Papadopoulos VN, Panidis S, Tzeveleki I, Karamanlis E, Mekras A, Apostolidis S, Michalopoulos A: Desmoid tumor of mesentery in familial adenomatous polyposis: a case report. Tech Coloproctol; 2010 Nov;14 Suppl 1:S61-2
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  • [Title] Desmoid tumor of mesentery in familial adenomatous polyposis: a case report.
  • Our case concerns a 52-year-old male with FAP, who was treated surgically by restorative colectomy and ileal pouch anal anastomosis.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Fibromatosis, Aggressive / surgery. Neoplasms, Second Primary / surgery. Peritoneal Neoplasms / surgery


18. Hu ZL, Fritz ER, Reecy JM: AnimalQTLdb: a livestock QTL database tool set for positional QTL information mining and beyond. Nucleic Acids Res; 2007 Jan;35(Database issue):D604-9
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  • The Animal Quantitative Trait Loci (QTL) database (AnimalQTLdb) is designed to house all publicly available QTL data on livestock animal species from which researchers can easily locate and compare QTL within species.
  • The database tools are also added to link the QTL data to other types of genomic information, such as radiation hybrid (RH) maps, finger printed contig (FPC) physical maps, linkage maps and comparative maps to the human genome, etc.
  • Currently, this database contains data on 1287 pig, 630 cattle and 657 chicken QTL, which are dynamically linked to respective RH, FPC and human comparative maps.
  • We plan to apply the tool to other animal species, and add more structural genome information for alignment, in an attempt to aid comparative structural genome studies (http://www.animalgenome.org/QTLdb/).

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  • (PMID = 17135205.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1781224
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19. Jin G, Kelley TR: Characterization of microbial communities in a pilot-scale constructed wetland using PLFA and PCR-DGGE analyses. J Environ Sci Health A Tox Hazard Subst Environ Eng; 2007 Sep;42(11):1639-47
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  • This pilot-scale constructed wetland system consists of three types: subsurface-flow (SSF), surface-flow (SF) and a floating aquatic plant (FAP) system.
  • Biomass content (total PFLA/sample) was highest in water samples collected from both SF and FAP system while highest metabolic activity was observed in FAP system.
  • This is consistent with the observed highest metal removal rate in FAP system.

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  • (PMID = 17849306.001).
  • [ISSN] 1093-4529
  • [Journal-full-title] Journal of environmental science and health. Part A, Toxic/hazardous substances & environmental engineering
  • [ISO-abbreviation] J Environ Sci Health A Tox Hazard Subst Environ Eng
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Bacterial; 0 / DNA, Ribosomal; 0 / Fatty Acids; 0 / Phospholipids; 0 / Water Pollutants
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20. Thorneloe SA, Kosson DS, Sanchez F, Garrabrants AC, Helms G: Evaluating the fate of metals in air pollution control residues from coal-fired power plants. Environ Sci Technol; 2010 Oct 1;44(19):7351-6
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  • Changes in emissions control at U.S. coal-fired power plants will shift metals content from the flue gas to the air pollution control (APC) residues.
  • To determine the potential fate of metals that are captured through use of enhanced APC practices, the leaching behavior of 73 APC residues was characterized following the approach of the Leaching Environmental Assessment Framework.
  • Leachate concentrations for most metals were highly variable over a range of coal rank, facility configurations, and APC residue types.
  • Variability in metals leaching was greater than the variability in totals concentrations by several orders of magnitude, inferring that total content is not predictive of leaching behavior.

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  • (PMID = 20806888.001).
  • [ISSN] 1520-5851
  • [Journal-full-title] Environmental science & technology
  • [ISO-abbreviation] Environ. Sci. Technol.
  • [Language] eng
  • [Publication-type] Journal Article; 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 / Air Pollutants; 0 / Coal; 0 / Metals
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21. Baudet JS, Díaz-Bethencourt D, Soler M, Vela M, Morales S, Avilés J: [Long-term follow-up of patients with gastric antral vascular ectasia treated with argon plasma coagulation]. Med Clin (Barc); 2009 Jul 11;133(6):217-20
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  • [Transliterated title] Seguimiento a largo plazo de pacientes con ectasia vascular del antro gástrico tratados mediante coagulación con argón plasma.
  • BACKGROUND AND OBJECTIVE: Due to its easy use and low complication rates, argon plasma coagulation (APC) it is most common method of endoscopic treatment for gastric antral vascular ectasia (GAVE).
  • We analyze both the long term effectiveness of APC for the treatment of GAVE and its side effects.
  • MATERIAL AND METHODS: A retrospective review of GAVE patients treated with APC and followed up for a minimum of 24 months was done.
  • CONCLUSIONS: APC is a safe and effective technique for the treatment of GAVE.
  • Early action on recurrence would require improved clinical follow-up and blood test monitoring.

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  • (PMID = 19394972.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 67XQY1V3KH / Argon
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22. Brugge JM, Simioni P, Bernardi F, Tormene D, Lunghi B, Tans G, Pagnan A, Rosing J, Castoldi E: Expression of the normal factor V allele modulates the APC resistance phenotype in heterozygous carriers of the factor V Leiden mutation. J Thromb Haemost; 2005 Dec;3(12):2695-702
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  • [Title] Expression of the normal factor V allele modulates the APC resistance phenotype in heterozygous carriers of the factor V Leiden mutation.
  • BACKGROUND: Functional defects of the protein C pathway, detectable in plasma as activated protein C (APC) resistance, are a prevalent risk factor for venous thrombosis.
  • The factor V (FV) Leiden mutation causes APC resistance by interfering with the APC-mediated inactivation of both FVa and FVIIIa.
  • Co-inheritance of FV Leiden and quantitative FV deficiency on different alleles, a rare condition known as pseudo-homozygous APC resistance, is associated with pronounced APC resistance and 50% reduced FV levels, because of non-expression of the non-Leiden FV allele.
  • OBJECTIVES: The role of normal FV in modulating the APC resistance phenotype in carriers of FV Leiden was investigated in patients with pseudo-homozygous APC resistance and in model systems.
  • PATIENTS/METHODS: Four functional plasma assays probing both components of APC resistance (susceptibility of FVa to APC and cofactor activity of FV in FVIIIa inactivation) were employed to compare seven clinically and genetically characterized FV Leiden pseudo-homozygotes to 30 relatives with different FV genotypes (including 12 FV Leiden heterozygotes and seven carriers of FV deficiency) and to 32 unrelated FV Leiden homozygotes.
  • RESULTS AND CONCLUSIONS: All assays consistently indicated that FV Leiden pseudo-homozygotes are significantly more APC-resistant than heterozygotes and indistinguishable from homozygotes.
  • Thrombin generation measurements in FV-deficient plasma reconstituted with purified normal FV and FV Leiden confirmed these observations and showed that the expression of the normal FV allele is an important modulator of APC resistance in FV Leiden heterozygotes.
  • [MeSH-major] Activated Protein C Resistance / etiology. Factor V / genetics

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  • (PMID = 16359508.001).
  • [ISSN] 1538-7933
  • [Journal-full-title] Journal of thrombosis and haemostasis : JTH
  • [ISO-abbreviation] J. Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / factor V Leiden; 9001-24-5 / Factor V
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23. Brosens LA, van Hattem WA, Jansen M, de Leng WW, Giardiello FM, Offerhaus GJ: Gastrointestinal polyposis syndromes. Curr Mol Med; 2007 Feb;7(1):29-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastrointestinal polyposis syndromes.
  • Rare hereditary gastrointestinal polyposis syndromes that predispose to colorectal cancer have provided a model for the investigation of cancer initiation and progression in the general population.
  • Many insights in the molecular genetic basis of cancer have emerged from the study of these syndromes.
  • This review discusses the genetics and clinical manifestations of the three most common syndromes with gastrointestinal polyposis and an increased risk of colorectal cancer: familial adenomatous polyposis (FAP), juvenile polyposis (JP) and Peutz-Jeghers syndrome (PJS).
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Gastrointestinal Neoplasms / pathology
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Animals. Humans. Peutz-Jeghers Syndrome / diagnosis. Peutz-Jeghers Syndrome / genetics. Peutz-Jeghers Syndrome / pathology. Peutz-Jeghers Syndrome / therapy. Signal Transduction. Transforming Growth Factor beta / metabolism

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  • (PMID = 17311531.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Transforming Growth Factor beta
  • [Number-of-references] 166
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24. Kimata Y, Baxter JE, Fry AM, Yamano H: A role for the Fizzy/Cdc20 family of proteins in activation of the APC/C distinct from substrate recruitment. Mol Cell; 2008 Nov 21;32(4):576-83
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  • [Title] A role for the Fizzy/Cdc20 family of proteins in activation of the APC/C distinct from substrate recruitment.
  • The Fizzy/Cdc20 family of proteins are essential activators of the anaphase-promoting complex/cyclosome (APC/C), a multisubunit E3 ubiquitin ligase.
  • Here we show that Nek2A, which directly binds the APC/C, can be ubiquitylated and destroyed in Fizzy/Cdc20-depleted Xenopus egg extracts when only the N-terminal domain of Fizzy/Cdc20 (N-Cdc20) is added.
  • This activity is dependent upon the C box and is conserved in the alternative activator, Fizzy-related/Cdh1.
  • In contrast, canonical substrates such as cyclin B and securin require both the N-terminal and WD40 domains, unless N-Cdc20 is fused to substrates when the WD40 domain becomes dispensable.
  • Furthermore, in Cdc20-depleted cells, N-Cdc20 can facilitate Nek2A destruction in a C box-dependent manner.
  • Our results reveal a role for the N-terminal domain of the Fizzy/Cdc20 family of activators in triggering substrate ubiquitylation by the APC/C.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Proteins / metabolism. Ubiquitin-Protein Ligase Complexes / metabolism. Xenopus Proteins / metabolism
  • [MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Animals. Cdc20 Proteins. Models, Biological. Protein Structure, Tertiary. Protein-Serine-Threonine Kinases / metabolism. Substrate Specificity. Ubiquitination. Xenopus / genetics. Xenopus / metabolism

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  • [CommentIn] Mol Cell. 2008 Nov 21;32(4):460-1 [19026776.001]
  • (PMID = 19026787.001).
  • [ISSN] 1097-4164
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] eng
  • [Grant] United Kingdom / Worldwide Cancer Research / / 07-0062
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdc20 Proteins; 0 / Cdc20 protein, Xenopus; 0 / Cell Cycle Proteins; 0 / Proteins; 0 / Xenopus Proteins; EC 2.3.2.23 / Ubiquitin-Protein Ligase Complexes; EC 2.3.2.27 / Anaphase-Promoting Complex-Cyclosome; EC 2.7.1.- / Nek2A protein, Xenopus; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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25. Church J, Berk T, Boman BM, Guillem J, Lynch C, Lynch P, Rodriguez-Bigas M, Rusin L, Weber T, Collaborative Group of the Americas on Inherited Colorectal Cancer: Staging intra-abdominal desmoid tumors in familial adenomatous polyposis: a search for a uniform approach to a troubling disease. Dis Colon Rectum; 2005 Aug;48(8):1528-34
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  • [Title] Staging intra-abdominal desmoid tumors in familial adenomatous polyposis: a search for a uniform approach to a troubling disease.
  • INTRODUCTION: Desmoid tumors are a clinical problem in 12 to 15 percent of patients with familial adenomatous polyposis.
  • CONCLUSION: A way of staging intra-abdominal desmoid tumors is proposed to facilitate stratification by disease severity during collaborative studies of various treatments.
  • [MeSH-major] Abdominal Neoplasms / pathology. Adenomatous Polyposis Coli / pathology. Fibromatosis, Aggressive / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Abdominal Wall / pathology. Clinical Protocols. Genes, APC. Genotype. Humans. Mesentery / pathology. Mutation / genetics. Neoplasm Staging. Patient Care Planning. Peritoneal Neoplasms / pathology. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis

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  • (PMID = 15906134.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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26. Qiu W, Wang X, Leibowitz B, Liu H, Barker N, Okada H, Oue N, Yasui W, Clevers H, Schoen RE, Yu J, Zhang L: Chemoprevention by nonsteroidal anti-inflammatory drugs eliminates oncogenic intestinal stem cells via SMAC-dependent apoptosis. Proc Natl Acad Sci U S A; 2010 Nov 16;107(46):20027-32
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  • [Title] Chemoprevention by nonsteroidal anti-inflammatory drugs eliminates oncogenic intestinal stem cells via SMAC-dependent apoptosis.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) such as sulindac effectively prevent colon cancer in humans and rodent models.
  • We found that dietary sulindac induced apoptosis to remove the intestinal stem cells with nuclear or phosphorylated β-catenin in APC(Min/+) mice.
  • Furthermore, deficiency in SMAC, a mitochondrial apoptogenic protein, attenuated the tumor-suppressive effect of sulindac in APC(Min/+) mice by blocking apoptosis and removal of stem cells with nuclear or phosphorylated β-catenin.
  • These results suggest that effective chemoprevention of colon cancer by NSAIDs lies in the elimination of stem cells that are inappropriately activated by oncogenic events through induction of apoptosis.

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  • (PMID = 21041628.001).
  • [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 / NCI NIH HHS / CA / CA121105; United States / NCI NIH HHS / CA / R01 CA121105; United States / NCI NIH HHS / CA / CA129829; United States / NIDDK NIH HHS / DK / U01 DK085570; United States / NIDDK NIH HHS / DK / U01-DK085570; United States / NCI NIH HHS / CA / R01 CA129829; United States / NCI NIH HHS / CA / CA106348; United States / NCI NIH HHS / CA / R01 CA106348
  • [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 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carrier Proteins; 0 / DIABLO protein, human; 0 / Diablo protein, mouse; 0 / Intracellular Signaling Peptides and Proteins; 0 / Mitochondrial Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 184SNS8VUH / Sulindac
  • [Other-IDs] NLM/ PMC2993406
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27. Cheah PY, Wong YH, Loi C, Koh PK, Eu KW: Novel human pathological mutations. Gene symbol: APC. Disease: adenomatous polyposis coli. Hum Genet; 2009 Apr;125(3):352
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  • [Title] Novel human pathological mutations. Gene symbol: APC. Disease: adenomatous polyposis coli.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. INDEL Mutation

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  • (PMID = 19320041.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ HX080001
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Codon; 0 / Codon, Nonsense
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28. Aziz O, Athanasiou T, Fazio VW, Nicholls RJ, Darzi AW, Church J, Phillips RK, Tekkis PP: Meta-analysis of observational studies of ileorectal versus ileal pouch-anal anastomosis for familial adenomatous polyposis. Br J Surg; 2006 Apr;93(4):407-17
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  • [Title] Meta-analysis of observational studies of ileorectal versus ileal pouch-anal anastomosis for familial adenomatous polyposis.
  • BACKGROUND: Surgery for familial adenomatous polyposis (FAP) aims to minimize cancer risk while providing good functional outcome.
  • Rectal cancer was a diagnosis only in the ileorectal group (5.5 per cent).
  • Further research is needed to determine which most benefits patients with FAP.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Colonic Pouches. Proctocolectomy, Restorative / methods


29. Lynch PM: Standards of care in diagnosis and testing for hereditary colon cancer. Fam Cancer; 2008;7(1):65-72
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  • [Title] Standards of care in diagnosis and testing for hereditary colon cancer.
  • Inherited colorectal cancer predisposition involves a rather heterogeneous range of rare, yet relatively well-defined disorders, including Familial Adenomatous Polyposis (FAP), Hereditary Non-polyposis Colorectal Cancer (HNPCC) or Lynch syndrome, Peutz-Jeghers syndrome, Juvenile Polyposis, and their respective variants.
  • It is not clear that such guidelines actually codify standards of care.
  • Since the medical-legal implications are evident, we expect these guidelines to impact the management of familial cancer, even in the persistent absence of clear precedents in the medical malpractice arena.
  • This paper undertakes to provide practitioners and academics some perspective on clinical practice guidelines and their potential for medical-legal application.
  • [MeSH-major] Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / genetics. Genetic Counseling / standards. Genetic Testing / standards. Peutz-Jeghers Syndrome / diagnosis. Peutz-Jeghers Syndrome / genetics. Practice Patterns, Physicians' / standards
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / genetics. Colonoscopy. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Genetic Predisposition to Disease. Humans. International Agencies / standards. Malpractice. Medical Oncology / legislation & jurisprudence. Medical Oncology / standards. Practice Guidelines as Topic. United States


30. Ponti G, Ponz de Leon M, Maffei S, Pedroni M, Losi L, Di Gregorio C, Gismondi V, Scarselli A, Benatti P, Roncari B, Seidenari S, Pellacani G, Varotti C, Prete E, Varesco L, Roncucci L: Attenuated familial adenomatous polyposis and Muir-Torre syndrome linked to compound biallelic constitutional MYH gene mutations. Clin Genet; 2005 Nov;68(5):442-7
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  • [Title] Attenuated familial adenomatous polyposis and Muir-Torre syndrome linked to compound biallelic constitutional MYH gene mutations.
  • Attenuated familial adenomatous polyposis and Muir-Torre syndrome linked to compound biallelic constitutional MYH gene mutations.Peculiar dermatologic manifestations are present in several heritable gastrointestinal disorders.
  • Muir-Torre syndrome (MTS) is a genodermatosis whose peculiar feature is the presence of sebaceous gland tumors associated with visceral malignancies.
  • We describe one patient in whom multiple sebaceous gland tumors were associated with early onset colon and thyroid cancers and attenuated polyposis coli.
  • Skin and visceral neoplasms were tested for microsatellite instability and immunohistochemical status of mismatch repair (MMR), APC and MYH proteins.
  • The proband colon and skin tumors were microsatellite stable and showed normal expression of MMR proteins.
  • Cytoplasmic expression of MYH protein was revealed in colonic cancer cells.
  • Compound heterozygosity due to biallelic mutations in MYH, R168H and 379delC, was identified in the proband.
  • The 11-year-old daughter was carrier of the monoallelic constitutional mutation 379delC in the MYH gene; in the sister, the R168H MYH gene mutation was detected.
  • This report presents an interesting case of association between MYH-associated polyposis and sebaceous gland tumors.
  • These findings suggest that patients with MTS phenotype that include colonic polyposis should be screened for MYH gene mutations.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colonic Neoplasms / genetics. DNA Glycosylases / genetics. Germ-Line Mutation. Sebaceous Gland Neoplasms / genetics
  • [MeSH-minor] Adult. Child. DNA Mutational Analysis. Female. Humans. Neoplastic Syndromes, Hereditary / genetics. Pedigree. Syndrome. Thyroid Neoplasms / genetics


31. Declich P, Carneiro F, Omazzi B, Tavani E, Grassini R, Ferrara A, Bortoli A, Bellone S, Gozzini C, Prada A: Immunophenotype of sporadic and familial adenomatous polyposis associated fundic gland polyps: a mucin and MIB1 study. Pol J Pathol; 2006;57(3):141-8
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  • [Title] Immunophenotype of sporadic and familial adenomatous polyposis associated fundic gland polyps: a mucin and MIB1 study.
  • BACKGROUND: Fundic Gland Polyps (FGPs) are small sessile (2-5 mm) usually multiple polyps arising in the gastric, acid-secreting mucosa, described both in a sporadic form, prevalently in middle aged females, and associated with familial adenomatosis coli (FAP)-Gardner's syndrome and their attenuated variants (syndromic form).
  • AIMS: We performed an immunohistochemical study on 5 syndromic (4 cases without and 1 case with dysplasia) and 28 sporadic FGPs, using monoclonal antibodies (MoAbs) against normal epitopes of fundic mucosa (Ck20, the surface gastric mucin M1, EMA, ChA), H. pylori and HLA-DR(Ia) antigens, CEA and mucin epitopes, and the Ki67 (MIB1) proliferation antigen, in order to establish the immunophenotype of FGPs; find any possible differences between sporadic and syndromic polyps.
  • Ck7, as expected, was negative in controls, whereas the 5 syndromic FGPs and 25 of 28 sporadic FGPs showed a diffuse superficial and deep expression. H. pylori anti-serum gave negative results on all cases, and only 3 sporadic FGPs showed epithelial expression of HLA-DR(Ia).
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Adenomatous Polyps / metabolism. Gastric Fundus / metabolism. Ki-67 Antigen / metabolism. Mucins / metabolism


32. Knutson KL, Disis ML: Tumor antigen-specific T helper cells in cancer immunity and immunotherapy. Cancer Immunol Immunother; 2005 Aug;54(8):721-8
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  • In addition, many putative tumor antigens are intracellular proteins, and CTL respond to peptides presented in the context of MHC class I which are most often derived from intracellular proteins.
  • Recently, increasing importance is being given to the stimulation of a CD4+ T helper cell (Th) response in cancer immunotherapy.
  • In addition, Th1 cells activate antigen-presenting cells (APC) and induce limited production of the type of antibodies that can enhance the uptake of infected cells or tumor cells into APC.
  • Th1 cells are already widely implicated in the tissue-specific destruction that occurs during the pathogenesis of autoimmune diseases, such as diabetes mellitus and multiple sclerosis.
  • We now know that cross-priming of the tumor-specific response by potent APC is a major mechanism of the developing endogenous immune response; therefore, even intracellular proteins can be presented in the context of MHC class II.
  • Early clinical trials have shown that focus on the Th effector arm of the immune system can result in significant levels of both antigen-specific Th cells and CTL, the generation of long lasting immunity, and a Th1 phenotype resulting in the development of epitope spreading.

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  • (PMID = 16010587.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24CA85218; United States / NCI NIH HHS / CA / R21CA105270; United States / NCI NIH HHS / CA / R41CA107590
  • [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.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Cytokines; 0 / Epitopes, T-Lymphocyte
  • [Number-of-references] 62
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33. Sievers S, Fritzsch C, Lehnhardt M, Zahn S, Kutzner N, Kuhnen C, Müller O: Hypermethylation of the APC promoter but lack of APC mutations in myxoid/round-cell liposarcoma. Int J Cancer; 2006 Nov 15;119(10):2347-52
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  • [Title] Hypermethylation of the APC promoter but lack of APC mutations in myxoid/round-cell liposarcoma.
  • The adenomatous polyposis coli (APC) protein is a key component of the WNT signalling pathway wherein it acts as a scaffolding protein in controlling the level of the proto-oncoprotein beta-catenin.
  • Although APC has been shown to be genetically or epigenetically inactivated in a variety of carcinomas, little is known about its role in sarcoma.
  • We assessed the extent of genetic and epigenetic inactivation of the APC gene in myxoid/round-cell LPS.
  • Sequencing of the mutation cluster region, the protein truncation test and a loss of heterozygosity (LOH) analysis did not reveal any genetic alterations of the APC gene in all of the liposarcoma samples.
  • Methylation of the APC promoter was detected by methylation-specific PCR in 9 of 20 (45%) tumours.
  • Analysis of APC expression by semiquantitative RT-PCR in a subset of the samples demonstrated that tumours with a methylated APC promoter showed a downregulation of the APC transcript.
  • However, APC downregulation was not correlated with a stabilisation of the beta-catenin protein.
  • Thus, the epigenetic regulation of the APC gene might play an important role in the pathogenesis of myxoid/round-cell LPS.
  • However, the impact of APC methylation on liposarcoma development is quite likely not mediated through WNT signalling.
  • [MeSH-major] DNA Methylation. Gene Silencing. Genes, APC. Liposarcoma, Myxoid / genetics. Liposarcoma, Myxoid / pathology. Mutation

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  • (PMID = 16858687.001).
  • [ISSN] 0020-7136
  • [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 / CTNNB1 protein, human; 0 / beta Catenin
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34. Chen Q, Sun B, Wu H, Peng Z, Fives-Taylor PM: Differential roles of individual domains in selection of secretion route of a Streptococcus parasanguinis serine-rich adhesin, Fap1. J Bacteriol; 2007 Nov;189(21):7610-7
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  • [Title] Differential roles of individual domains in selection of secretion route of a Streptococcus parasanguinis serine-rich adhesin, Fap1.
  • Fimbria-associated protein 1 (Fap1) is a high-molecular-mass glycosylated surface adhesin required for fimbria biogenesis and biofilm formation in Streptococcus parasanguinis.
  • The secretion of mature Fap1 is dependent on the presence of SecA2, a protein with some homology to, but with a different role from, SecA.
  • The signals that direct the secretion of Fap1 to the SecA2-dependent secretion pathway rather than the SecA-dependent secretion pathway have not yet been identified.
  • In this study, Fap1 variants containing different domains were expressed in both secA2 wild-type and mutant backgrounds and were tested for their ability to be secreted by the SecA- or SecA2-dependent pathway.
  • The presence or absence of the cell wall anchor domain (residues 2531 to 2570) at the C terminus did not alter the selection of the Fap1 secretion route.
  • The Fap1 signal peptide (residues 1 to 68) was sufficient to support the secretion of a heterologous protein via the SecA-dependent pathway, suggesting that the signal peptide was sufficient for recognition by the SecA-dependent pathway.
  • The minimal sequences of Fap1 required for the SecA2-dependent pathway included the N-terminal signal peptide, nonrepetitive region I (residues 69 to 102), and part of nonrepetitive region II (residues 169 to 342).
  • The two serine-rich repeat regions (residues 103 to 168 and 505 to 2530) were not required for Fap1 secretion.
  • However, they were both involved in the specific inhibition of Fap1 secretion via the SecA-dependent pathway.

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  • (PMID = 17766425.001).
  • [ISSN] 0021-9193
  • [Journal-full-title] Journal of bacteriology
  • [ISO-abbreviation] J. Bacteriol.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R01 DE011000; United States / NIDCR NIH HHS / DE / K22 DE014726; United States / NIDCR NIH HHS / DE / R01-DE11000; United States / PHS HHS / / R01-017954; United States / NIDCR NIH HHS / DE / K22-DE14726
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Bacterial; 0 / fap1 protein, Streptococcus; 147680-16-8 / Fimbriae Proteins; 452VLY9402 / Serine
  • [Other-IDs] NLM/ PMC2168744
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35. Beggs AD, Hodgson SV: The genomics of colorectal cancer: state of the art. Curr Genomics; 2008 Mar;9(1):1-10
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  • The concept of the adenoma-carcinoma sequence, as first espoused by Morson et al. whereby the development of colorectal cancer is dependent on a stepwise progression from adenomatous polyp to carcinoma is well documented.
  • Initial studies of the genetics of inherited colorectal cancer susceptibility concentrated on the inherited colorectal cancer syndromes, such as Familial Adenomatous Polyposis (FAP) and Lynch Syndrome (also known as HNPCC).
  • These syndromes, whilst easily characterisable, have a well understood sequence of genetic mutations that predispose the sufferer to developing colorectal cancer, initiated for example in FAP by the loss of the second, normal allelle of the tumour supressor APC gene.
  • Later research has identified other inherited variants such as MUTYH (MYH) polyposis and Hyperplastic Polyposis Syndrome.
  • Recent research has concentrated on the pathways by which colorectal adenomatous polyps not due to one of these known inherited susceptibilities undergo malignant transformation, and determination of the types of polyps most likely to do so.
  • In this article, we will discuss briefly the current state of knowledge of the genomics of the classical inherited colorectal cancer syndromes.

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  • (PMID = 19424478.001).
  • [ISSN] 1389-2029
  • [Journal-full-title] Current genomics
  • [ISO-abbreviation] Curr. Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2674304
  • [Keywords] NOTNLM ; Colorectal / cancer / epigenomics. / genomics
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36. Jimeno A, Rudek MA, Purcell T, Laheru DA, Messersmith WA, Dancey J, Carducci MA, Baker SD, Hidalgo M, Donehower RC: Phase I and pharmacokinetic study of UCN-01 in combination with irinotecan in patients with solid tumors. Cancer Chemother Pharmacol; 2008 Mar;61(3):423-33
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  • PURPOSE: 7-Hydroxystaurosporine (UCN-01) is a protein kinase inhibitor that inhibits several serine-threonine kinases including PKC and PDK1.
  • Due to the preclinical synergistic effects seen with topoisomerase I inhibitors and non-overlapping toxicity, UCN-01 and irinotecan were combined in a dose-finding study designed to determine the maximum tolerated dose (MTD), toxicity profile, and pharmacokinetics (PK) of UCN-01 and irinotecan.
  • METHODS: Patients with incurable solid malignancies received UCN-01 intravenously (IV) as a 3-h infusion on day 1 and irinotecan IV over 90 min on days 1 and 8 of a 21-day cycle.
  • No objective responses were documented, and four patients had stable disease for at least ten cycles.
  • There was a significant decrease in C(max) of APC, AUC of APC and SN-38, and AUC ratio of SN-38:irinotecan when comparing days 1 and 8 PK.
  • CONCLUSIONS: APC and SN-38 exposure decreased when administered in combination with UCN-01.
  • The MTD of the combination based on protocol criteria was defined as 70 mg/m(2) of UCN-01 on day 1 and 60 mg/m(2) of irinotecan on days 1 and 8 in a 21-day cycle.

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  • (PMID = 17429623.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / U01 CA 70095
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 0 / Topoisomerase I Inhibitors; 7673326042 / irinotecan; 7BU5H4V94A / 7-hydroxystaurosporine; H88EPA0A3N / Staurosporine; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ NIHMS433906; NLM/ PMC3557498
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37. Lahat G, Nachmany I, Itzkowitz E, Abu-Abeid S, Barazovsky E, Merimsky O, Klauzner J: Surgery for sporadic abdominal desmoid tumor: is low/no recurrence an achievable goal? Isr Med Assoc J; 2009 Jul;11(7):398-402
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  • BACKGROUND: Sporadic abdominal desmoid tumors are rare and data on these tumors as a distinct disease entity are lacking.
  • Although desmoids are benign, invasion and a high recurrence rate are common.
  • OBJECTIVES: To evaluate outcomes of surgery for this rare disease.
  • All familial adenomatous polyposis patients were excluded.

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  • (PMID = 19911489.001).
  • [ISSN] 1565-1088
  • [Journal-full-title] The Israel Medical Association journal : IMAJ
  • [ISO-abbreviation] Isr. Med. Assoc. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Israel
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38. Misra MV, Bhattacharya K, Nompleggi DJ, Uknis ME, Rastellini C, Cicalese L: Magnification endoscopy as a reliable tool for the early diagnosis of rejection in living related small bowel transplants: a case report. Transplant Proc; 2006 Jul-Aug;38(6):1738-9
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  • [Title] Magnification endoscopy as a reliable tool for the early diagnosis of rejection in living related small bowel transplants: a case report.
  • The purpose was to determine whether magnification endoscopy (ME) accurately diagnosed rejection in living related small bowel transplants (LRSBTx) during initial morphological adaptation of segmental intestinal grafts.
  • The small bowel recipient was a 44-year-old woman with short gut syndrome following multiple bowel surgeries for familial adenomatous polyposis.
  • The first endoscopy, at 5 days posttransplant, showed no evidence of intestinal ischemia.
  • The superior imaging of small bowel mucosa created by ME chromoendoscopy enables early diagnosis and delivery of more prompt antirejection therapy to prevent progression of rejection.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Endoscopy, Digestive System / methods. Graft Rejection / diagnosis. Intestine, Small / transplantation

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  • (PMID = 16908267.001).
  • [ISSN] 0041-1345
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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39. Angel CE, George E, Brooks AE, Ostrovsky LL, Brown TL, Dunbar PR: Cutting edge: CD1a+ antigen-presenting cells in human dermis respond rapidly to CCR7 ligands. J Immunol; 2006 May 15;176(10):5730-4
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  • Recent data from murine models have confirmed that Langerhans cells are not the only population of APCs in the skin involved in initiating immune responses.
  • In healthy human skin, we identify CD1a(+) dermal APCs located close to the lymphatic vessels in the upper layers of the dermis that are unequivocally distinct from migrating Langerhans cells but exhibit both potent allostimulatory capacity and a chemotactic response to CCR7 ligands.
  • CD1a(+) dermal APCs therefore represent an APC population distinct from Langerhans cells that are capable of migrating to lymph nodes and stimulating naive T cells.

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  • (PMID = 16670277.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / CCR7 protein, human; 0 / CD1a antigen; 0 / Ligands; 0 / Receptors, CCR7; 0 / Receptors, Chemokine
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40. Lee HC, Kim M, Wands JR: Wnt/Frizzled signaling in hepatocellular carcinoma. Front Biosci; 2006;11:1901-15
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  • As an example, over 90% of the colorectal cancers have mutations in adenomatous polyposis coli (APC) or beta-catenin genes.
  • In addition, hepatocellular carcinoma (HCC) is another tumor with frequent aberrant activation of beta-catenin signaling.
  • However, mutations of APC and/or beta-catenin genes are found only in about 20-30% of HCCs, suggesting that the predominant mechanism(s) activating Wnt/FZD signaling pathway may be different from that found in colorectal cancers.
  • There is accumulating evidence to suggest that regulatory mechanisms other than mutations involving beta-catenin or proteins in its destruction complex, many of which involve upstream components of the Wnt/FZD cascade, are important in HCC.
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Carcinoma, Hepatocellular / metabolism. Frizzled Receptors / metabolism. Gene Expression Regulation, Neoplastic. Liver Neoplasms / embryology. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 16368566.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NIAAA NIH HHS / AA / AA02666; United States / NIAAA NIH HHS / AA / AA20169; United States / NCI NIH HHS / CA / CA35711; United States / NCRR NIH HHS / RR / P20 RR 015578
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Frizzled Receptors; 0 / Ligands; 0 / Wnt Proteins; 0 / beta Catenin
  • [Number-of-references] 134
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41. Milner JM, Kevorkian L, Young DA, Jones D, Wait R, Donell ST, Barksby E, Patterson AM, Middleton J, Cravatt BF, Clark IM, Rowan AD, Cawston TE: Fibroblast activation protein alpha is expressed by chondrocytes following a pro-inflammatory stimulus and is elevated in osteoarthritis. Arthritis Res Ther; 2006;8(1):R23
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  • [Title] Fibroblast activation protein alpha is expressed by chondrocytes following a pro-inflammatory stimulus and is elevated in osteoarthritis.
  • We have previously shown that serine proteinases are involved in the activation cascades leading to cartilage collagen degradation.
  • The aim of this study was to use an active-site probe, biotinylated fluorophosphonate, to identify active serine proteinases present on the chondrocyte membrane after stimulation with the pro-inflammatory cytokines IL-1 and oncostatin M (OSM), agents that promote cartilage resorption.
  • Fibroblast activation protein alpha (FAPalpha), a type II integral membrane serine proteinase, was identified on chondrocyte membranes stimulated with IL-1 and OSM.
  • [MeSH-major] Chondrocytes / drug effects. Chondrocytes / metabolism. Cytokines / pharmacology. Gelatinases / metabolism. Interleukin-1 / pharmacology. Membrane Proteins / metabolism. Osteoarthritis / metabolism. Serine Endopeptidases / metabolism
  • [MeSH-minor] Animals. Cartilage / metabolism. Cartilage, Articular / metabolism. Cattle. Cell Membrane / chemistry. Cells, Cultured. Gene Expression Regulation. Humans. Immunohistochemistry. Oncostatin M. Recombinant Proteins / pharmacology. Tissue Culture Techniques

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  • (PMID = 16507127.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1; 0 / Membrane Proteins; 0 / OSM protein, human; 0 / Recombinant Proteins; 106956-32-5 / Oncostatin M; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ PMC1526559
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42. Foley PJ, Scheri RP, Smolock CJ, Pippin J, Green DW, Drebin JA: Targeted suppression of beta-catenin blocks intestinal adenoma formation in APC Min mice. J Gastrointest Surg; 2008 Aug;12(8):1452-8
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  • [Title] Targeted suppression of beta-catenin blocks intestinal adenoma formation in APC Min mice.
  • INTRODUCTION: Mutations involving the adenomatous polyposis coli (APC) tumor suppressor gene leading to activation of beta-catenin have been identified in the majority of sporadic colonic adenocarcinomas and in essentially all colonic tumors from patients with Familial Adenomatous Polyposis.
  • The C57BL/6J-APC(min) (Min) mouse, which carries a germ line mutation in the murine homolog of the APC gene is a useful model for intestinal adenoma formation linked to loss of APC activity.
  • One of the critical downstream molecules regulated by APC is beta-catenin; molecular targeting of beta-catenin is, thus, an attractive chemopreventative strategy in colon cancer.
  • ANALYSIS OF beta-CATENIN PROTEIN EXPRESSION IN LIVER TISSUE AND INTESTINAL ADENOMAS: Adenomas harvested from mice treated for 7 days with beta-catenin AODNs demonstrated clear downregulation of beta-catenin expression, which was accompanied by a significant reduction in proliferation.
  • There was no effect on proliferation in normal intestinal epithelium.
  • Min mice treated systemically with beta-catenin AODNs over a 6-week period had a statistically significant reduction in the number of intestinal adenomas.
  • These studies provide direct evidence that targeted suppression of beta-catenin inhibits the formation of intestinal adenomas in APC-mutant mice.
  • Furthermore, these studies suggest that molecular targeting of beta-catenin holds significant promise as a chemopreventative strategy in colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / therapy. Colonic Neoplasms / therapy. Gene Expression Regulation, Neoplastic. Gene Targeting / methods. RNA, Neoplasm / genetics. beta Catenin / genetics
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Proliferation. Disease Progression. Female. Immunohistochemistry. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasms, Experimental. Treatment Outcome

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  • (PMID = 18521697.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100189
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / RNA, Neoplasm; 0 / beta Catenin
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43. Kim DS, Cha SI, Lee JH, Lee YM, Choi JE, Kim MJ, Lim JS, Lee EB, Kim CH, Park TI, Jung TH, Park JY: Aberrant DNA methylation profiles of non-small cell lung cancers in a Korean population. Lung Cancer; 2007 Oct;58(1):1-6
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  • The aberrant promoter methylation of eight genes (GSTP1, p16, FHIT, APC, RASSF1A, hMLH1, hMSH2, AGT) was determined by MSP in 99 surgically resected NSCLCs and their corresponding nonmalignant lung tissues.
  • Methylation in the tumor samples was detected at 15% for GSTP1, 22% for p16, 34% for FHIT1, 48% for APC, 40% for RASSF1A, 18% for hMLH1, 8% for hMSH2 and 21% for AGT, whereas it occurred at lower frequencies in the corresponding nonmalignant lung tissues, particularly in the p16 (1%) and RASSF1A (1%) genes.

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  • (PMID = 17532092.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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44. Iatsenko LD: [Improvement of the quality of life in patients with non-operable pancreatic cancer treated with polyplatillen]. Lik Sprava; 2007 Jul-Sep;(5-6):65-9
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  • The authors summarize in the article experience of a new anticancer drug Polyplatillen use in the chemotherapy of advanced pancreatic cancer.


45. Parker D, Hodgkinson B: A comparison of palliative care outcome measures used to assess the quality of palliative care provided in Residential Aged Care Facilities: a systematic review. JBI Libr Syst Rev; 2010;8(3):90-120
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  • METHODOLOGICAL QUALITY: Included studies were assessed by two independent reviewers for methodological quality prior to inclusion in the review using an appraisal checklist developed for the review based on the review methods of Zwakhalen et al to evaluate validity, reliability and feasibility.
  • The Family Perceptions of Care Scale (FPCS) is considered by the authors as the most suitable outcome measure for use in RACFs.
  • The FPCS has a number of properties that has led to its preferred selection, in particular the development and testing of the scale which occurred exclusively in the RACF population.

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  • (PMID = 27820164.001).
  • [ISSN] 1838-2142
  • [Journal-full-title] JBI library of systematic reviews
  • [ISO-abbreviation] JBI Libr Syst Rev
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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46. Wu J, Ohlsson M, Warner EA, Loo KK, Hoang TX, Voskuhl RR, Havton LA: Glial reactions and degeneration of myelinated processes in spinal cord gray matter in chronic experimental autoimmune encephalomyelitis. Neuroscience; 2008 Oct 15;156(3):586-96
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  • Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) result in inflammatory white matter lesions in the CNS.
  • However, information is sparse with regard to the effects of autoimmune demyelinating disease on gray matter regions.
  • Here, EAE induced marked astrocytic, microglial, and macrophage activation in the ventral horn gray matter, without any motoneuron loss.
  • Furthermore, activated poly (ADP-ribose) polymerase (PARP), another apoptotic marker, co-localized with myelin basic protein (MBP) of oligodendrocyte processes, but not with the oligodendroglial cell body marker, adenomatous polyposis coli gene clone CC1 (APC-CC1), or with neurofilament marker (RT-97) or synaptophysin of axonal arbors.
  • However, there was no associated increase in the number of terminal deoxynucleotidyl transferase (TdT) mediated-dUTP nick end labeling positive nuclei in the spinal cord gray matter of EAE mice.

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  • (PMID = 18718511.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K24 NS062117; United States / NINDS NIH HHS / NS / K24 NS062117-01; United States / NCRR NIH HHS / RR / U54 RR021813; United States / NCRR NIH HHS / RR / 1 U54 RR021813
  • [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 / Glial Fibrillary Acidic Protein; 0 / Myelin Basic Protein; 0 / Neurofilament Proteins; 0 / Receptor, Nerve Growth Factor; 0 / Synaptophysin; EC 2.4.2.30 / Parp1 protein, mouse; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS101002; NLM/ PMC2670892
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47. Zhang T, Fields JZ, Opdenaker L, Otevrel T, Masuda E, Palazzo JP, Isenberg GA, Goldstein SD, Brand M, Boman BM: Survivin-induced Aurora-B kinase activation: A mechanism by which APC mutations contribute to increased mitoses during colon cancer development. Am J Pathol; 2010 Dec;177(6):2816-26
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  • [Title] Survivin-induced Aurora-B kinase activation: A mechanism by which APC mutations contribute to increased mitoses during colon cancer development.
  • APC mutations initiate most colorectal cancers (CRCs), but cellular mechanisms linking this to CRC pathology are unclear.
  • We reported that wild-type APC in the colon down-regulates the anti-apoptotic protein survivin, and APC mutation up-regulates it, explaining why most CRCs display survivin overexpression and apoptosis inhibition.
  • However, it does not explain another hallmark of CRC pathology--increased mitotic figures and cell proliferation.
  • Because survivin activates aurora-B kinase (ABK) in vitro, catalyzing mitosis, we hypothesized that in normal colonic crypts, APC controls ABK activity, while in neoplastic APC-mutant crypts, ABK activity is up-regulated, increasing mitosis.
  • We quantitatively mapped intracryptal distributions of survivin, ABK, and markers of activated downstream signaling and mitosis (INCENP, phospho-histone-H3, phospho-centromere-protein-A).
  • In normal crypts, gradients for these markers, ABK:survivin:INCENP complexes, and ABK activity were highest in the lower crypt (inverse to the APC gradient).
  • In neoplastic crypts that harbor APC mutations, proliferating (Ki-67+) cells and cells expressing survivin, ABK, and phospho-histone-H3 were distributed farther up the crypt.
  • In CRC cell lines, increasing wild-type APC, inhibiting TCF-4, or decreasing survivin expression down-regulated ABK activity.
  • Thus, APC mutation-induced up-regulation of the survivin/ABK cascade can explain delayed crypt cell maturation, expansion of proliferative cell populations (including mitotic figures), and promotion of colon tumorigenesis.

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  • (PMID = 21057000.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R21 DE019713; United States / NIDDK NIH HHS / DK / R21 DK062146; United States / NIDDK NIH HHS / DK / 5R21DK62146
  • [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 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Small Interfering; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2993266
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48. Beamish H, de Boer L, Giles N, Stevens F, Oakes V, Gabrielli B: Cyclin A/cdk2 regulates adenomatous polyposis coli-dependent mitotic spindle anchoring. J Biol Chem; 2009 Oct 16;284(42):29015-23
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  • [Title] Cyclin A/cdk2 regulates adenomatous polyposis coli-dependent mitotic spindle anchoring.
  • Mutations in adenomatous polyposis coli (APC) protein is a major contributor to tumor initiation and progression in several tumor types.
  • These mutations affect APC function in the Wnt-beta-catenin signaling and influence mitotic spindle anchoring to the cell cortex and orientation.
  • Here we report that the mitotic anchoring and orientation function of APC is regulated by cyclin A/cdk2.
  • Knockdown of cyclin A and inhibition of cdk2 resulted in cells arrested in mitosis with activation of the spindle assembly checkpoint.
  • We have demonstrated that cyclin A/cdk2 specifically associates with APC in late G2 phase and phosphorylates it at Ser-1360, located in the mutation cluster region of APC.
  • Mutation of APC Ser-1360 to Ala results in identical off-centered mitotic spindles.
  • Thus, this cyclin A/cdk2-dependent phosphorylation of APC affects astral microtubule attachment to the cortical surface in mitosis.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Cyclin A / metabolism. Cyclin-Dependent Kinase 2 / metabolism. Spindle Apparatus
  • [MeSH-minor] Cell Line, Tumor. Glutathione Transferase / metabolism. HeLa Cells. Humans. Microscopy, Fluorescence / methods. Mitosis. Mutation. Phosphorylation. Time Factors. Wnt Proteins / metabolism. beta Catenin / metabolism


49. Cattaneo F, Molatore S, Mihalatos M, Apessos A, Venesio T, Bione S, Grignani P, Nasioulas G, Ranzani GN: Heterogeneous molecular mechanisms underlie attenuated familial adenomatous polyposis. Genet Med; 2007 Dec;9(12):836-41
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  • [Title] Heterogeneous molecular mechanisms underlie attenuated familial adenomatous polyposis.
  • PURPOSE: Familial adenomatous polyposis is a phenotypically heterogeneous disease predisposing to colorectal cancer.
  • It is dominantly transmitted, when associated with the APC gene, and recessively inherited, when associated with MUTYH gene.
  • We searched for APC and MUTYH germline alterations in Italian and Greek patients with attenuated polyposis, a phenotypic variant whose genetic cause remains unknown in many cases.
  • METHODS: We studied 26 unrelated patients (and 16 relatives) with multiple colorectal adenomas (3-100, by endoscopic analysis) that had screened APC mutation-negative by protein truncation test.
  • We searched for APC rearrangements by multiplex ligation-dependent probe amplification and for MUTYH mutations by sequencing.
  • RESULTS: One patient proved to carry an APC whole-gene deletion; 4 of 25 (16%) patients showed biallelic and 3 of 25 (12%) monoallelic MUTYH mutations.
  • CONCLUSION: Attenuated polyposis patients without "conventional" APC mutations are genetically heterogeneous, and the phenotype is not directly related to the germline defect.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Mutation
  • [MeSH-minor] Adult. DNA Glycosylases / genetics. Female. Genes, APC. Genetic Heterogeneity. Genetic Testing. Germ-Line Mutation. Humans. Male. Middle Aged. Phenotype


50. Bolaños JP, Almeida A, Moncada S: Glycolysis: a bioenergetic or a survival pathway? Trends Biochem Sci; 2010 Mar;35(3):145-9
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  • Following inhibition of mitochondrial respiration neurons die rapidly, whereas astrocytes utilize glycolytically-generated ATP to increase their mitochondrial membrane potential, thus becoming more resistant to pro-apoptotic stimuli.
  • In neurons, PFKFB3 is degraded constantly via the E3 ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C)- CDH1.
  • In addition to their relevance to brain physiology and pathophysiology, these observations suggest that APC/C-CDH1 might link activation of glycolysis and cell proliferation as it is also involved in the regulation of cell cycle proteins.
  • [MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Brain / cytology. Brain / metabolism. Cell Cycle Proteins / metabolism. Cell Proliferation. Glucose / metabolism. Phosphofructokinase-2 / genetics. Phosphofructokinase-2 / metabolism. Ubiquitin-Protein Ligase Complexes / metabolism

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20006513.001).
  • [ISSN] 0968-0004
  • [Journal-full-title] Trends in biochemical sciences
  • [ISO-abbreviation] Trends Biochem. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; EC 2.7.1.105 / Phosphofructokinase-2; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes; IY9XDZ35W2 / Glucose
  • [Number-of-references] 53
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51. Matsui C, Kaieda S, Ikegami T, Mimori-Kiyosue Y: Identification of a link between the SAMP repeats of adenomatous polyposis coli tumor suppressor and the Src homology 3 domain of DDEF. J Biol Chem; 2008 Nov 21;283(47):33006-20
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  • [Title] Identification of a link between the SAMP repeats of adenomatous polyposis coli tumor suppressor and the Src homology 3 domain of DDEF.
  • The adenomatous polyposis coli (APC) tumor suppressor protein is a multifunctional protein with a well characterized role in the Wnt signal transduction pathway and in cytoskeletal regulation.
  • The SAMP repeats region of APC, an Axin-binding site, is known to be important for tumor suppression and for the developmental function of APC.
  • We performed a yeast two-hybrid screening using the first SAMP motif-containing region of Xenopus APC as bait and obtained several SAMP binding candidates including DDEF2 (development and differentiation enhancing factor 2), which is an ADP-ribosylation factor (Arf) GTPase-activating protein (GAP (ArfGAP)) involved in the regulation of focal adhesions.
  • In vitro and in cells the Src homology 3 (SH3) domain of DDEF2 and its close homolog, DDEF1, are associated with the SAMP motif of APC competitively with Axin1.
  • When fluorescent protein-tagged APC and DDEF are expressed in Xenopus A6 cells, co-localization at microtubule ends is observed.
  • Overexpression and RNA interference experiments indicate that APC and DDEFs cooperatively regulate the distributions of microtubules and focal adhesions.
  • Our findings reveal that the SAMP motif of APC specifically binds to the SH3 domains of DDEFs, providing new insights into the functions of APC in cell migration.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / chemistry. Adenomatous Polyposis Coli Protein / chemistry. src Homology Domains / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Humans. Magnetic Resonance Spectroscopy. Mice. Molecular Sequence Data. Protein Conformation. Protein Structure, Tertiary. Rats. Recombinant Proteins / chemistry. Sequence Homology, Amino Acid. Xenopus laevis


52. Kovács M, Pák P, Pák G, Fehér J: [Screening and surveillance for hereditary polyposis and non-polyposis syndromes with capsule endoscopy]. Orv Hetil; 2008 Apr 6;149(14):639-44
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  • [Title] [Screening and surveillance for hereditary polyposis and non-polyposis syndromes with capsule endoscopy].
  • [Transliterated title] Hereditaer intestinalis polyposis- és nem polyposisos szindrómák követése és szurése kapszulás endoszkópiával.
  • The hereditary polyposis syndromes and non-polyposis colorectal carcinoma have been considered as scarcely occurring but inheritable dominant autosomal syndromes.
  • Earlier the diagnosis of these symptoms was difficult to establish because traditional radiological methods have a low yield for small polyps.
  • The "wireless" capsule endoscopy has opened the way then for the non-invasive and painless test of the entire small intestine.
  • - Test results have been cumulated to justify the efficiency and safety of capsule endoscopy concerning the syndromes above.
  • As the results compared of the diagnosed familial adenomatous polyposis and of Peutz-Jeghers syndrome reflect on capsule endoscopy, its diagnostic sensitiveness is stated as significantly higher than the Barium-contrast X-Ray and MR-enterography.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis. Capsule Endoscopy. Colorectal Neoplasms / prevention & control. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Mass Screening / methods. Peutz-Jeghers Syndrome / diagnosis. Population Surveillance / methods
  • [MeSH-minor] Humans. Intestinal Polyps / diagnosis. Intestinal Polyps / genetics. Intestinal Polyps / prevention & control. Magnetic Resonance Imaging. Syndrome. Tomography, X-Ray Computed. Video Recording

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  • (PMID = 18375363.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Number-of-references] 42
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53. Xinopoulos D, Dimitroulopoulos D, Karanikas I, Fotopoulou A, Oikonomou N, Korkolis D, Kouroumalis E, Antsaklis G, Vassilopoulos P, Paraskevas E: Gemcitabine as palliative treatment in patients with unresectable pancreatic cancer previously treated with placement of a covered metal stent. A randomized controlled trial. J BUON; 2008 Jul-Sep;13(3):341-7
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  • [Title] Gemcitabine as palliative treatment in patients with unresectable pancreatic cancer previously treated with placement of a covered metal stent. A randomized controlled trial.
  • PURPOSE: To evaluate the efficacy of gemcitabine as palliative treatment in patients with advanced pancreatic cancer (PC) previously treated with placement of a covered metal biliary stent, taking into account survival and quality of life (QoL).
  • PATIENTS AND METHODS: Forty-nine patients with unresectable PC and obstructive jaundice, previously treated with the placement of a covered metal biliary endoprosthesis, were randomized to receive gemcitabine (group A: 9 males, 7 females) or to be followed without any anticancer intervention (group B: 18 males, 15 females).

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  • (PMID = 18979547.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / Ribonucleotide Reductases
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54. Chauffert B, Mornex F, Bonnetain F, Rougier P, Mariette C, Bouché O, Bosset JF, Aparicio T, Mineur L, Azzedine A, Hammel P, Butel J, Stremsdoerfer N, Maingon P, Bedenne L: Phase III trial comparing intensive induction chemoradiotherapy (60 Gy, infusional 5-FU and intermittent cisplatin) followed by maintenance gemcitabine with gemcitabine alone for locally advanced unresectable pancreatic cancer. Definitive results of the 2000-01 FFCD/SFRO study. Ann Oncol; 2008 Sep;19(9):1592-9
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  • PATIENTS AND METHODS: One hundred and nineteen patients with LAPC, World Health Organization performance status of zero to two were randomly assigned to either the induction CHRT group (60 Gy, 2 Gy/fraction; concomitant 5-fluorouracil infusion, 300 mg/m(2)/day, days 1-5 for 6 weeks; cisplatin, 20 mg/m(2)/day, days 1-5 during weeks 1 and 5) or the induction gemcitabine group (GEM: 1000 mg/m(2) weekly for 7 weeks).
  • Maintenance gemcitabine (1000 mg/m(2) weekly, 3/4 weeks) was given in both arms until disease progression or toxicity.

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  • (PMID = 18467316.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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55. Feistritzer C, Riewald M: Endothelial barrier protection by activated protein C through PAR1-dependent sphingosine 1-phosphate receptor-1 crossactivation. Blood; 2005 Apr 15;105(8):3178-84
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  • [Title] Endothelial barrier protection by activated protein C through PAR1-dependent sphingosine 1-phosphate receptor-1 crossactivation.
  • Activated protein C (APC) inhibits thrombin generation and has potent anti-inflammatory effects.
  • Here, we show that APC enhanced endothelial barrier integrity in a dual-chamber system dependent on binding to endothelial protein C receptor, activation of PAR1, and activity of cellular sphingosine kinase.
  • Small interfering RNA that targets sphingosine kinase-1 or S1P receptor-1 blocked this protective signaling by APC.
  • These results demonstrate that PAR1 activation on endothelial cells can have opposite biologic effects, reveal a role for cross-communication between the prototypical barrier-protective S1P and barrier-disruptive PAR1 pathway, and suggest that S1P receptor-1 mediates protective effects of APC in systemic inflammation.
  • [MeSH-major] Capillary Permeability / physiology. Protein C / metabolism. Receptor Cross-Talk / physiology. Receptor, PAR-1 / metabolism. Receptors, Lysosphingolipid / metabolism

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  • (PMID = 15626732.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL 73318
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Protein C; 0 / RNA, Small Interfering; 0 / Receptor, PAR-1; 0 / Receptors, Lysosphingolipid
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56. Aissa A, Debbabi M, Gruselle M, Thouvenot R, Flambard A, Gredin P, Beaunier P, Tõnsuaadu K: Sorption of tartrate ions to lanthanum (III)-modified calcium fluor- and hydroxyapatite. J Colloid Interface Sci; 2009 Feb 1;330(1):20-8
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  • Chemical analyses, FT-IR and (31)P NMR spectroscopies, XRD powder, TGA, and TEM analyses were employed for studying the reaction between Ca(10)(PO(4))(6)(OH)(2) (HAp) or Ca(10)(PO(4))(6)(F)(2) (FAp) and LaCl(3).
  • The reaction was found to take place mainly through partial dissolution of the apatite followed by precipitation of a new phase containing lanthanum phosphate.
  • When La(3+) was introduced in the presence of L(+)-tartaric acid (TAH(2)), no fundamental changes were observed in the HAp or FAp structures.
  • However, there did occur a formation of a new phase of Ca or/and La tartrate salt.

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  • (PMID = 18996541.001).
  • [ISSN] 1095-7103
  • [Journal-full-title] Journal of colloid and interface science
  • [ISO-abbreviation] J Colloid Interface Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anions; 0 / Apatites; 0 / Tartrates; 6I3K30563S / Lanthanum; 91D9GV0Z28 / Durapatite; M4CM1H238J / fluorapatite; SY7Q814VUP / Calcium
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57. Ozhalici-Unal H, Pow CL, Marks SA, Jesper LD, Silva GL, Shank NI, Jones EW, Burnette JM 3rd, Berget PB, Armitage BA: A rainbow of fluoromodules: a promiscuous scFv protein binds to and activates a diverse set of fluorogenic cyanine dyes. J Am Chem Soc; 2008 Sep 24;130(38):12620-1
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  • [Title] A rainbow of fluoromodules: a promiscuous scFv protein binds to and activates a diverse set of fluorogenic cyanine dyes.
  • Combined magnetic and fluorescence cell sorting were used to select Fluorogen Activating Proteins (FAPs) from a yeast surface-displayed library for binding to the fluorogenic cyanine dye Dimethyl Indole Red (DIR).
  • Several FAPs were selected that bind to the dye with low nanomolar Kd values and enhance fluorescence more than 100-fold.
  • One of these FAPs also exhibits considerable promiscuity, binding with high affinity to several other fluorogenic cyanine dyes with emission wavelengths covering most of the visible and near-IR regions of the spectrum.

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  • (PMID = 18761447.001).
  • [ISSN] 1520-5126
  • [Journal-full-title] Journal of the American Chemical Society
  • [ISO-abbreviation] J. Am. Chem. Soc.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / U54 RR022241; United States / NCRR NIH HHS / RR / U54 RR022241-04; United States / Howard Hughes Medical Institute / / 52005865
  • [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 / Carbocyanines; 0 / Coloring Agents; 0 / Fluorescent Dyes; 0 / Fungal Proteins; 0 / Immunoglobulin Fragments; 0 / Immunoglobulin Variable Region; 0 / Peptide Library
  • [Other-IDs] NLM/ NIHMS86288; NLM/ PMC2633110
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58. Dymerska D, Serrano-Fernández P, Suchy J, Pławski A, Słomski R, Kaklewski K, Scott RJ, Gronwald J, Kładny J, Byrski T, Huzarski T, Lubiński J, Kurzawski G: Combined iPLEX and TaqMan assays to screen for 45 common mutations in Lynch syndrome and FAP patients. J Mol Diagn; 2010 Jan;12(1):82-90
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  • [Title] Combined iPLEX and TaqMan assays to screen for 45 common mutations in Lynch syndrome and FAP patients.
  • Mutations of genes associated with the mismatch repair mechanism and mutations of the APC gene are the most frequent causes of hereditary colorectal cancer.
  • The iPLEX test included two plexes, which comprised seven mutations of the APC gene and 29 mutations of three of the mismatch repair genes.
  • TaqMan assays were designed for nine mutations not covered by the iPLEX assays: one mutation in the APC gene and eight mutations in the mismatch repair genes.
  • These results suggest that the combined iPLEX/TaqMan test is an outstanding tool for identification of recurrent mutations among hereditary colorectal cancer patients.
  • [MeSH-major] Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA / analysis. DNA Mutational Analysis / methods. Genes, APC. Mutation

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  • (PMID = 20007843.001).
  • [ISSN] 1943-7811
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2797722
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59. Nascimbeni R, Di Fabio F, Casella C, Cader M, Bonardi M, Villanacci V: [Accuracy and acceptability of surveillance tests after total colectomy and ileorectal anastomosis]. Ann Ital Chir; 2007 Mar-Apr;78(2):103-9
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  • BACKGROUND AND AIMS: Surveillance of the rectal stump after total colectomy for familial adenomatous polyposis (FAP) or chronic ulcerative colitis (CUC) is empirically based on periodic outpatient visit with digital exploration and proctoscopy.
  • PATIENTS AND METHODS: Forty patients who underwent total colectomy were prospectively enrolled, including 12 FAP patients, 16 CUC patients, 12 patients with slow-transit constipation.
  • [MeSH-minor] Adult. Aged. Anastomosis, Surgical / adverse effects. Female. Follow-Up Studies. Humans. Male. Middle Aged. Patient Satisfaction. Postoperative Complications / diagnosis. Prospective Studies. Reproducibility of Results. Sensitivity and Specificity. Surveys and Questionnaires

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  • (PMID = 17583119.001).
  • [ISSN] 0003-469X
  • [Journal-full-title] Annali italiani di chirurgia
  • [ISO-abbreviation] Ann Ital Chir
  • [Language] ita
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Italy
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60. Giardiello FM, Hylind LM, Trimbath JD, Hamilton SR, Romans KE, Cruz-Correa M, Corretti MC, Offerhaus GJ, Yang VW: Oral contraceptives and polyp regression in familial adenomatous polyposis. Gastroenterology; 2005 Apr;128(4):1077-80
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  • [Title] Oral contraceptives and polyp regression in familial adenomatous polyposis.
  • We describe a patient in the placebo arm of a 4-year primary chemoprevention trial who developed adenomatous polyps and then had eradication of polyps after the administration of oral contraceptives.
  • No change in the prostaglandin levels in the colonic mucosa was noted after polyp elimination, making nonsteroidal anti-inflammatory drug ingestion unlikely as a cause.
  • [MeSH-major] Adenomatous Polyposis Coli / physiopathology. Contraceptives, Oral / therapeutic use
  • [MeSH-minor] Child. Colon / metabolism. Female. Humans. Intestinal Mucosa / metabolism. Menstruation Disturbances / drug therapy. Prostaglandins / metabolism. Remission Induction

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  • (PMID = 15825088.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 51085; United States / NCI NIH HHS / CA / CA 53801; United States / NCI NIH HHS / CA / CA 63721; United States / NCI NIH HHS / CA / P50 CA 9316
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contraceptives, Oral; 0 / Prostaglandins
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61. Taira K, Boku N, Fukutomi A, Onozawa Y, Hironaka S, Yoshino T, Yasui H, Yamazaki K, Taku K, Hashimoto T, Nishimura T: Results of a retrospective analysis of gemcitabine as a second-line treatment after chemoradiotherapy and maintenance chemotherapy using 5-fluorouracil in patients with locally advanced pancreatic cancer. J Gastroenterol; 2008;43(11):875-80
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  • [Title] Results of a retrospective analysis of gemcitabine as a second-line treatment after chemoradiotherapy and maintenance chemotherapy using 5-fluorouracil in patients with locally advanced pancreatic cancer.
  • The clinical outcome of chemoradiation therapy in conjunction with 5-FU and second-line chemotherapy with GEM after disease progression has not been clarified.
  • METHODS: Patients with locally advanced pancreatic cancer were treated with concurrent radiation therapy (1.8 Gy/fraction; total dose, 50.4 Gy) with 5-FU (200 mg/m(2) every day) until disease progression, followed by GEM (1000 mg/m(2), days 1, 8, 15, and every 4 weeks) as second-line therapy.
  • [MeSH-minor] Adult. Aged. Disease Progression. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Ribonucleotide Reductases / antagonists & inhibitors. Tomography, X-Ray Computed. Treatment Outcome

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  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
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62. Xu KC, Niu LZ, Hu YZ, He WB, He YS, Zuo JS: Cryosurgery with combination of (125)iodine seed implantation for the treatment of locally advanced pancreatic cancer. J Dig Dis; 2008 Feb;9(1):32-40
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  • The diagnosis was confirmed by pathology in 31 patients.
  • Fourteen patients underwent two procedures of cryosurgery and three underwent three procedures of cryosurgery. (125)Iodine seed implantation was performed during the freezing procedure in 29 patients and within 3-7 days after cryosurgery in nine patients under ultrasound and CT guidance.
  • A complete response of the tumor was seen in 23.6% of patients, a partial response in 42.1%, stable disease in 26.3% and progressive disease in 7.9%.
  • The adverse effects associated with cryosurgery mainly included pain of the upper abdomen and increased serum amylase activity.
  • Acute pancreatitis was seen in five patients, one of whom presented a severe type of pancreatitis.
  • During the followed-up of a median of 16 months (range of 5-37) median overall survival was 12 months, 19 patients (50.0%) survived for 12 months or longer and four survived for 24 months or longer.

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  • (PMID = 18251792.001).
  • [ISSN] 1751-2972
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
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63. Huang JY, Morley G, Li D, Whitaker M: Cdk1 phosphorylation sites on Cdc27 are required for correct chromosomal localisation and APC/C function in syncytial Drosophila embryos. J Cell Sci; 2007 Jun 15;120(Pt 12):1990-7
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  • [Title] Cdk1 phosphorylation sites on Cdc27 are required for correct chromosomal localisation and APC/C function in syncytial Drosophila embryos.
  • Anaphase-promoting complex or cyclosome (APC/C) controls the metaphase-to-anaphase transition and mitosis exit by triggering the degradation of key cell cycle regulators such as securin and B-type cyclins.
  • However, little is known about the functions of individual APC/C subunits and how they might regulate APC/C activity in space and time.
  • Here, we report that two potential Cdk1 kinase phosphorylation sites are required for the chromosomal localisation of GFP::Cdc27 during mitosis.
  • The singly mutated fusion proteins, GFP::Cdc27P304A and GFP::Cdc27P456A, can still localise to mitotic chromosomes in a manner identical to wild-type GFP::Cdc27 and are functional in that they can rescue the phenotype of the cdc27L7123 mutant in vivo.
  • However, when both of the Cdk1 phosphorylation sequence motifs were mutated, the resulting GFP::Cdc27P304A,P456A construct was not localised to the chromosomes during mitosis and was no longer functional, as it failed to rescue mutant phenotypes of the cdc27L7123 gene.
  • High levels of cyclin B and cyclin A were detected in mutant third instar larvae brain samples compared with its wild-type control.
  • These results show for the first time that the two potential Cdk1 phosphorylation sites on Drosophila Cdc27 are required for its chromosomal localisation during mitosis and imply that these localisations specific to Cdc27 are crucial for APC/C functions.
  • [MeSH-major] CDC2 Protein Kinase / metabolism. Cell Cycle Proteins / metabolism. Chromosomes / metabolism. Drosophila Proteins / metabolism. Drosophila melanogaster / embryology. Recombinant Fusion Proteins / metabolism. Ubiquitin-Protein Ligase Complexes / metabolism

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  • (PMID = 17519285.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 072445; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome; 0 / Cdc27 protein, Drosophila; 0 / Cell Cycle Proteins; 0 / Drosophila Proteins; 0 / Recombinant Fusion Proteins; 0 / Tubulin Modulators; EC 2.3.2.23 / Ubiquitin-Protein Ligase Complexes; EC 2.3.2.27 / Anaphase-Promoting Complex-Cyclosome; EC 2.7.11.22 / CDC2 Protein Kinase; SML2Y3J35T / Colchicine
  • [Other-IDs] NLM/ PMC2082081; NLM/ UKMS1186
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64. Loubele ST, ten Cate H, Spronk HM: Anticoagulant therapy in critical organ ischaemia/reperfusion injury. Thromb Haemost; 2010 Jul;104(1):136-42
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  • Besides for their anti-coagulant function, anticoagulant proteins such as activated protein C (APC), active site inhibited factor VIIa (ASIS), tissue factor pathway inhibitor (TFPI), and antithrombin (AT) are also known for their anti-inflammatory or cell protective effects.
  • This review gives an overview of the application of these anti-coagulants in several animal models of I/R injury in critical organs and describes the effects of these proteins on cellular processes including inflammation and apoptosis.
  • The future testing of mutant forms of some of these inhibitors including APC in a clinical setting should be actively explored.
  • [MeSH-minor] Animals. Antithrombins / immunology. Antithrombins / metabolism. Apoptosis. Disease Models, Animal. Factor VIIa / immunology. Factor VIIa / metabolism. Humans. Inflammation. Lipoproteins / immunology. Lipoproteins / metabolism. Protein C / immunology. Protein C / metabolism

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  • (PMID = 20431846.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Anticoagulants; 0 / Antithrombins; 0 / Lipoproteins; 0 / Protein C; 0 / lipoprotein-associated coagulation inhibitor; EC 3.4.21.21 / Factor VIIa
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65. Mewhort-Buist TA, Liaw PC, Patel S, Atkinson HM, Berry LR, Chan AK: Treatment of endothelium with the chemotherapy agent vincristine affects activated protein C generation to a greater degree in newborn plasma than in adult plasma. Thromb Res; 2008;122(3):418-26
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  • [Title] Treatment of endothelium with the chemotherapy agent vincristine affects activated protein C generation to a greater degree in newborn plasma than in adult plasma.
  • INTRODUCTION: Activated protein C (APC) is well-established as a physiologically important anticoagulant.
  • During development, plasma concentrations of protein C and alpha(2)macroglobulin, factors involved in APC generation, differ from adult levels.
  • This study examines the effect of chemotherapy treatment of endothelium on APC generation in newborn and adult plasma.
  • MATERIALS AND METHODS: APC generations were initiated on endothelial cells treated with vincristine or media by recalcifying defibrinated plasma with buffer containing thromboplastin.
  • APC generation was terminated by mixing timed subsamples into FFRCMK-EDTA or heparin, followed by EDTA.
  • APC-PCI and APC-alpha(1)AT were assayed by ELISA.
  • APC-alpha(2)M was measured chromogenically.
  • Since heparin converts free APC to APC-PCI, the difference between APC-PCI detected in heparin subsamples and APC-PCI detected in FFRCMK-EDTA subsamples gave the free APC.
  • RESULTS: Vincristine-treated endothelium decreased free APC generation in newborn plasma to a greater degree than in adult plasma.
  • APC-PCI levels in both adult and newborn plasma were unaffected by chemotherapy.
  • Vincristine treatment reduced levels of APC-alpha(1) AT and APC-alpha(2) M to a greater degree in newborn plasma versus adult plasma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Blood Proteins / pharmacology. Endothelial Cells / drug effects. Protein C / metabolism. Thrombosis / prevention & control. Vincristine / pharmacology
  • [MeSH-minor] Adult. Age Factors. Cells, Cultured. Humans. Infant, Newborn. Membrane Proteins / metabolism. Plasma. Protein Binding / drug effects. Protein C Inhibitor / metabolism. Thrombomodulin / metabolism. Umbilical Veins / cytology. alpha 1-Antitrypsin / metabolism. alpha-Macroglobulins / metabolism

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  • (PMID = 18206217.001).
  • [ISSN] 0049-3848
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Blood Proteins; 0 / Membrane Proteins; 0 / Protein C; 0 / Protein C Inhibitor; 0 / Thrombomodulin; 0 / alpha 1-Antitrypsin; 0 / alpha-Macroglobulins; 5J49Q6B70F / Vincristine
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66. McQuillan K, Lynch MA, Mills KH: Activation of mixed glia by Abeta-specific Th1 and Th17 cells and its regulation by Th2 cells. Brain Behav Immun; 2010 May;24(4):598-607
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  • [Title] Activation of mixed glia by Abeta-specific Th1 and Th17 cells and its regulation by Th2 cells.
  • Microglia are innate immune cells of the CNS, that act as antigen-presenting cells (APC) for antigen-specific T cells and respond to inflammatory stimuli, such as amyloid-beta (Abeta), resulting in the release of neurotoxic factors and pro-inflammatory cytokines.
  • Astrocytes can also act as APC and modulate the function of microglia.
  • However, the role of distinct T cell subtypes, in particular Th17 cells, in glial activation and subsequent modulatory effects of Th2 cells are poorly understood.
  • Here, we generated Abeta-specific Th1, Th2, and Th17 cells and examined their role in modulating Abeta-induced activation of microglia in a mixed glial culture, a preparation which mimics the complex APC types in the brain.
  • We demonstrated that mixed glia acted as an effective APC for Abeta-specific Th1 and Th17 cells.
  • Addition of Abeta-specific Th2 cells suppressed the Abeta-induced IFN-gamma production by Th1 cells and IL-17 production by Th17 cells with glia as the APC.
  • The modest enhancement of MHC class II and CD86 expression on astrocytes by Abeta-specific Th1 and Th17 was not attenuated by Th2 cells.
  • These data indicate that Abeta-specific Th1 and Th17 cells induce inflammatory activation of glia, and that this is in part regulated by Th2 cells.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20060887.001).
  • [ISSN] 1090-2139
  • [Journal-full-title] Brain, behavior, and immunity
  • [ISO-abbreviation] Brain Behav. Immun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Antigens, CD40; 0 / Antigens, CD86; 0 / Interleukin-17; 0 / Interleukin-1beta; 0 / Interleukin-6; 82115-62-6 / Interferon-gamma
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67. Stewart S, Fang G: Destruction box-dependent degradation of aurora B is mediated by the anaphase-promoting complex/cyclosome and Cdh1. Cancer Res; 2005 Oct 1;65(19):8730-5
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  • Aurora B kinase, a subunit of the chromosomal passenger protein complex, plays essential roles in spindle assembly, chromosome bi-orientation, and cytokinesis.
  • Modulation of Aurora B protein levels could partly account for the regulation of its kinase activity in the cell cycle.
  • Here, we examined Aurora B protein levels and confirmed that they fluctuate during the cell cycle, peaking in mitosis and dropping drastically in G1.
  • This profile for Aurora B in the cell cycle is reminiscent of those for substrates of the anaphase-promoting complex/cyclosome (APC/C), a ubiquitin ligase essential for mitotic progression.
  • Indeed, Aurora B is a substrate of APC/C both in vitro and in vivo.
  • Aurora B is efficiently ubiquitinated in an in vitro reconstituted system by APC/C that had been activated by Cdh1.
  • The recognition of Aurora B by APC/C-Cdh1 is specific as it requires the presence of a conserved D-box at the COOH terminus of Aurora B.
  • Degradation of Aurora B at the end of mitosis requires Cdh1 in vivo as a reduction of the Cdh1 level by RNA interference stabilizes the Aurora B protein.
  • We conclude that, as a key mitotic regulator, Aurora B is regulated both by its activation during early mitosis and by its destruction by APC/C-Cdh1 in late mitosis and in G1.

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  • (PMID = 16204042.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009151; United States / NCI NIH HHS / CA / CA09151; United States / NIGMS NIH HHS / GM / GM062852
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ubiquitin; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
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68. Heffernan RT, Barrett NL, Gallagher KM, Hadler JL, Harrison LH, Reingold AL, Khoshnood K, Holford TR, Schuchat A: Declining incidence of invasive Streptococcus pneumoniae infections among persons with AIDS in an era of highly active antiretroviral therapy, 1995-2000. J Infect Dis; 2005 Jun 15;191(12):2038-45
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  • BACKGROUND: Our goal was to describe trends in invasive pneumococcal disease incidence among persons with acquired immunodeficiency syndrome (AIDS) since the introduction of highly active antiretroviral therapy (HAART).
  • METHODS: We used time-trend analysis of annual invasive pneumococcal disease incidence rates from a population-based, active surveillance system.
  • RESULTS: The annual incidence of invasive pneumococcal disease declined from 1094 cases/100,000 persons with AIDS (July 1995-June 1996) to 467 cases/100,000 persons living with AIDS (July 1999-June 2000).
  • During the final year of the study, the invasive pneumococcal disease incidence in persons with AIDS was half that of the pre-HAART era but was still 35 times higher than that in similarly aged non-HIV-infected adults.
  • CONCLUSIONS: In the United States, invasive pneumococcal disease incidence declined sharply across a range of subgroups living with AIDS during the period after widespread introduction of HAART.
  • Despite these gains, persons with AIDS remain at high risk for invasive pneumococcal disease.
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / drug therapy. Adolescent. Adult. African Americans. European Continental Ancestry Group. Female. Hispanic Americans. Humans. Incidence. Male. Middle Aged. Retrospective Studies. United States / epidemiology


69. Harris DL, Washington MK, Hood DB, Roberts LJ 2nd, Ramesh A: Dietary fat-influenced development of colon neoplasia in Apc Min mice exposed to benzo(a)pyrene. Toxicol Pathol; 2009 Dec;37(7):938-46
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  • [Title] Dietary fat-influenced development of colon neoplasia in Apc Min mice exposed to benzo(a)pyrene.
  • Consumption of well-done red meat and saturated fats rich in polycyclic aromatic hydrocarbons may be one of the causative factors for sporadic colon cancer.
  • The objective of this study was to investigate whether the formation of colon tumors in adult Apc(Min) mice was influenced by the ingestion of different types of fat containing benzo(a)pyrene [B(a)P], a polycyclic aromatic hydrocarbon compound.
  • Treatment consisted of 50 and 100 microg B(a)P/kg body weight dissolved in peanut or coconut oil (representatives of unsaturated and saturated fats, respectively) administered daily to six-week-old male Apc(Min) mice via oral gavage for sixty days.
  • On the other hand, the B(a)P-alone and unsaturated-fat groups did not show significant differences in the numbers of adenomas and invasive tumors in the both jejunum and the colon.
  • Our studies established that dietary fat, especially saturated fat, potentiates the development of colon tumors caused by B(a)P in the Apc(Min) mouse.

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  • (PMID = 19841130.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / F31 ES017391-01; United States / NCI NIH HHS / CA / R03 CA130112; United States / NIEHS NIH HHS / ES / F31 ES017391; United States / NIEHS NIH HHS / ES / 1S11ES014156-01A1; United States / NHLBI NIH HHS / HL / T32 HL007735-12; United States / NIEHS NIH HHS / ES / S11 ES014156; United States / NCI NIH HHS / CA / R03 CA130112-01; United States / NCI NIH HHS / CA / R01 CA142845; United States / NCI NIH HHS / CA / 1R03CA130112-01; United States / NHLBI NIH HHS / HL / 5T32HL007735-12; United States / NHLBI NIH HHS / HL / T32 HL007735; United States / NIEHS NIH HHS / ES / S11 ES014156-01A1; United States / NIEHS NIH HHS / ES / 1F31ES017391-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Dietary Fats; 3417WMA06D / Benzo(a)pyrene
  • [Other-IDs] NLM/ NIHMS248414; NLM/ PMC2982189
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70. Poulsen ML, Bisgaard ML: MUTYH Associated Polyposis (MAP). Curr Genomics; 2008 Sep;9(6):420-35
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  • [Title] MUTYH Associated Polyposis (MAP).
  • MUTYH Associated Polyposis (MAP), a Polyposis predisposition caused by biallelic mutations in the Base Excision Repair (BER) gene MUTYH, confers a marked risk of colorectal cancer (CRC).
  • The MAP phenotype is difficult to distinguish from other hereditary CRC syndromes.
  • Especially from Familial Adenomatous Polyposis (FAP) and to a lesser extend Lynch Syndrome, which are caused by germline mutations in the APC and Mismatch Repair (MMR) genes, respectively.Here we review research findings regarding MUTYH interactions, genotypic and phenotypic characteristics of MAP, as well as surveillance and treatment of the disease.
  • The applied papers, published between 1/1 2002- 1/2 2008, were found through PubMed.The exact role of MUTYH in CRC tumorgenesis is still uncertain, although MAP tumors show distinct molecular features, including somatic G:C>T:A transversions in the APC gene.
  • Most thoroughly investigated are the two most common MUTYH variants, Y179C and G396D, both generating dysfunctional gene products.PHENOTYPIC FEATURES OF MAP INCLUDE: development of 10-100 colorectal adenomas, debuting at 46-47 years, often CRC at time of clinical diagnosis, and in some, development of extracolonic manifestations.

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  • (PMID = 19506731.001).
  • [ISSN] 1389-2029
  • [Journal-full-title] Current genomics
  • [ISO-abbreviation] Curr. Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2691665
  • [Keywords] NOTNLM ; (Attenuated) familial adenomatous polyposis / Colorectal cancer / MUTYH associated polyposis / The MUTYH gene / base excision repair / lynch syndrome.
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71. Sugita A, Koganei K, Kimura H, Yamada K, Futatuki R, Kitoh F, Fukushima T: [Reconstruction of proctocolectomy: which is the best surgical procedure?]. Nihon Geka Gakkai Zasshi; 2008 Sep;109(5):269-73
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  • [Title] [Reconstruction of proctocolectomy: which is the best surgical procedure?].
  • Total proctocolectomy is commonly performed in patients with ulcerative colitis or familial adenomatosis coli.
  • The standard surgical procedure for reconstruction is the ileal pouch anal anastomosis with rectal mucosal stripping (IPAA), which is radical treatment for the disease, or stapled ileal pouch anal anastomosis with preserved anal canal (stapled IPAA), which results in a lower incidence of soiling with a high possibility of one-stage surgery.
  • Quality of life (QOL) studies (SF36, etc.) found good QOL after surgery in patients who underwent both procedures.
  • The surgical procedure for reconstruction should be determined based on surgical indications, preoperative anal function, and patient's request.
  • For improved QOL in the future, pouch surgery should have a lower incidence of diverting ileostomy and result in fewer bowel movements and a lower incidence of soiling, with optimal management of pouchitis.

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  • (PMID = 18939461.001).
  • [ISSN] 0301-4894
  • [Journal-full-title] Nihon Geka Gakkai zasshi
  • [ISO-abbreviation] Nihon Geka Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Japan
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72. Hashimoto K, Shimizu Y, Suehiro Y, Okayama N, Hashimoto S, Okada T, Hiura M, Ueno K, Hazama S, Higaki S, Hamanaka Y, Oka M, Sakaida I, Hinoda Y: Hypermethylation status of APC inversely correlates with the presence of submucosal invasion in laterally spreading colorectal tumors. Mol Carcinog; 2008 Jan;47(1):1-8
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  • [Title] Hypermethylation status of APC inversely correlates with the presence of submucosal invasion in laterally spreading colorectal tumors.
  • Methylation of MINT1, MINT2, MINT31, p16, O(6)-methylguanine-DNA methyltransferase (MGMT), adenomatous polyposis coli (APC), and human MutL homologue 1 (hMLH1) in 42 LSTs was assessed by methylation-specific polymerase chain reaction (MSP) and compared with clinicopathologic parameters.
  • The frequency of hypermethylation was 12.5% (4/32) for MINT1, 40.0% (16/40) for MINT2, 25.0% (10/40) for MINT31, 25.7% (9/35) for p16, 7.7% (3/39) for hMLH1, 26.5% (9/34) for MGMT, and 35.9% (14/39) for APC.
  • APC methylation was inversely associated with submucosal invasion (P = 0.034), which was not found in any of 14 LST cases with APC methylation, whereas submucosal invasion was present in 8 of 25 (32.0%) cases without APC methylation.
  • These data suggest that hypermethylation of APC could be a predictive marker for the absence of submucosal invasion of LSTs.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. DNA Methylation. DNA, Neoplasm / genetics. Genes, APC
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Aged. Cell Division. DNA Primers. Dinucleoside Phosphates / genetics. Female. Humans. Male. Middle Aged. Mutation. Neoplasm Invasiveness

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17620311.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm; 0 / Dinucleoside Phosphates; 2382-65-2 / cytidylyl-3'-5'-guanosine
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73. Whitfield JF: Calcium, calcium-sensing receptor and colon cancer. Cancer Lett; 2009 Mar 8;275(1):9-16
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  • [Title] Calcium, calcium-sensing receptor and colon cancer.
  • There is much evidence that dietary Ca(2+) loading reduces colon cell proliferation and carcinogenesis in humans and rodents, but during carcinogenesis it becomes ineffective or even tumor-promoting.
  • We are beginning to see how Ca(2+) balances the continuous massive cell production in colon crypts by driving the terminal differentiation and eventually the apoptosis of the cells mainly on the mucosal surface, and how this Ca(2+) control is lost during colon carcinogenesis.
  • The rapid proliferation of the transit-amplifying (TA) progeny of the colon stem cells is driven by the so-called "Wnt" signaling mechanism, which involves the stimulation of proliferogenic genes such as those for c-Myc and cyclin D1 and the silencing of the gene for the cell cycle-stopping p21(Cip1/WAF1) protein by nuclear beta-catenin*Tcf-4 complexes.
  • TA cells avoid mitotic damage and premature apoptosis by expressing the protein survivin.
  • It appears that TA cell cycling stops and terminal differentiation starts when the cells reach a higher level in the crypt where there is enough lumenal Ca(2+) to stimulate the expression and activation of CaSRs (Ca(2+)-sensing receptors), the signals from which stimulate the expression of E-cadherin.
  • Along with this, the APC (adenomatous polyposis coli) protein appears and some of it enters the nucleus.
  • There it makes the TA cells susceptible to the eventual apoptotic balancing by stopping survivin expression and the beta-catenin*Tcf-4 complex from driving further cell cycling by releasing beta-catenin from the nucleus, and delivering it to cytoplasmic APC*axin*GSK-3beta complexes for ultimate proteasomal destruction.
  • Cytoplasmic beta-catenin is then prevented from returning to the nucleus by either being intercepted and destroyed by APC*axin*GSK-3beta complexes or locked by the emerging E-cadherin into membrane adherens junctions which tie the cell into the sheet of proliferatively shut-down cells with APC-dependent cytoskeletons moving to the mouth of the crypt and onto the flat mucosal surface.
  • A common first step in sporadic colon carcinogenesis is the loss of functional APC which disorients upwardly directed migration and causes the retention of nuclear beta-catenin and proliferogenic beta-catenin*Tcf-4 complexes as well as genomic instability.
  • [MeSH-minor] Animals. Apoptosis. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Nucleus / metabolism. Cell Proliferation. Cyclin D1 / metabolism. Cytoplasm / metabolism. DNA-Binding Proteins / metabolism. Glycogen Synthase Kinase 3 / metabolism. Humans. Inhibitor of Apoptosis Proteins. Microtubule-Associated Proteins / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Transcription Factors / metabolism. beta Catenin / metabolism

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  • (PMID = 18725175.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / DNA-Binding Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptors, Calcium-Sensing; 0 / TCF4 protein, human; 0 / Transcription Factors; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; SY7Q814VUP / Calcium
  • [Number-of-references] 80
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74. Guo H, Singh I, Wang Y, Deane R, Barrett T, Fernández JA, Chow N, Griffin JH, Zlokovic BV: Neuroprotective activities of activated protein C mutant with reduced anticoagulant activity. Eur J Neurosci; 2009 Mar;29(6):1119-30
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  • [Title] Neuroprotective activities of activated protein C mutant with reduced anticoagulant activity.
  • The anticoagulant activated protein C (APC) protects neurons and endothelium via protease activated receptor (PAR)1, PAR3 and endothelial protein C receptor.
  • APC is neuroprotective in stroke models.
  • Bleeding complications may limit the pharmacologic utility of APC.
  • Here, we compared the 3K3A-APC mutant with 80% reduced anticoagulant activity and wild-type (wt)-APC.
  • Murine 3K3A-APC compared with wt-APC protected mouse cortical neurons from N-methyl-D-aspartate-induced apoptosis with twofold greater efficacy and more potently reduced N-methyl-D-aspartate excitotoxic lesions in vivo.
  • Human 3K3A-APC protected human brain endothelial cells (BECs) from oxygen/glucose deprivation with 1.7-fold greater efficacy than wt-APC.
  • 3K3A-APC neuronal protection required PAR1 and PAR3, as shown by using PAR-specific blocking antibodies and PAR1- and PAR3-deficient cells and mice.
  • BEC protection required endothelial protein C receptor and PAR1.
  • In neurons and BECs, 3K3A-APC blocked caspase-9 and -3 activation and induction of p53, and decreased the Bax/Bcl-2 pro-apoptotic ratio.
  • After distal middle cerebral artery occlusion (dMCAO) in mice, murine 3K3A-APC compared with vehicle given 4:00 h after dMCAO improved the functional outcome and reduced the infarction volume by 50% within 3 days.
  • 3K3A-APC compared with wt-APC multi-dosing therapy at 12:00 h, 1, 3, 5 and 7 days after dMCAO significantly improved functional recovery and reduced the infarction volume by 75% and 38%, respectively, within 7 days.
  • The wt-APC, but not 3K3A-APC, significantly increased the risk of intracerebral bleeding as indicated by a 50% increase in hemoglobin levels in the ischemic hemisphere.
  • Thus, 3K3A-APC offers a new approach for safer and more efficacious treatments of neurodegenerative disorders and stroke with APC.
  • [MeSH-major] Anticoagulants / therapeutic use. Mutation / physiology. Neuroprotective Agents / therapeutic use. Protein C / genetics. Protein C / therapeutic use
  • [MeSH-minor] Analysis of Variance. Animals. Antibodies / pharmacology. Apoptosis / drug effects. Brain / cytology. Caspase 3 / metabolism. Caspase 9 / metabolism. Cells, Cultured. Embryo, Mammalian. Endothelial Cells / drug effects. Enzyme Inhibitors / pharmacology. Excitatory Amino Acid Agonists / toxicity. Female. Glucose / deficiency. Hemoglobins / metabolism. Humans. Hypoxia / drug therapy. In Situ Nick-End Labeling / methods. Infarction, Middle Cerebral Artery / drug therapy. Infarction, Middle Cerebral Artery / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. N-Methylaspartate / toxicity. Neurons / drug effects. Neurons / physiology. Pregnancy. Receptors, Proteinase-Activated / genetics. Time Factors. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19302148.001).
  • [ISSN] 1460-9568
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL063290; United States / NHLBI NIH HHS / HL / HL81528; United States / NHLBI NIH HHS / HL / HL63290; United States / NHLBI NIH HHS / HL / R01 HL052246; United States / NHLBI NIH HHS / HL / R01 HL063290-10; United States / NHLBI NIH HHS / HL / R01 HL021544; United States / NHLBI NIH HHS / HL / R01 HL081528-03; United States / NHLBI NIH HHS / HL / R01 HL081528
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies; 0 / Anticoagulants; 0 / Enzyme Inhibitors; 0 / Excitatory Amino Acid Agonists; 0 / Hemoglobins; 0 / Neuroprotective Agents; 0 / Protein C; 0 / Receptors, Proteinase-Activated; 0 / Tumor Suppressor Protein p53; 6384-92-5 / N-Methylaspartate; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ NIHMS105284; NLM/ PMC2692517
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75. Kanda Y, Komatsu Y, Akahane M, Kojima S, Asano-Mori Y, Tada M, Oshima K, Isayama H, Ogawa S, Motokura T, Chiba S, Ohtomo K, Omata M, Hirai H: Graft-versus-tumor effect against advanced pancreatic cancer after allogeneic reduced-intensity stem cell transplantation. Transplantation; 2005 Apr 15;79(7):821-7
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  • METHODS: Only patients with pathologically proven pancreatic cancer that was locally advanced or metastatic and not amenable to curative resection were included.
  • In addition, some of these responses were associated with an increase in the serum anticarcinoembryonic antigen antibody level.

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  • (PMID = 15818325.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Carcinoembryonic Antigen
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76. El-Rayes BF, Jasti P, Severson RK, Almhanna K, Philip PA, Shields A, Zalupski M, Heilbrun LK: Impact of race, age, and socioeconomic status on participation in pancreatic cancer clinical trials. Pancreas; 2010 Oct;39(7):967-71
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  • OBJECTIVES: Over 18 years, 7 phase 2 trials in advanced pancreatic cancer (APC) were conducted at Karmanos Cancer Institute (KCI).
  • METHODS: The target population was patients with APC diagnosed between January 1, 1986, and December 31, 2003.
  • Patients were divided into 3 mutually exclusive groups: treated on clinical trials at KCI (t-KCI), treated at KCI but not on a clinical trial (KCI), or treated at non-KCI institutions (n-KCI).
  • Median OS was higher in t-KCI (8.5 months) than in KCI (5.0 months) or n-KCI (2.8 months) and could not be accounted for by variations in baseline characteristics.
  • Patients with APC treated at academic institutions may have longer OS than patients treated in the community.
  • Clinical trials seem to offer a survival advantage for patients with APC.


77. Celecoxib: new indication. Colorectal cancer: no preventive benefit. Prescrire Int; 2006 Feb;15(81):13-5
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  • (1) Familial adenomatous polyposis is a genetic disorder associated with multiple adenomatous colorectal polyps that invariably progress to colorectal cancer.
  • Gastroduodenal polyposis and extra-gastrointestinal desmoid tumours are other major sources of morbidity in these patients. (2) The current strategy used to prevent colorectal cancer in patients with APC gene mutations consists of yearly monitoring starting in adolescence, and prophylactic colectomy in early adulthood if polyposis occurs. (3) On the basis of pathophysiological, experimental and epidemiological evidence, some specialists have postulated that certain nonsteroidal antiinflammatory drugs (NSAIDs) might have a preventive effect on colorectal adenomas and cancer. (4) Aspirin and sulindac were tested for the prevention of polyps in patients with familial adenomatous polyposis, with uncertain results and weak evidence of effectiveness. (5) Celecoxib was tested in a comparative randomised double-blind trial lasting 6 months.
  • It involved 77 patients with familial polyposis and colorectal polyps, and 6 patients with only duodenal polyps.
  • On the basis of composite endoscopic criteria, a celecoxib dose of 800 mg/day (but not 200 mg/day) reduced the number and surface area of adenomatous colorectal polyps in patients with familial adenomatous polyposis.
  • It is not known whether celecoxib also reduced the risk of colorectal cancer.
  • Another preventive trial was stopped when an excess of cardiovascular events was found in patients taking celecoxib. (7) The long-term risk-benefit balance of celecoxib 800 mg/day is not known nor whether efficacy persists after treatment discontinuation. (8) In practice, it is better not to use celecoxib to prevent colorectal cancer: its efficacy has not been demonstrated, even in familial polyposis, and it carries a major risk of bleeding and cardiovascular events.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use

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  • (PMID = 16548099.001).
  • [ISSN] 1167-7422
  • [Journal-full-title] Prescrire international
  • [ISO-abbreviation] Prescrire Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides
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78. Ito Y, Okusaka T, Kagami Y, Ueno H, Ikeda M, Sumi M, Imai A, Fujimoto N, Ikeda H: Evaluation of acute intestinal toxicity in relation to the volume of irradiated small bowel in patients treated with concurrent weekly gemcitabine and radiotherapy for locally advanced pancreatic cancer. Anticancer Res; 2006 Sep-Oct;26(5B):3755-9
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  • [Title] Evaluation of acute intestinal toxicity in relation to the volume of irradiated small bowel in patients treated with concurrent weekly gemcitabine and radiotherapy for locally advanced pancreatic cancer.
  • BACKGROUND: Treatment of concurrent gemcitabine and radiotherapy for pancreatic cancer was reported to have a higher rate of severe acute intestinal toxicity.
  • This study evaluated the acute intestinal toxicity in relation to the volume of irradiated small bowel and other factors using dosimetric analyses in pancreatic cancer patients treated with gemcitabine-based chemoradiotherapy.
  • A dose-volume histogram was generated for the small bowel, colon and planning target volume (PTV) and dosimetric parameters were recorded.
  • Correlations between the acute intestinal toxicity and the volume of irradiated small bowel and other factors were evaluated.
  • Grade 3+ acute intestinal toxicities were observed in twenty-four (62%) patients.
  • There was no correlation between the acute intestinal toxicity and the volume of irradiated small bowel.
  • However, the total volume of PTV was shown to be significantly correlated with the development of Grade 3+ acute intestinal toxicity (p = 0.021).
  • CONCLUSION: The volume of irradiated small bowel did not directly influence the acute intestinal toxicity, but only the volume of PTV significantly correlated with severe acute intestinal toxicity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Deoxycytidine / analogs & derivatives. Intestine, Small / drug effects. Intestine, Small / radiation effects. Pancreatic Neoplasms / therapy. Radiotherapy / adverse effects


79. Park S, Gwak J, Cho M, Song T, Won J, Kim DE, Shin JG, Oh S: Hexachlorophene inhibits Wnt/beta-catenin pathway by promoting Siah-mediated beta-catenin degradation. Mol Pharmacol; 2006 Sep;70(3):960-6
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  • Aberrant activation of Wnt/beta-catenin signaling and subsequent up-regulation of beta-catenin response transcription (CRT) is a critical event in the development of human colon cancer.
  • This degradation pathway is Siah-1 and adenomatous polyposis colidependent, but glycogen synthase kinase-3beta and F-box beta-transducin repeat-containing protein-independent.
  • In addition, hexachlorophene represses the expression of cyclin D1, which is a known beta-catenin target gene, and inhibits the growth of colon cancer cells.
  • [MeSH-major] Anti-Infective Agents, Local / pharmacology. Hexachlorophene / pharmacology. Nuclear Proteins / metabolism. Protein Processing, Post-Translational / drug effects. Signal Transduction / drug effects. Ubiquitin-Protein Ligases / metabolism. Wnt Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Cell Proliferation / drug effects. Cells, Cultured. Colonic Neoplasms / pathology. Down-Regulation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Glycogen Synthase Kinase 3 / metabolism. Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tumor Suppressor Protein p53 / metabolism. Wnt3 Protein. Wnt3A Protein. beta-Transducin Repeat-Containing Proteins / metabolism

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  • (PMID = 16735606.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents, Local; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; 0 / WNT3A protein, human; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / Wnt3A Protein; 0 / beta Catenin; 0 / beta-Transducin Repeat-Containing Proteins; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / seven in absentia proteins; IWW5FV6NK2 / Hexachlorophene
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80. Sinicrope FA, Penington RC: Sulindac sulfide-induced apoptosis is enhanced by a small-molecule Bcl-2 inhibitor and by TRAIL in human colon cancer cells overexpressing Bcl-2. Mol Cancer Ther; 2005 Oct;4(10):1475-83
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  • [Title] Sulindac sulfide-induced apoptosis is enhanced by a small-molecule Bcl-2 inhibitor and by TRAIL in human colon cancer cells overexpressing Bcl-2.
  • Sulindac is a nonsteroidal anti-inflammatory drug (NSAID) that induces apoptosis in cultured colon cancer cells and in intestinal epithelia in association with its chemopreventive efficacy.
  • Resistance to sulindac is well documented in patients with familial adenomatous polyposis; however, the molecular mechanisms underlying such resistance remain unknown.
  • We determined the effect of ectopic Bcl-2 expression upon sulindac-induced apoptotic signaling in SW480 human colon cancer cells.
  • Coadministration of sulindac sulfide and the small-molecule Bcl-2 inhibitor HA14-1 increased apoptosis induction and enhanced caspase-8 and caspase-9 cleavage, Bax redistribution, and cytochrome c and second mitochondria-derived activator of caspase release.
  • Given that sulindac sulfide activated caspase-8 and increased membrane death receptor (DR4 and DR5) protein levels, we evaluated its combination with the endogenous death receptor ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
  • Together, these data indicate that HA14-1 or TRAIL can enhance sulindac sulfide-induced apoptosis and represent novel strategies for circumventing Bcl-2-mediated apoptosis resistance in human colon cancer cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Apoptosis Regulatory Proteins / pharmacology. Benzopyrans / pharmacology. Colonic Neoplasms / drug therapy. Membrane Glycoproteins / pharmacology. Nitriles / pharmacology. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Sulindac / analogs & derivatives. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16227396.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA104683
  • [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 / Apoptosis Regulatory Proteins; 0 / Benzopyrans; 0 / Enzyme Inhibitors; 0 / Membrane Glycoproteins; 0 / Nitriles; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate; 184SNS8VUH / Sulindac; 6UVA8S2DEY / sulindac sulfide; 9007-43-6 / Cytochromes c; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
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81. Coleman P, Barnard NA: Congenital hypertrophy of the retinal pigment epithelium: prevalence and ocular features in the optometric population. Ophthalmic Physiol Opt; 2007 Nov;27(6):547-55
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  • The progression of the condition could not be accurately described without follow-up.
  • No evidence was found to suggest a relationship between true CHRPE and familial adenomatous polyposis coli, Gardner's or Turcot's syndromes.
  • [MeSH-minor] Adenomatous Polyposis Coli / complications. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Diagnosis, Differential. Female. Gardner Syndrome / complications. Humans. Hypertrophy / complications. Hypertrophy / congenital. Hypertrophy / pathology. Infant. Male. Middle Aged. Prevalence. Retrospective Studies

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  • (PMID = 17956359.001).
  • [ISSN] 0275-5408
  • [Journal-full-title] Ophthalmic & physiological optics : the journal of the British College of Ophthalmic Opticians (Optometrists)
  • [ISO-abbreviation] Ophthalmic Physiol Opt
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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82. Lindqvist P, Olofsson BO, Backman C, Suhr O, Waldenström A: Pulsed tissue Doppler and strain imaging discloses early signs of infiltrative cardiac disease: a study on patients with familial amyloidotic polyneuropathy. Eur J Echocardiogr; 2006 Jan;7(1):22-30
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  • [Title] Pulsed tissue Doppler and strain imaging discloses early signs of infiltrative cardiac disease: a study on patients with familial amyloidotic polyneuropathy.
  • BACKGROUND: Familial amyloidotic polyneuropathy (FAP) is a hereditary systemic amyloidosis with cardiac involvement.
  • As early identification of the cardiac involvement is of major clinical interest we performed this study to test the hypothesis that tissue Doppler imaging (TDI) and strain imaging (SI) might disclose cardiac involvement in patients with early stages of FAP.
  • METHODS: Twenty-two patients with FAP and 36 healthy controls were studied.
  • CONCLUSIONS: This is the first clinical study using TDI and strain in patients with FAP showing functional abnormalities before any morphological echocardiographic abnormalities were present.
  • Both the left and right heart functions are involved and the disease should therefore be regarded as biventricular.
  • [MeSH-major] Amyloid Neuropathies, Familial / ultrasonography. Echocardiography, Doppler, Pulsed. Heart Diseases / ultrasonography

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  • (PMID = 15869906.001).
  • [ISSN] 1525-2167
  • [Journal-full-title] European journal of echocardiography : the journal of the Working Group on Echocardiography of the European Society of Cardiology
  • [ISO-abbreviation] Eur J Echocardiogr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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83. Grubben MJ, van den Braak CC, Nagengast FM, Peters WH: Low colonic glutathione detoxification capacity in patients at risk for colon cancer. Eur J Clin Invest; 2006 Mar;36(3):188-92
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  • [Title] Low colonic glutathione detoxification capacity in patients at risk for colon cancer.
  • BACKGROUND: Colon carcinogenesis is a multifactorial process influenced by hereditary as well as environmental factors.
  • The glutathione/glutathione S-transferase detoxification system in the colon is important for protection against carcinogens.
  • We investigated the levels of glutathione/glutathione S-transferase in normal colon mucosa of patients with colorectal cancer and in patients at high risk for colorectal cancer compared with those in healthy controls.
  • Normal colon tissue of patients with colon adenoma (n = 64), colorectal cancer (n = 37), familial adenomatous polyposis (FAP; n = 19), hereditary non-polyposis colorectal cancer families with (HNPCC+Ad; n = 34) or without (HNPCC-Ad; n = 33) adenoma was investigated.
  • RESULTS: Glutathione levels were significantly lower in the normal colon mucosa of patients with cancer, FAP, HNPCC-Ad or HNPCC+Ad compared with adenoma patients or healthy controls.
  • Glutathione S-transferase enzyme activity in the distal colon was significantly lower in patients with cancer or FAP compared with the adenoma patients or healthy controls, whereas values in carcinoma patients were significantly lower compared with both the HNPCC-Ad and HNPCC+Ad groups.
  • This low glutathione detoxification capacity might contribute to the colon cancer risk.
  • [MeSH-major] Colon / chemistry. Colorectal Neoplasms / chemistry. Glutathione / analysis
  • [MeSH-minor] Adenoma / chemistry. Adenoma / enzymology. Adenomatous Polyposis Coli / chemistry. Adenomatous Polyposis Coli / enzymology. Adult. Colonic Neoplasms / chemistry. Colonic Neoplasms / enzymology. Colorectal Neoplasms, Hereditary Nonpolyposis / chemistry. Colorectal Neoplasms, Hereditary Nonpolyposis / enzymology. Female. Glutathione Transferase / metabolism. Humans. Intestinal Mucosa / chemistry. Intestinal Mucosa / enzymology. Male. Middle Aged. Risk Factors

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  • (PMID = 16506964.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.5.1.18 / Glutathione Transferase; GAN16C9B8O / Glutathione
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84. Heinemann V, Boeck S, Hinke A, Labianca R, Louvet C: Meta-analysis of randomized trials: evaluation of benefit from gemcitabine-based combination chemotherapy applied in advanced pancreatic cancer. BMC Cancer; 2008;8:82
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  • RESULTS: The meta-analysis revealed a significant survival benefit for GEM+X with a pooled hazard ratio (HR) of 0.91 (95% CI: 0.85 - 0.97, p = 0.004).
  • The analysis of platinum-based combinations indicated a HR of 0.85 (95% CI: 0.76 - 0.96, p = 0.010), while for fluoropyrimidine-based combinations the HR was 0.90 (95% CI: 0.81 - 0.99, p = 0.030).
  • This analysis indicated that patients with a good PS had a marked survival benefit when receiving combination chemotherapy (HR = 0.76; 95% CI: 0.67 - 0.87; p < 0.0001).
  • By contrast, application of combination chemotherapy to patients with an initially poor PS appeared to be ineffective (HR = 1.08; 95% CI: 0.90 - 1.29, p = 0.40).

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  • (PMID = 18373843.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Meta-Analysis
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoacridines; 0 / Antimetabolites, Antineoplastic; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 0W860991D6 / Deoxycytidine; 316-83-6 / fluoroquinacrine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2292732
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85. Miller JJ, Summers MK, Hansen DV, Nachury MV, Lehman NL, Loktev A, Jackson PK: Emi1 stably binds and inhibits the anaphase-promoting complex/cyclosome as a pseudosubstrate inhibitor. Genes Dev; 2006 Sep 01;20(17):2410-20
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  • The periodic destruction of mitotic cyclins is triggered by the activation of the anaphase-promoting complex/cyclosome (APC/C) in mitosis.
  • Although the ability of the APC/C to recognize destruction box (D-box) substrates oscillates throughout the cell cycle, the mechanism regulating APC/C binding to D-box substrates remains unclear.
  • Here, we show that the APC/C inhibitor Emi1 tightly binds both the APC/C and its Cdh1 activator, binds to the D-box receptor site on the APC/C(Cdh1), and competes with APC/C substrates for D-box binding.
  • Emi1 itself contains a conserved C-terminal D-box, which provides APC/C-binding affinity, and a conserved zinc-binding region (ZBR), which antagonizes APC/C E3 ligase activity independent of tight APC binding.
  • Mutation of the ZBR converts Emi1 into a D-box-dependent APC/C substrate.
  • The identification of a direct Emi1-APC/C complex further explains how Emi1 functions as a stabilizing factor for cyclin accumulation and the need to destroy Emi1 for APC/C activation in mitosis.
  • The combination of a degron/E3 recognition site and an anti-ligase function in Emi1 suggests a general model for how E3 substrates evolve to become pseudosubstrate inhibitors.
  • [MeSH-major] Cell Cycle Proteins / physiology. Enzyme Inhibitors. F-Box Proteins / physiology. Ubiquitin-Protein Ligase Complexes / antagonists & inhibitors. Ubiquitin-Protein Ligase Complexes / metabolism
  • [MeSH-minor] Amino Acid Motifs. Anaphase-Promoting Complex-Cyclosome. Binding, Competitive. Cadherins / metabolism. Cadherins / physiology. Cell Nucleus / enzymology. Cell Nucleus / metabolism. Conserved Sequence. HeLa Cells. Humans. Interphase / physiology. Protein Binding. Substrate Specificity

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  • (PMID = 16921029.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM054811; United States / NIGMS NIH HHS / GM / T32 GM007365; United States / NCI NIH HHS / CA / T32 CA009151; United States / NIGMS NIH HHS / GM / R01 GM060439; United States / NIGMS NIH HHS / GM / GM07365; United States / NINDS NIH HHS / NS / K08 NS045077; United States / NCI NIH HHS / CA / CA09151; United States / NIGMS NIH HHS / GM / R01 GM54811; United States / NIGMS NIH HHS / GM / R01 GM60439
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDH1 protein, human; 0 / Cadherins; 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / F-Box Proteins; 0 / FBXO5 protein, human; EC 2.3.2.23 / Ubiquitin-Protein Ligase Complexes; EC 2.3.2.27 / Anaphase-Promoting Complex-Cyclosome
  • [Other-IDs] NLM/ PMC1560415
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86. Cohen Z, Senagore AJ, Dayton MT, Koruda MJ, Beck DE, Wolff BG, Fleshner PR, Thirlby RC, Ludwig KA, Larach SW, Weiss EG, Bauer JJ, Holmdahl L: Prevention of postoperative abdominal adhesions by a novel, glycerol/sodium hyaluronate/carboxymethylcellulose-based bioresorbable membrane: a prospective, randomized, evaluator-blinded multicenter study. Dis Colon Rectum; 2005 Jun;48(6):1130-9
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  • INTRODUCTION: Postoperative abdominal adhesions are associated with significant morbidity and mortality, placing a substantial burden on healthcare systems worldwide.
  • Development of a bioresorbable membrane containing up to 23 percent glycerol and chemically modified sodium hyaluronate/carboxymethylcellulose offers ease of handling and has been shown to provide significant postoperative adhesion prevention in animals.
  • METHODS: Twelve centers enrolled 120 patients with ulcerative colitis or familial polyposis who were scheduled for a restorative proctocolectomy and ileal pouch-anal anastomosis with diverting loop ileostomy.
  • Safety profiles for the treatment and no treatment control groups were similar with the exception of more infection complications associated with glycerol hyaluronate/carboxymethylcellulose use.
  • Animal models did not predict these complications.

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  • (PMID = 15868230.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Biocompatible Materials; 0 / Membranes, Artificial; 9004-32-4 / Carboxymethylcellulose Sodium; 9004-61-9 / Hyaluronic Acid; PDC6A3C0OX / Glycerol
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87. Abbas O, Richards JE, Mahalingam M: Fibroblast-activation protein: a single marker that confidently differentiates morpheaform/infiltrative basal cell carcinoma from desmoplastic trichoepithelioma. Mod Pathol; 2010 Nov;23(11):1535-43
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  • [Title] Fibroblast-activation protein: a single marker that confidently differentiates morpheaform/infiltrative basal cell carcinoma from desmoplastic trichoepithelioma.
  • Fibroblast-activation protein, a type II membrane-bound glycoprotein belonging to the serine protease family, is expressed in the granulation tissue of healing wounds.
  • More recently, it has been identified as a marker of reactive tumor stromal fibroblasts, as it is reportedly selectively expressed in peritumoral stromal fibroblasts of multiple epithelial cancers including cutaneous malignancies such as basal cell carcinoma.
  • Given this, we sought to ascertain the use of fibroblast-activation protein in distinguishing morpheaform/infiltrative basal cell carcinoma from desmoplastic trichoepithelioma.
  • Immunohistochemical staining for fibroblast-activation protein was performed on desmoplastic trichoepithelioma (n=25) and morpheaform/infiltrative basal cell carcinoma (n=25), with the control group comprising scars from reexcision specimens (n=10).
  • As expected, fibroblast-activation protein expression was observed in stromal fibroblasts of all control cases (10 of 10, 100%).
  • Of interest, fibroblast-activation protein expression was observed in peritumoral fibroblasts of all cases of morpheaform/infiltrative basal cell carcinoma (25 of 25, 100%) but not in any cases of desmoplastic trichoepithelioma (0 of 25, 0%).
  • A gradient of fibroblast-activation protein expression was observed in morpheaform/infiltrative basal cell carcinoma with more intense expression noted in fibroblasts abutting the tumor cells, a less intense expression in the distal peritumoral stromal portion, and minimal to loss of expression in adjacent normal tissue.
  • In summary, findings from this study underscore the use of fibroblast-activation protein as a histologic adjunct in confidently differentiating morpheaform/infiltrative basal cell carcinoma from desmoplastic trichoepithelioma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Basal Cell / diagnosis. Fibroblasts / enzymology. Gelatinases / analysis. Membrane Proteins / analysis. Serine Endopeptidases / analysis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biopsy. Boston. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Predictive Value of Tests. Young Adult


88. Elligers KT, Davies M, Sanchis D, Ferencz T, Saif MW: Rechallenge with cisplatin in a patient with pancreatic cancer who developed a hypersensitivity reaction to oxaliplatin. Is skin test useful in this setting? JOP; 2008;9(2):197-202
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  • In an event of a platinum hypersensitivity reaction, the particular platinum salt is likely discontinued.
  • The patient has tolerated multiple additional cycles with further decrease in tumor size and tumor markers.


89. Kashyap MK, Marimuthu A, Kishore CJ, Peri S, Keerthikumar S, Prasad TS, Mahmood R, Rao S, Ranganathan P, Sanjeeviah RC, Vijayakumar M, Kumar KV, Montgomery EA, Kumar RV, Pandey A: Genomewide mRNA profiling of esophageal squamous cell carcinoma for identification of cancer biomarkers. Cancer Biol Ther; 2009 Jan;8(1):36-46
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  • Esophageal squamous cell carcinoma (ESCC) is predominant type of esophageal cancers worldwide comprising almost 95% of cases.
  • In spite of its higher prevalence, ESCC has not been studied as intensively as esophageal adenocarcinoma.
  • In order to identify molecules as candidates for early diagnosis and/or as therapeutic targets, we analyzed the mRNA expression profiles of 20 cases of ESCC using whole genome DNA microarrays.
  • We validated two molecules that were not previously reported to be overexpressed in ESCC, oral cancer overexpressed 2 (ORAOV2) and fibroblast activation protein (FAP), by immunohistochemical labeling of tissue microarrays and archival tissue sections and found that they were overexpressed in 98% (116/118) and 68% (79/116) of cases, respectively.
  • Overall, using this approach we have identified a number of promising novel candidates that can be validated further for their potential to serve as biomarkers for ESCC.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Squamous Cell / genetics. Esophageal Neoplasms / genetics. Genome-Wide Association Study. Neoplasm Proteins / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Antigens, Neoplasm / genetics. DNA, Neoplasm / genetics. Gelatinases. Gene Expression Regulation, Neoplastic. Humans. Membrane Proteins. Oligonucleotide Array Sequence Analysis. RNA, Neoplasm / genetics. Serine Endopeptidases / genetics. Up-Regulation

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  • (PMID = 18981721.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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90. Mátrai Z, Papp J, Polgár C, Hitre E, Köves I, Oláh E, Andi J, Kiss A, Vámosi Nagy I, Tóth L, Orosz Z: [Long-term experience with therapy of a female patient with Gardner's syndrome, first presenting with extra-abdominal desmoid tumor, and review of the literature]. Magy Seb; 2009 Apr;62(2):75-82
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  • [Title] [Long-term experience with therapy of a female patient with Gardner's syndrome, first presenting with extra-abdominal desmoid tumor, and review of the literature].
  • Gardner's syndrome is a clinical subgroup of familial adenomatous polyposis, an autosomal dominant disease.
  • It is characterized by gastrointestinal polyps and extra-intestinal manifestations including multiple osteomas, skin and soft tissue tumours.
  • Aggressive desmoid tumours can be very difficult to manage in patients with Gardner's syndrome.
  • We present a case of a 17-year-old female who presented with an aggressive desmoid tumor arising of the lumbar area as part of her Gardner's syndrome.
  • We conclude that desmoid tumors can precede gastrointestinal manifestations of familial adenomatous polyposis or Gardner's syndrome.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fibromatosis, Aggressive / diagnosis. Fibromatosis, Aggressive / genetics. Gardner Syndrome / diagnosis. Gardner Syndrome / genetics. Genes, APC

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  • (PMID = 19386568.001).
  • [ISSN] 0025-0295
  • [Journal-full-title] Magyar sebészet
  • [ISO-abbreviation] Magy Seb
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 30
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91. Norhana MN, Azman MN, Poole SE, Deeth HC, Dykes GA: Effects of bilimbi (Averrhoa bilimbi L.) and tamarind (Tamarindus indica L.) juice on Listeria monocytogenes Scott A and Salmonella Typhimurium ATCC 14028 and the sensory properties of raw shrimps. Int J Food Microbiol; 2009 Nov 30;136(1):88-94
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  • [Title] Effects of bilimbi (Averrhoa bilimbi L.) and tamarind (Tamarindus indica L.) juice on Listeria monocytogenes Scott A and Salmonella Typhimurium ATCC 14028 and the sensory properties of raw shrimps.
  • The potential of using juice of bilimbi (Averrhoa bilimbi L.) and tamarind (Tamarindus indica L.) to reduce Listeria monocytogenes Scott A and Salmonella Typhimurium ATCC 14028 populations on raw shrimps after washing and during storage (4 degrees C) was investigated.
  • The uninoculated raw shrimps and those inoculated with approximately 9 log cfu/ml of L. monocytogenes Scott A and S.
  • Naturally occurring aerobic bacteria (APC), L. monocytogenes Scott A and S.
  • Compared to SDW, bilimbi and tamarind juice significantly (p<0.05) reduced APC (0.40-0.70 log cfu/g), L. monocytogenes Scott A (0.84-1.58 log cfu/g) and S.
  • There was a significant difference (p<0.05) in bacterial reduction between the dipping (0.40-0.41 log for APC; 0.84 for L. monocytogenes Scott A and 1.03-1.09 log for S.
  • Typhimurium ATCC 14028) and rubbing (0.68-0.70 log for APC; 1.34-1.58 for L. monocytogenes Scott A and 1.67-2.00 log for S.
  • Regardless of washing treatments or methods, populations of S.
  • Typhimurium ATCC 14028 decreased slightly (5.10-6.29 log cfu/g on day 7 of storage) while populations of L. monocytogenes Scott A (8.74-9.20 log cfu/g) and APC (8.68-8.92 log cfu/g) increased significantly during refrigerated storage.
  • The control, bilimbi or tamarind-washed shrimps did not differ in sensory panellist acceptability (p>0.05) throughout the storage except for odour (p<0.05) attributes at 0 day when acidic or lemony smell was noticed in bilimbi- and tamarind-washed shrimps and not in control shrimps.

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  • (PMID = 19818521.001).
  • [ISSN] 1879-3460
  • [Journal-full-title] International journal of food microbiology
  • [ISO-abbreviation] Int. J. Food Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Disinfectants; 0 / Plant Extracts
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92. Labori KJ, Hjermstad MJ, Wester T, Buanes T, Loge JH: Symptom profiles and palliative care in advanced pancreatic cancer: a prospective study. Support Care Cancer; 2006 Nov;14(11):1126-33
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  • OBJECTIVES: To describe prospectively the prevalence and severity of disease-related symptoms, quality of life (QOL) and need for palliative care in patients with advanced pancreatic cancer.
  • RESULTS: Of the 22 women and 29 men (mean age, 62 years), 20 had locally unresectable cancer, 19 had metastatic disease, and 12 had recurrent disease after curative resection.
  • A multidisciplinary approach is necessary for the best palliation of symptoms at the time of diagnosis and during follow-up.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Humans. Male. Middle Aged. Norway / epidemiology. Prevalence. Prospective Studies. Quality of Life. Severity of Illness Index. Surveys and Questionnaires. Survival Analysis. Time Factors

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  • (PMID = 16601947.001).
  • [ISSN] 0941-4355
  • [Journal-full-title] Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
  • [ISO-abbreviation] Support Care Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
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93. Lage A: On the cross-fertilization between biotechnology and immunology: current situation in Cuba. Vaccine; 2006 Apr 12;24 Suppl 2:S2-3-6
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  • Current understanding of antigen presentation and the maturation of dendritic cells has opened the way for a more rational design of new adjuvants, intended not only to deliver the antigen to antigen presenting cells (APC) and to induce APC maturation, but also to direct lymphocyte differentiation towards either Th1 or Th2 phenotypes, and to deal with disease-induced immunodepression.

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  • (PMID = 16823906.001).
  • [ISSN] 0264-410X
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Vaccines
  • [Number-of-references] 10
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94. Markova M, Koratkar RA, Silverman KA, Sollars VE, MacPhee-Pellini M, Walters R, Palazzo JP, Buchberg AM, Siracusa LD, Farber SA: Diversity in secreted PLA2-IIA activity among inbred mouse strains that are resistant or susceptible to Apc Min/+ tumorigenesis. Oncogene; 2005 Sep 22;24(42):6450-8
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  • [Title] Diversity in secreted PLA2-IIA activity among inbred mouse strains that are resistant or susceptible to Apc Min/+ tumorigenesis.
  • The secreted phospholipase A2 type IIA (Pla2g2a) gene was previously identified as a modifier of intestinal adenoma multiplicity in Apc Min/+ mice.
  • To determine if intestinal secreted phospholipase A2 (sPLA2) activity was also attenuated in susceptible strains, we developed a sensitive assay to directly quantitate sPLA2 activity in the murine intestinal tract utilizing a fluorescent BODIPY-labeled phospholipid substrate.
  • Here, we report assay conditions that distinguish between secreted and cytosolic PLA2 enzyme activities in extracts of intestinal tissue.
  • The small intestine exhibited higher activity levels than the large intestine.
  • Consistent with predictions from the sPLA2-IIA gene sequence in inbred strains, we detected low levels of enzyme activity in inbred strains containing sPLA2-IIA mutations; these strains were also associated with greater numbers of intestinal polyps.
  • Additionally, the assay was able to distinguish differences in levels of sPLA2 activity between neoplasia-resistant strains, which were then shown by sequencing to carry variant wild-type sPLA2-IIA alleles.
  • Immunohistochemical analyses of intestinal tissues were consistent with sPLA2-IIA activity levels.
  • This approach enables further studies of the mechanisms of sPLA2 action influencing the development and tumorigenesis of the small intestine and colon in both mice and humans.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Genes, APC. Phospholipases A / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Boron Compounds. Group II Phospholipases A2. Immunohistochemistry. Intestinal Neoplasms / enzymology. Intestine, Large / enzymology. Intestine, Small / enzymology. Mice. Mice, Inbred Strains. Molecular Sequence Data. Molecular Weight. Phospholipases A2. Sequence Homology, Amino Acid. Species Specificity

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  • (PMID = 16007193.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA72027; United States / NCI NIH HHS / CA / R01 CA89560; United States / NIDDK NIH HHS / DK / R01 DK060369
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4,4-difluoro-4-bora-3a,4a-diaza-s-indacene; 0 / Boron Compounds; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Group II Phospholipases A2; EC 3.1.1.4 / Phospholipases A2; EC 3.1.1.4 / Pla2g2a protein, mouse
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95. Lavergne SN, Wang H, Callan HE, Park BK, Naisbitt DJ: "Danger" conditions increase sulfamethoxazole-protein adduct formation in human antigen-presenting cells. J Pharmacol Exp Ther; 2009 Nov;331(2):372-81
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  • [Title] "Danger" conditions increase sulfamethoxazole-protein adduct formation in human antigen-presenting cells.
  • Antigen-presenting cells (APC) are thought to play an important role in the pathogenesis of drug-induced immune reactions.
  • Various pathological factors can activate APC and therefore influence the immune equilibrium.
  • It is interesting that several diseases have been associated with an increased rate of drug allergy.
  • The aim of this project was to evaluate the impact of such "danger signals" on