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Items 1 to 100 of about 7647
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. Nasu J, Ohsumi S, Masuta H, Tanimizu M: [Familial tumor]. Nihon Rinsho; 2010 Aug;68 Suppl 8:494-500
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  • [Title] [Familial tumor].
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Breast Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics

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  • (PMID = 20976925.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
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3. 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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4. 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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5. Li CF, Wei RY, Baliko F, Bapat B, Alman BA: An association between the 4G polymorphism in the PAI-1 promoter and the development of aggressive fibromatosis (desmoid tumor) in familial adenomatous polyposis patients. Fam Cancer; 2007;6(1):89-95
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  • [Title] An association between the 4G polymorphism in the PAI-1 promoter and the development of aggressive fibromatosis (desmoid tumor) in familial adenomatous polyposis patients.
  • Aggressive fibromatosis is a mesenchymal neoplasm associated with mutations resulting in beta-catenin mediated transcriptional activation.
  • Familial adenomatous polyposis is associated with Adenomatous Polyposis Coli gene mutations resulting in beta-catenin mediated transcriptional activation, yet only some patients develop aggressive fibromatosis.
  • Since PAI-1 expression is influenced by a promoter 4G/5G polymorphism, we investigated the incidence of this polymorphism in familial adenomatous polyposis patients who did and who did not develop aggressive fibromatosis, as well as sporadic aggressive fibromatosis patients.
  • There was a trend towards association of the 4G allele (associated with high PAI-1 expression) with the development of aggressive fibromatosis in familial adenomatous polyposis patients (50% vs. 19%, P = 0.1).
  • In familial adenomatous polyposis patients who did not develop aggressive fibromatosis, there was a significantly lower proportion of patients with a 4G allele compared to the healthy control (19% vs. 51%, P = 0.0286).
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Fibromatosis, Aggressive / genetics. Gene Expression Regulation, Neoplastic. Plasminogen Activator Inhibitor 1 / genetics. Polymorphism, Genetic. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Adult. Causality. Comorbidity. Genetic Predisposition to Disease. Humans. Incidence. Severity of Illness Index. Transcriptional Activation


6. Ishikawa H, Nakamura T, Kawano A, Gondo N, Sakai T: Chemoprevention of colorectal cancer in Japan: a brief introduction to current clinical trials. J Gastroenterol; 2009;44 Suppl 19:77-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The rapidly increasing incidence of colorectal cancer in Japan poses a great challenge to researchers to develop preventive strategies against this disease.
  • Also, the Ministry of Health, Labour and Welfare of Japan recognizes the significance of cancer prevention studies, especially against colorectal cancer, including it as one of the pillars in the "Third Research Project on General Strategies against Cancer" and funding several large-scale projects.
  • Among them are two chemoprevention studies currently being performed: in patients with previous sporadic colorectal tumors (J-CAPP study) and in patients with familial adenomatous polyposis (J-FAPP study II).
  • Both are double-blind randomized controlled trials with low-dose aspirin (100 mg/day), which is generally considered to be safe for long-term use.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Adenomatous Polyposis Coli / drug therapy. Chemoprevention / methods. Humans. Japan / epidemiology. Randomized Controlled Trials as Topic

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  • [Cites] J Surg Oncol. 1983 Sep;24(1):83-7 [6887943.001]
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  • (PMID = 19148798.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin
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7. 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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8. 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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9. 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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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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11. 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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  • [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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12. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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13. Lewis A, Segditsas S, Deheragoda M, Pollard P, Jeffery R, Nye E, Lockstone H, Davis H, Clark S, Stamp G, Poulsom R, Wright N, Tomlinson I: Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5. Gut; 2010 Dec;59(12):1680-6
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  • [Title] Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5.
  • BACKGROUND AND AIMS: Adenomatous polyposis coli (APC) is a tumour suppressor gene mutated in the germline of patients with familial adenomatous polyposis (FAP) and somatically in most colorectal cancers.
  • APC mutations impair β-catenin degradation, resulting in increased Wnt signalling.
  • The most frequent APC mutation is a codon 1309 truncation that is associated with severe FAP.
  • A previous study compared two mouse models of intestinal tumorigenesis, Apc(R850X) (Min) and Apc(1322T) (1322T), the latter a model of human codon 1309 changes.
  • 1322T mice had more severe polyposis but, surprisingly, these tumours had lower levels of nuclear β-catenin than Min tumours.
  • RESULTS: As expected, lower nuclear β-catenin levels in 1322T lesions were associated with generally lower levels of Wnt target expression.
  • CONCLUSIONS: The severe phenotype caused by truncation of Apc at codon 1322 is associated with an increased number of stem cells.

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  • (PMID = 20926645.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lgr5 protein, mouse; 0 / Neoplasm Proteins; 0 / Receptors, G-Protein-Coupled; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC3002835
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14. 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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  • [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


15. 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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  • [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


16. Vandrovcova J, Lagerstedt-Robinsson K, Påhlman L, Lindblom A: Somatic BRAF-V600E mutations in familial colorectal cancer. Cancer Epidemiol Biomarkers Prev; 2006 Nov;15(11):2270-3
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  • [Title] Somatic BRAF-V600E mutations in familial colorectal cancer.
  • However, it has been shown that activating BRAF mutations are almost never found in tumors from hereditary nonpolyposis colorectal cancer patients.
  • To evaluate the role of oncogenic BRAF mutations in non-hereditary nonpolyposis colorectal cancer/non-familial adenomatous polyposis familial colorectal cancer, we did a mutation screening of the most common BRAF mutation, the V600E mutation, in 194 colorectal tumors from patients with a positive family history of the disease.
  • These findings indicate that adenomas might be less important in the cancer development in the group of families with BRAF-V600E mutations and indirectly support a previous hypothesis that tumors might develop through the hyperplastic polyp-serrated adenoma pathway.
  • [MeSH-major] Colorectal Neoplasms / genetics. Genetic Predisposition to Disease. Mutation. Proto-Oncogene Proteins B-raf / genetics

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  • (PMID = 17119056.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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17. 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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18. 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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19. 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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20. Johnson MW, Maestranzi S, Duffy AM, Dewar DH, Forbes A, Bjarnason I, Sherwood RA, Ciclitira P, Nicholls JR: Faecal calprotectin: a noninvasive diagnostic tool and marker of severity in pouchitis. Eur J Gastroenterol Hepatol; 2008 Mar;20(3):174-9
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  • INTRODUCTION: In pouchitis, the mucosa is infiltrated by activated polymorphonuclear neutrophils capable of producing calprotectin, a stable antimicrobial myelomonocytic protein.
  • METHOD: Fifty-four stool samples were collected from patients who had undergone restorative proctocolectomy; 46 from patients with ulcerative colitis and eight from those with familial adenomatous polyposis coli.
  • Of the familial adenomatous polyposis patients, one had pouchitis and pre-pouch ileitis (305 microg/g), and seven had noninflamed pouches (9, 6-26 microg/g).
  • Faecal calprotectin concentrations correlated closely with the Objective Pouchitis Score, the Pouch Disease Activity Index and endoscopic and histological inflammatory scores (Spearman rank test: P values <0.0001).
  • Using a faecal calprotectin threshold of >or=92.5 microg/g to define a positive result, Receiver Operating Characteristic analysis demonstrated a sensitivity of 90% and a specificity of 76.5%.
  • CONCLUSION: Faecal calprotectin measurement is a useful noninvasive tool in the diagnosis of acutely inflamed ileal pouches and correlates well with the severity of pouchitis.
  • [MeSH-major] Feces / chemistry. Leukocyte L1 Antigen Complex / analysis. Pouchitis / diagnosis
  • [MeSH-minor] Adenomatous Polyposis Coli / surgery. Adult. Biomarkers / analysis. Colitis, Ulcerative / surgery. Diagnosis, Differential. Endoscopy, Gastrointestinal. Female. Humans. Male. Middle Aged. Sensitivity and Specificity. Severity of Illness Index

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  • (PMID = 18301296.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Leukocyte L1 Antigen Complex
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21. Menko FH, Ligtenberg MJ, Brouwer T, Hahn DE, Ausems MG: [DNA-based diagnosis of hereditary tumour predisposition]. Ned Tijdschr Geneeskd; 2007 Feb 3;151(5):295-8
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  • [Title] [DNA-based diagnosis of hereditary tumour predisposition].
  • DNA diagnosis is currently used in families with hereditary tumour syndromes, such as familial adenomatous polyposis, hereditary non-polyposis colorectal carcinoma (Lynch syndrome), and hereditary breast and ovarian cancer.
  • Those persons who have not inherited the predisposition no longer have to undergo regular examinations.
  • DNA diagnosis for a hereditary predisposition is currently also performed in patients with cancer at a relatively young age, even if the family history is unclear or negative.
  • This is true of both diagnostic and presymptomatic DNA diagnosis.
  • For these reasons, the clinical application of the DNA diagnosis of hereditary tumours has become an integral part of the work of the multidisciplinary cancer family clinics of the university medical centres and the cancer centres.
  • Guidelines for the management of hereditary tumours have recently been issued, with criteria for referral to the specialised outpatient clinics.
  • [MeSH-major] DNA, Neoplasm / analysis. Genetic Predisposition to Disease. Neoplasms / diagnosis. Neoplasms / genetics

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  • (PMID = 17326472.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  • [Number-of-references] 11
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22. 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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23. 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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24. 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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25. Venkatachalam R, Ligtenberg MJ, Hoogerbrugge N, de Bruijn DR, Kuiper RP, Geurts van Kessel A: The epigenetics of (hereditary) colorectal cancer. Cancer Genet Cytogenet; 2010 Nov;203(1):1-6
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  • [Title] The epigenetics of (hereditary) colorectal cancer.
  • In the last decade, it has become apparent that not only DNA sequence variations but also epigenetic modifications may contribute to disease, including cancer.
  • Interestingly, it was found that sporadic and inherited cancers may exhibit similar DNA methylation patterns, and many genes that are mutated in familial cancers have also been found to be hypermethylated, mutated, or deleted in sporadic cancers.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adenomatous Polyposis Coli / genetics. DNA Methylation. Genes, APC. Germ-Line Mutation. Humans. MutS Homolog 2 Protein / genetics. Nuclear Proteins / genetics

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20951312.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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26. Anaya DA, Chang GJ, Rodriguez-Bigas MA: Extracolonic manifestations of hereditary colorectal cancer syndromes. Clin Colon Rectal Surg; 2008 Nov;21(4):263-72
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  • [Title] Extracolonic manifestations of hereditary colorectal cancer syndromes.
  • Familial colorectal adenocarcinoma (CRC) accounts for approximately 15 to 20% of CRC.
  • Of these, hereditary nonpolyposis colorectal cancer (HNPCC) and familial adenomatous polyposis (FAP) represent the most common hereditary syndromes associated with CRC, followed by other less common diseases including juvenile polyposis (JP) and Peutz-Jeghers syndrome (PJS).
  • Extracolonic manifestations are common in each of these syndromes having significant implications for surveillance and management in at-risk individuals.
  • The authors review the most common and clinically relevant extracolonic manifestations for each of these syndromes focusing on incidence, presentation, genotype/phenotype correlations, and management (including surveillance) strategies.

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  • (PMID = 20011437.001).
  • [ISSN] 1530-9681
  • [Journal-full-title] Clinics in colon and rectal surgery
  • [ISO-abbreviation] Clin Colon Rectal Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2780251
  • [Keywords] NOTNLM ; Hereditary polyposis / colorectal cancer / extracolonic manifestations
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27. 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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28. 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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29. 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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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. Ignatenko NA, Besselsen DG, Stringer DE, Blohm-Mangone KA, Cui H, Gerner EW: Combination chemoprevention of intestinal carcinogenesis in a murine model of familial adenomatous polyposis. Nutr Cancer; 2008;60 Suppl 1:30-5
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  • [Title] Combination chemoprevention of intestinal carcinogenesis in a murine model of familial adenomatous polyposis.
  • Familial adenomatous polyposis (FAP) is an autosomal dominantly inherited syndrome in humans.
  • The Apc(Min/+) mouse, which expresses a mutant homolog of the adenomatous polyposis coli gene, is a model of FAP in humans.
  • Treatment with the nonsteroidal anti-inflammatory drugs (NSAIDS) sulindac or celecoxib can suppress polyp development in FAP patients, but responses are generally transient and incomplete.
  • Combination chemoprevention with the ornithine decarboxylase inhibitor difluoromethylornithine (DFMO) and either celecoxib or sulindac was evaluated in the Apc(Min/+) mouse.
  • Combinations of DFMO and either NSAID reduced intestinal tumor number by more than 80% (P < 0.0001) compared to untreated controls.
  • In addition to the dramatic reduction in tumor number, the combination of DFMO and sulindac reduced the development of high-grade intestinal adenomas compared to sulindac alone (P = 0.003).
  • The fraction of high-grade intestinal adenomas remaining after treatment was similar for the combination of DFMO and celecoxib and celecoxib alone.
  • Only combinations of DFMO plus sulindac reduced total intestinal polyamine contents compared to untreated mice.
  • These data support the rationale for treatment of FAP patients postcolectomy with DFMO combined with either celecoxib or sulindac but indicate that sulindac may be more effective than celecoxib in reducing intestinal polyamine contents and the incidence of high-grade intestinal adenomas when combined with DFMO.
  • [MeSH-major] Adenoma / prevention & control. Adenomatous Polyposis Coli / drug therapy. Intestinal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Biogenic Polyamines / analysis. Celecoxib. Chemoprevention. Eflornithine / administration & dosage. Female. Genes, APC. Intestinal Polyps / prevention & control. Male. Mice. Mice, Inbred C57BL. Pyrazoles / administration & dosage. Sulfonamides / administration & dosage. Sulindac / administration & dosage

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  • (PMID = 19003578.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA123065; United States / NCI NIH HHS / CA / CA23074; United States / NCI NIH HHS / CA / CA72008; United States / NCI NIH HHS / CA / CA95060
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biogenic Polyamines; 0 / Pyrazoles; 0 / Sulfonamides; 184SNS8VUH / Sulindac; JCX84Q7J1L / Celecoxib; ZQN1G5V6SR / Eflornithine
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32. Davis T, Song B, Cram DS: Preimplantation genetic diagnosis of familial adenomatous polyposis. Reprod Biomed Online; 2006 Nov;13(5):707-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preimplantation genetic diagnosis of familial adenomatous polyposis.
  • Familial adenomatous polyposis is a severe autosomal dominant cancer predisposition syndrome.
  • It is characterized by the development of hundreds to thousands of polyps in the gastrointestinal tract, primarily in the colon, at a mean age of 16 years.
  • Without a colectomy, colon cancer is inevitable.
  • FAP is caused by mutations in the adenomatous polyposis coli (APC) gene.
  • A couple was referred to Monash IVF following a request to undertake preimplantation genetic diagnosis for FAP.
  • The female proband had an AGTT deletion mutation in exon 15 of the APC gene.
  • Analysis of the APC-linked marker D5S346 showed that the parental alleles were fully informative.
  • Following standard hormone stimulation and IVF procedures, 14 oocytes were collected, 11 inseminated and nine embryos were biopsied on day 3.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis. Genes, APC. Preimplantation Diagnosis / methods


33. 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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34. 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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35. Miroglio A, Jammes H, Tost J, Ponger L, Gut IG, El Abdalaoui H, Coste J, Chaussade S, Arimondo PB, Lamarque D, Dandolo L: Specific hypomethylated CpGs at the IGF2 locus act as an epigenetic biomarker for familial adenomatous polyposis colorectal cancer. Epigenomics; 2010 Jun;2(3):365-75
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  • [Title] Specific hypomethylated CpGs at the IGF2 locus act as an epigenetic biomarker for familial adenomatous polyposis colorectal cancer.
  • AIMS: The identification of specific biomarkers for colorectal cancer is of primary importance for early diagnosis.
  • The aim of this study was to evaluate if methylation changes at the IGF2/H19 locus could be predictive for individuals at high risk for developing sporadic or hereditary colorectal cancer.
  • MATERIALS & METHODS: Quantitative methylation analysis using pyrosequencing was performed on three differentially methylated regions (DMRs): IGF2 DMR0 and DMR2 and the H19 DMR in DNA samples from sporadic colorectal cancer (n = 26), familial adenomatous polyposis (n = 35) and hereditary nonpolyposis colorectal cancer (n = 19) patients.
  • In lymphocyte DNA, a striking hypomethylation of nine contiguous correlated CpGs was found in the IGF2 DMR2 but only in familial adenomatous polyposis patients.
  • CONCLUSION: Methylation alterations at the IGF2 locus are more extensive than previously reported and DMR2 hypomethylation in lymphocyte DNA might be a specific epigenetic biomarker for familial adenomatous polyposis patients.
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Biomarkers / metabolism. Colorectal Neoplasms / metabolism. CpG Islands / genetics. DNA Methylation / genetics. Insulin-Like Growth Factor II / genetics


36. 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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37. 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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38. Senda T, Shimomura A, Iizuka-Kogo A: Adenomatous polyposis coli (Apc) tumor suppressor gene as a multifunctional gene. Anat Sci Int; 2005 Sep;80(3):121-31
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  • [Title] Adenomatous polyposis coli (Apc) tumor suppressor gene as a multifunctional gene.
  • The adenomatous polyposis coli (Apc) gene is mutated in familial adenomatous polyposis and in sporadic colorectal tumors.
  • The Apc gene product (APC), basically a cytoplasmic protein, blocks cell cycle progression and plays crucial roles in development.
  • The APC binds to beta-catenin, axin and glycogen synthase kinase 3beta to form a large protein complex, in which beta-catenin is phosphorylated and broken down, resulting in negative regulation of the Wnt signaling pathway.
  • Most of the mutated Apc genes in colorectal tumors lack beta-catenin-binding regions and fail to inhibit Wnt signaling, leading to overproliferation of tumor cells.
  • The APC, having some nuclear localizing signals in its molecule, can also be localized in the nucleus.
  • The nuclear APC exports excess beta-catenin to the cytoplasm.
  • Through its C-terminus, APC binds to post-synaptic density discs large zonula occludens domain-containing proteins, such as discs large (DLG) and post-synaptic density (PSD)-95, and may play important roles in epithelial morphogenesis, brain development and neuronal functions.
  • In addition, APC is involved in cell motility through its association with microtubules and APC-stimulated guanine nucleotide exchange factor.
  • Colocalization of APC and DLG is dependent on microtubules.
  • The Apc gene is highly expressed in the embryonic and postnatal developing brain.
  • Recently, we found that APC is required for the activity of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors by facilitating the clustering of PSD-95 and these receptors at the postsynapse.
  • In addition, APC is present in astrocytes, although its role in astrocytes is, as yet, unknown.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Cytoskeletal Proteins / genetics. Genes, APC
  • [MeSH-minor] Animals. Cell Line. Dogs. Gene Expression Regulation, Neoplastic. Humans. Intercellular Signaling Peptides and Proteins / metabolism. Signal Transduction / physiology. Trans-Activators / metabolism. Wnt Proteins. beta Catenin

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  • (PMID = 16158975.001).
  • [ISSN] 1447-6959
  • [Journal-full-title] Anatomical science international
  • [ISO-abbreviation] Anat Sci Int
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / APC2 protein, human; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Trans-Activators; 0 / Wnt Proteins; 0 / beta Catenin
  • [Number-of-references] 72
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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. Ohge H, Furne JK, Springfield J, Rothenberger DA, Madoff RD, Levitt MD: Association between fecal hydrogen sulfide production and pouchitis. Dis Colon Rectum; 2005 Mar;48(3):469-75
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  • METHODS: During incubation at 37 degrees C, the production of hydrogen sulfide, methylmercaptan, carbon dioxide, and hydrogen were studied using fresh fecal specimens obtained from 50 patients with ileoanal pouches constructed after total proctocolectomy for ulcerative colitis (n = 45) or for familial adenomatous polyposis (n = 5).
  • b) past episode(s) of pouchitis but no active disease for the previous year (n = 9);.
  • Antibiotic therapy was associated with very low hydrogen sulfide release (0.68 +/- 0.29 micromol g(-1) 4 h(-1)).
  • Pouch contents from familial adenomatous polyposis patients produced significantly less hydrogen sulfide (0.75 +/- 0.09 micromol g(-1) 4 h(-1)) than did any group of nonantibiotic-treated ulcerative colitis patients.
  • No statistically significant differences in carbon dioxide and hydrogen were observed among the groups not receiving antibiotics.
  • CONCLUSIONS: Pouch contents of patients with ongoing pouchitis or an episode within the previous year released significantly more hydrogen sulfide than did the contents of patients who never had an attack of pouchitis and those with longstanding inactive disease.
  • The response to therapy with metronidazole or ciprofloxacin was associated with marked reductions in hydrogen sulfide release and sulfate-reducing bacteria.
  • The lower hydrogen sulfide production by pouch contents of familial adenomatous polyposis vs. patients with ulcerative colitis suggests a fundamental difference in gut sulfide metabolism that could have implications for the etiology of ulcerative colitis as well as the pouchitis of patients with ulcerative colitis.


43. Namba H: [Familial thyroid cancer]. Nihon Rinsho; 2006 May 28;Suppl 1:489-91
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  • [Title] [Familial thyroid cancer].
  • [MeSH-minor] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / genetics. Combined Modality Therapy. Hamartoma Syndrome, Multiple / complications. Hamartoma Syndrome, Multiple / genetics. Humans. Lymph Node Excision. Molecular Diagnostic Techniques. Thyroid Hormones / administration & dosage. Thyroidectomy

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  • (PMID = 16776197.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Thyroid Hormones
  • [Number-of-references] 14
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44. 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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45. 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.


46. Kim DW, Kim IJ, Kang HC, Jang SG, Kim K, Yoon HJ, Ahn SA, Han SY, Hong SH, Hwang JA, Sohn DK, Jeong SY, Choi HS, Hong CW, Lim SB, Park JG: Germline mutations of the MYH gene in Korean patients with multiple colorectal adenomas. Int J Colorectal Dis; 2007 Oct;22(10):1173-8
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  • [Title] Germline mutations of the MYH gene in Korean patients with multiple colorectal adenomas.
  • BACKGROUND: Most investigations on MutY human homolog (MYH)-associated polyposis (MAP) have been conducted in Western countries.
  • Limited data on MAP in Asia are currently available.
  • The present study investigated germline mutations of the MYH gene among patients with 10 to 99 adenomatous colorectal polyps and familial adenomatous polyposis (FAP) without adenomatous polyposis coli (APC) germline mutations in Korea.
  • MATERIALS AND METHODS: The study population included 46 patients with 10 to 99 adenomatous polyps in the colorectum and 16 FAP patients with no identified APC germline mutations.
  • Subjects were screened for MYH germline mutations, and we additionally screened for MYH mutations in 96 normal control individuals.
  • RESULTS: Two of 46 (4.3%) patients with multiple polyps displayed heterozygous biallelic germline mutations of the MYH gene.
  • A 39-year-old male patient with biallelic MYH mutations (p.G272E and p.A359V) received total proctocolectomy for rectal cancer and 36 colorectal polyps.
  • A 58-year-old female patient with biallelic MYH mutations (p.Q253X and p.Q440P) received right hemicolectomy for ascending colon cancer and 16 colonic polyps.
  • The frequency of biallelic MYH mutation in 14 of 46 multiple-polyp patients, who had 15 to 99 polyps, was 14.3% (2 of 14).
  • No biallelic MYH mutations were detected in the 32 patients with 10 to 14 colorectal polyps, 16 FAP patients, or 96 normal controls.
  • CONCLUSION: We identified biallelic MYH germline mutations in 2 of 14 (14.3%) Korean patients with 15 to 99 colorectal polyps.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colonic Polyps / genetics. DNA Glycosylases / genetics. Mutation / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Asian Continental Ancestry Group. Base Sequence. Female. Genetic Predisposition to Disease / genetics. Humans. Male. Middle Aged

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  • (PMID = 17703316.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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47. 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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48. 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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49. 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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50. Jaiswal AS, Balusu R, Narayan S: Involvement of adenomatous polyposis coli in colorectal tumorigenesis. Front Biosci; 2005;10:1118-34
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  • [Title] Involvement of adenomatous polyposis coli in colorectal tumorigenesis.
  • Mutation in the adenomatous polyposis coli (APC) gene is considered to be one of the earliest events in the colon cancer development.
  • The familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC) are the most commonly inherited colorectal cancers.
  • FAP and HNPCC develop due to mutations in APC and DNA mismatch repair (MMR) genes, respectively.
  • APC is known to regulate the levels of beta-catenin, an important mediator of cell-cell adhesion and transcriptional regulator.
  • Mutations in APC gene are also linked with chromosomal instability in colon cancer cells.
  • The role of APC is also implicated in cell migration, cell-cell adhesion, cell cycle control, and apoptosis.
  • This article summarizes the structure-function studies and the role of APC mutations in colon cancer development.
  • [MeSH-major] Adenomatous Polyposis Coli / physiopathology. Adenomatous Polyposis Coli Protein / physiology. Colorectal Neoplasms / etiology

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  • (PMID = 15769611.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-097031; United States / NCI NIH HHS / CA / CA-100247
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / beta Catenin
  • [Number-of-references] 174
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51. 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


52. 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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53. 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


54. 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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55. 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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56. 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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57. 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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58. 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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59. 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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  • [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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60. 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
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Radiation-Sensitizing Agents; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / Ribonucleotide Reductases; U3P01618RT / Fluorouracil
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61. 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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62. 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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63. 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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64. 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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65. 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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66. 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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67. 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


68. 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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69. 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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70. 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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71. 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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72. 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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73. 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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74. 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.


75. 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


76. 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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77. 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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78. Sato Y, Takayama T, Waga E, Sagawa T, Okamoto T, Miyanishi K, Sato T, Takimoto R, Sato Y, Sato Y, Oku T, Araki H, Takada K, Takanashi K, Kato J, Niitsu Y: [A family of attenuated familial adenomatous polyposis (AFAP)]. Nihon Shokakibyo Gakkai Zasshi; 2005 Apr;102(4):453-8
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  • [Title] [A family of attenuated familial adenomatous polyposis (AFAP)].
  • [MeSH-major] Adenomatous Polyposis Coli / genetics
  • [MeSH-minor] Aged. Female. Genes, APC. Humans. Male. Middle Aged


79. 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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80. 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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81. 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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82. 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


83. 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.


84. 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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85. Pho LN, Coffin CM, Burt RW: Abdominal desmoid in familial adenomatous polyposis presenting as a pancreatic cystic lesion. Fam Cancer; 2005;4(2):135-8
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  • [Title] Abdominal desmoid in familial adenomatous polyposis presenting as a pancreatic cystic lesion.
  • A 17-year-old male with familial adenomatous polyposis (FAP) presented with chest pain and significant weight loss.
  • The patient therefore underwent surgical resection of the distal pancreas, which included the lesion, because of the known association of pancreatic cancer with FAP.
  • Histopathological examination of the resected specimen showed a benign pancreatic cyst and fibrous plaque with desmoid fibromatosis adherent to the surface of the pancreas, serosa of the stomach, and colon.
  • The fibrous plaque was histologically identical to the fibrous mesenteric plaque known to occur in FAP and associated mesenteric fibromatosis.
  • We present pathologic evidence that the pancreatic cyst formation was induced by FAP-associated desmoid invasion.
  • Desmoid growth should be considered in the differential diagnosis of a pancreatic cystic mass lesion in patients with FAP or its Gardner syndrome variant.
  • This case report provides the first pathologic evidence for benign epithelial cyst formation in the pancreas caused by fibromatosis invasion of that organ as a part of FAP.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / pathology. Fibromatosis, Aggressive / complications. Fibromatosis, Aggressive / diagnosis. Pancreatic Cyst / diagnosis. Pancreatic Cyst / etiology
  • [MeSH-minor] Adolescent. Chest Pain. Diagnosis, Differential. Humans. Male. Weight Loss

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  • (PMID = 15951964.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 73992; United States / NCI NIH HHS / CA / P30 CA 42014; United States / NCI NIH HHS / CA / R01 CA 40641
  • [Publication-type] Case Reports; 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] Netherlands
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86. 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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87. Goodin GS, McCarville MB, Thibodeau SN, Skapek SX, Khoury JD, Spunt SL: Prolactinoma as the first manifestation of Gardner's syndrome. Pediatr Blood Cancer; 2008 Feb;50(2):409-12
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  • [Title] Prolactinoma as the first manifestation of Gardner's syndrome.
  • Familial adenomatous polyposis (FAP) is an inherited condition causing numerous adenomatous colorectal polyps and a markedly elevated risk of colon cancer.
  • FAP may be associated with various extracolonic manifestations such as desmoid fibromatosis and osteomas (termed Gardner's syndrome) and brain tumors, usually medulloblastoma or glioma [termed Brain Tumor Polyposis (BTP) syndrome type 2].
  • We describe a pediatric patient who initially presented with prolactinoma and later was found to have Gardner's syndrome.
  • A germline mutation of the APC (adenomatous polyposis coli) gene was identified.
  • Our case illustrates the association between prolactinoma and FAP, which may represent a rare subtype of Gardner's and BTP syndromes.
  • [MeSH-major] Gardner Syndrome / genetics. Prolactinoma / genetics
  • [MeSH-minor] Child. Genes, APC. Humans. Male. Mutation

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 16862550.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 23099; United States / NCI NIH HHS / CA / P30 CA 21765
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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88. 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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89. 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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90. 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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91. Plevová P, Drobcinská L, Stekrová J, Silhánová E: [Single nucleotide c.645+32c&gt;T substitution in the APC gene is a non-pathogenic polymorphism appearing in about 16% of the Czech population]. Cas Lek Cesk; 2008;147(5):266-8
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  • [Title] [Single nucleotide c.645+32c>T substitution in the APC gene is a non-pathogenic polymorphism appearing in about 16% of the Czech population].
  • [Transliterated title] Jednonukleotidová substituce c.645+32c>T v genu APC je nepatogenním polymorfismem s výskytem priblizne u 16% ceské populace.
  • BACKGROUND: Familial adenomatous polyposis is an autosomal dominant disease characterised by predisposition to colon polyposis and colorectal cancer and caused by germline mutations in the APC gene.
  • The aim of the study was to establish the frequency of c.645+32C>T substitution in intron 5 of the APC gene in patients with multiple colon polyposis and in the general population and to determine if this substitution is a nonpathogenic polymorphism or a pathogenic mutation associated with multiple polyposis coli.
  • METHODS AND RESULTS: The frequency of c.645+32C>T substitution in the APC gene was established in 170 patients with the clinical phenotype of familial adenomatous polyposis or its attenuated form using denaturating gradient gel electrophoresis and direct sequencing.
  • The c.645+32C>T substitution was detected in 27 of 170 patients with multiple colon polyposis (i.e. 15.9%).
  • The difference between patients with polyposis and the control group was not statistically significant (p = 0.979; chí-square test).
  • CONCLUSIONS: Our results suggest that the c.645+32C>T substitution is a non-pathogenic single nucleotide polymorphism appearing in about 16% of the Czech population.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Polymorphism, Single Nucleotide

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  • (PMID = 18630182.001).
  • [ISSN] 0008-7335
  • [Journal-full-title] Casopís lékar̆ů c̆eských
  • [ISO-abbreviation] Cas. Lek. Cesk.
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
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92. 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 sulfamethoxazole (SMX) metabolism in human APC (peripheral blood mononuclear cells, Epstein-Barr virus-modified B lymphocytes, monocyte-derived dendritic cells, and two cell lines).
  • APC were incubated with SMX (100 microM-2 mM; 5 min-24 h), in the presence of pathological factors: bacterial endotoxins (lipopolysaccharide and staphylococcal enterotoxin B), flu viral proteins, cytokines [interleukin (IL)-1beta, IL-6, IL-10; tumor necrosis factor-alpha; interferon-gamma; and transforming growth factor-beta], inflammatory molecules (prostaglandin E2, human serum complement, and activated protein C), oxidants (buthionine sulfoximine and H(2)O(2)), and hyperthermia (37.5-39.5 degrees C).
  • SMX-protein adduct formation was time- and concentration-dependent for each cell type tested, in both physiological and danger conditions.
  • A danger environment significantly increased the formation of SMX-protein adducts and significantly shortened the delay for their detection.
  • Various enzyme inhibitors were associated with a significant decrease in SMX-adduct levels, with a pattern varying depending on the cell type and the culture conditions.
  • These results illustrate that danger signals enhance the formation of intracellular SMX-protein adducts in human APC.
  • These findings might be relevant to the increased frequency of drug allergy in certain disease states.

  • MedlinePlus Health Information. consumer health - Drug Reactions.
  • Hazardous Substances Data Bank. SULFAMETHOXAZOLE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 19666748.001).
  • [ISSN] 1521-0103
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / / 078598/Z/05/Z; United Kingdom / Medical Research Council / / G0700654
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Cyclohexanones; 0 / Cytokines; 0 / Endotoxins; 0 / Enzyme Inhibitors; 0 / Inflammation Mediators; 0 / Oxidants; 0 / Viral Proteins; B2B5DSX2FC / dimedone; JE42381TNV / Sulfamethoxazole
  • [Other-IDs] NLM/ PMC2775259
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93. Li Q, Ishikawa TO, Oshima M, Taketo MM: The threshold level of adenomatous polyposis coli protein for mouse intestinal tumorigenesis. Cancer Res; 2005 Oct 1;65(19):8622-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The threshold level of adenomatous polyposis coli protein for mouse intestinal tumorigenesis.
  • The adenomatous polyposis coli (APC) gene, whose mutations are responsible for familial adenomatous polyposis, is a major negative controller of the Wnt/beta-catenin pathway.
  • To investigate the dose-dependent effects of APC protein in suppressing intestinal tumorigenesis, we constructed mutant mice carrying hypomorphic Apc alleles Apc(neoR) and Apc(neoF) whose expression levels were reduced to 20% and 10% of the wild type, respectively.
  • Although both hypomorphic heterozygotes developed intestinal polyps, tumor multiplicities were much lower than that in Apc(Delta716) mice, heterozygotes of an Apc null allele.
  • Like in Apc(Delta716) mice, loss of the wild-type Apc allele was confirmed for all polyps examined in the Apc(neoR) and Apc(neoF) mice.
  • In the embryonic stem cells homozygous for these hypomorphic Apc alleles, the level of the APC protein was inversely correlated with both the beta-catenin accumulation and beta-catenin/T-cell factor transcriptional activity.
  • These results suggest that the reduced APC protein level increases intestinal polyp multiplicity through quantitative stimulation of the beta-catenin/T-cell factor transcription.
  • We further estimated the threshold of APC protein level that forms one polyp per mouse as approximately 15% of the wild type.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Genes, APC. Intestinal Neoplasms / genetics
  • [MeSH-minor] Alleles. Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Female. Intestinal Polyps / genetics. Intestinal Polyps / metabolism. Intestinal Polyps / pathology. Loss of Heterozygosity. Male. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. beta Catenin / metabolism

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. Marmoset Gene list: Data: Gene Annotation .
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  • (PMID = 16204028.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / beta Catenin
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94. Koom WS, Seong J, Kim YB, Pyun HO, Song SY: CA 19-9 as a predictor for response and survival in advanced pancreatic cancer patients treated with chemoradiotherapy. Int J Radiat Oncol Biol Phys; 2009 Mar 15;73(4):1148-54
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  • The median survival time (MST) was 12 months (range, 4-48 months), and 1-year survival rate was 44%.
  • In addition, patients with multiple unfavorable CA 19-9 levels had significantly worse outcomes than those without.