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1. Sie MP, van der Wiel HE, Smedts FM, de Boer AC: Human recombinant insulin and amyloidosis: an unexpected association. Neth J Med; 2010 Mar;68(3):138-40
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  • Additional pathological-anatomical investigations demonstrated insulin in one (the most recent) amyloid tumour.


2. Malle E, Sodin-Semrl S, Kovacevic A: Serum amyloid A: an acute-phase protein involved in tumour pathogenesis. Cell Mol Life Sci; 2009 Jan;66(1):9-26
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  • [Title] Serum amyloid A: an acute-phase protein involved in tumour pathogenesis.
  • The synthesis of acute-phase protein serum amyloid A (SAA) is largely regulated by inflammation- associated cytokines and a high concentration of circulating SAA may represent an ideal marker for acute and chronic inflammatory diseases.
  • This review is meant to provide a broad overview of the many ways that SAA could contribute to tumour development, and accelerate tumour progression and metastasis, and to gain a better understanding of this acute-phase reactant as a possible link between chronic inflammation and neoplasia.
  • [MeSH-major] Biomarkers, Tumor / blood. Neoplasms / metabolism. Serum Amyloid A Protein / physiology
  • [MeSH-minor] ATP Binding Cassette Transporter 1. ATP-Binding Cassette Transporters / metabolism. Advanced Glycosylation End Product-Specific Receptor. Animals. Biomarkers. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. Mice. Receptors, Formyl Peptide / metabolism. Receptors, Immunologic / metabolism. Receptors, Lipoxin / metabolism. Scavenger Receptors, Class B / metabolism

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  • (PMID = 18726069.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / FWF/ P 19074
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / ATP Binding Cassette Transporter 1; 0 / Advanced Glycosylation End Product-Specific Receptor; 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / FPR2 protein, human; 0 / Receptors, Formyl Peptide; 0 / Receptors, Immunologic; 0 / Receptors, Lipoxin; 0 / SCARB1 protein, human; 0 / Scavenger Receptors, Class B; 0 / Serum Amyloid A Protein
  • [Number-of-references] 203
  • [Other-IDs] NLM/ EMS34540; NLM/ PMC4864400
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3. Bate C, Kempster S, Last V, Williams A: Interferon-gamma increases neuronal death in response to amyloid-beta1-42. J Neuroinflammation; 2006;3:7
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  • [Title] Interferon-gamma increases neuronal death in response to amyloid-beta1-42.
  • The amyloid hypothesis proposes that neuronal damage results from the accumulation of insoluble, hydrophobic, fibrillar peptides such as amyloid-beta1-42.
  • In the current study we examined the effects of interferon (IFN)-gamma, tumour necrosis factor (TNF)alpha, interleukin (IL)-1beta and IL-6 on neurons.
  • RESULTS: While none of the cytokines tested were directly neurotoxic, pre-treatment with IFN-gamma sensitised neurons to the toxic effects of amyloid-beta1-42 or HuPrP82-146 (a neurotoxic peptide found in prion diseases).
  • Pre-treatment with IFN-gamma increased the levels of cytoplasmic phospholipase A2 in SH-SY5Y cells and increased prostaglandin E2 production in response to amyloid-beta1-42.
  • CONCLUSION: Treatment of neuronal cells with IFN-gamma increased neuronal death in response to amyloid-beta1-42 or HuPrP82-146.
  • IFN-gamma increased the levels of cytoplasmic phospholipase A2 in cultured neuronal cells and increased expression of cytoplasmic phospholipase A2 was associated with increased production of prostaglandin E2 in response to amyloid-beta1-42 or HuPrP82-146.

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  • (PMID = 16569229.001).
  • [ISSN] 1742-2094
  • [Journal-full-title] Journal of neuroinflammation
  • [ISO-abbreviation] J Neuroinflammation
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1435873
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4. Shiels SA, Hasan SI, Darowski A: Collapse in a 79-year-old: a rare case of amyloid tumour of the pelvis. Age Ageing; 2005 Nov;34(6):648-9
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  • [Title] Collapse in a 79-year-old: a rare case of amyloid tumour of the pelvis.
  • Further investigations showed that the mass contained amyloid protein.
  • With no evidence of systemic amyloidosis or malignancy a diagnosis of amyloidoma/amyloid tumour was made.
  • This is the largest amyloid tumour reported in the literature to date.
  • Clearly amyloidomas are rare, but patients can present acutely and may have a poor prognosis, especially when the tumour is of considerable size.
  • [MeSH-major] Amyloid Neuropathies / complications. Leg. Lumbosacral Plexus. Pain / etiology. Pelvis

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  • (PMID = 16267196.001).
  • [ISSN] 0002-0729
  • [Journal-full-title] Age and ageing
  • [ISO-abbreviation] Age Ageing
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 10
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5. Oluk MA, Murphy J: Nasopharyngeal amyloidosis: an unusual cause for epistaxis. J Laryngol Otol; 2010 Feb;124(2):209-12
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  • The amyloid tumour, which recurred in correlation with the progressive transformation of the multiple myeloma, was treated surgically.
  • Subsequent localised radiotherapy decreased the size and growth rate of the tumour.
  • CONCLUSION: Amyloid should be considered as a cause of resistant or recurrent epistaxis provided a mass lesion is seen on radiological imaging.

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  • (PMID = 19527533.001).
  • [ISSN] 1748-5460
  • [Journal-full-title] The Journal of laryngology and otology
  • [ISO-abbreviation] J Laryngol Otol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 37
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6. Hanoun M, Schmitz KJ, Dührsen U, Röth A: Amyloid tumour. Br J Haematol; 2010 Aug;150(4):387
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  • [Title] Amyloid tumour.

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  • (PMID = 19344394.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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7. Melchior B, Garcia AE, Hsiung BK, Lo KM, Doose JM, Thrash JC, Stalder AK, Staufenbiel M, Neumann H, Carson MJ: Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease. ASN Neuro; 2010 Jul 12;2(3):e00037
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  • [Title] Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease.
  • Vaccine-based autoimmune (anti-amyloid) treatments are currently being examined for their therapeutic potential in Alzheimer's disease.
  • In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b).
  • Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone.
  • Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits.
  • Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production.
  • TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells.
  • Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid.
  • Instead, plaque-associated TREM2(+) microglia have the potential to evoke neuroprotective immune responses that may serve to support CNS function during pro-inflammatory anti-amyloid immune therapies.

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  • (PMID = 20640189.001).
  • [ISSN] 1759-0914
  • [Journal-full-title] ASN neuro
  • [ISO-abbreviation] ASN Neuro
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS039508; United States / NINDS NIH HHS / NS / R01 NS045735; United States / NINDS NIH HHS / NS / NS045735; United States / NINDS NIH HHS / NS / NS39508
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic; 0 / TREM1 protein, mouse; 0 / Trem2 protein, mouse
  • [Other-IDs] NLM/ PMC2905103
  • [Keywords] NOTNLM ; Aβ, amyloid β peptide / CCL2, chemokine ligand 2 / CFSE, carboxyfluorescein succinimidyl ester / CNS, central nervous system / Clast1 / DAMP, danger-associated molecular pattern / DMEM, Dulbecco's modified Eagle's medium / EAE, experimentally induced autoimmune encephalomyelitis / FBS, fetal bovine serum / GFP, green fluorescent protein / HPRT, hypoxanthine phosphoribosyl transferase / IFNγ, interferon γ / IL, interleukin / KO, knockout / LPS, lipopolysaccharide / PFA, paraformaldehyde / TNF, tumour necrosis factor / TREM2, triggering receptor expressed on myeloid cells 2 / Thio-S, thioflavine-S / Tmem176b, transmembrane domain protein 176b / Torid / WT, wild-type / antigen presentation / autoimmunity / neuroinflammation / qPCR, quantitative PCR
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8. Kotilinek LA, Westerman MA, Wang Q, Panizzon K, Lim GP, Simonyi A, Lesne S, Falinska A, Younkin LH, Younkin SG, Rowan M, Cleary J, Wallis RA, Sun GY, Cole G, Frautschy S, Anwyl R, Ashe KH: Cyclooxygenase-2 inhibition improves amyloid-beta-mediated suppression of memory and synaptic plasticity. Brain; 2008 Mar;131(Pt 3):651-64
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  • [Title] Cyclooxygenase-2 inhibition improves amyloid-beta-mediated suppression of memory and synaptic plasticity.
  • Non-steroidal anti-inflammatory agents (NSAIDs) are associated with a marked reduction in the risk of developing Alzheimer's disease, a form of dementia characterized by the accumulation of amyloid plaques containing the amyloid-beta protein (Abeta).
  • Studies of the effects of NSAIDs upon the inflammatory response surrounding amyloid plaques and upon the generation of Abeta from the amyloid precursor protein (APP) have led to two proposed mechanisms by which NSAIDs may protect against Alzheimer's disease: one, the selective lowering of Abeta42 by a subset of NSAIDs; and two, the reduction of inflammation.
  • The beneficial effects on memory did not depend upon lowered levels of Abeta42 or the inflammatory cytokines, tumour necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta).

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  • (PMID = 18292081.001).
  • [ISSN] 1460-2156
  • [Journal-full-title] Brain : a journal of neurology
  • [ISO-abbreviation] Brain
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS033249-13; United States / NIMH NIH HHS / MH / MH065465-03; United States / NIA NIH HHS / AG / AG013741-07A2; United States / NIMH NIH HHS / MH / R01 MH065465-04; United States / NIA NIH HHS / AG / R01 AG013741-07A2; United States / NIA NIH HHS / AG / AG015453-05S1; United States / NIA NIH HHS / AG / R01 AG021975-04; United States / NIA NIH HHS / AG / R01 AG013741-06; United States / NINDS NIH HHS / NS / NS033249-12; United States / NIMH NIH HHS / MH / R01 MH065465; United States / NIA NIH HHS / AG / R01-AG13471; United States / NIA NIH HHS / AG / AG015453-030001; United States / NIA NIH HHS / AG / P01 AG015453-05; United States / NIA NIH HHS / AG / AG015453-04; United States / NIA NIH HHS / AG / U01 AG028583-03; United States / NIA NIH HHS / AG / AG013741-06; United States / NIA NIH HHS / AG / P01 AG018357; United States / NIA NIH HHS / AG / U01 AG028583; United States / NIA NIH HHS / AG / AG021975-04; United States / NIA NIH HHS / AG / AG015453-040001; United States / NIA NIH HHS / AG / P01 AG015453-04; United States / NIMH NIH HHS / MH / R01 MH065465-01; United States / NIA NIH HHS / AG / AG028583-03; United States / NIA NIH HHS / AG / R01 AG013741-08; United States / NIMH NIH HHS / MH / R01 MH065465-05; United States / NIMH NIH HHS / MH / R01-MH65465; United States / NIA NIH HHS / AG / P01 AG015453; United States / NIA NIH HHS / AG / R01 AG013741; United States / NINDS NIH HHS / NS / NS033249-11; United States / NINDS NIH HHS / NS / R01 NS033249; United States / NINDS NIH HHS / NS / R01-NS33249; United States / NIA NIH HHS / AG / R01 AG021975-03; United States / NIA NIH HHS / AG / AG015453-05; United States / NIMH NIH HHS / MH / R01 MH065465-02; United States / NIA NIH HHS / AG / U01 AG028583-02; United States / NIA NIH HHS / AG / P01 AG015453-05S2; United States / NIA NIH HHS / AG / P01 AG015453-040001; United States / NIA NIH HHS / AG / AG028583-02; United States / NIA NIH HHS / AG / P01 AG015453-030001; United States / NIA NIH HHS / AG / P01-AG15453; United States / NIMH NIH HHS / MH / MH065465-01; United States / NIMH NIH HHS / MH / MH065465-02; United States / NIA NIH HHS / AG / P01-AG18357; United States / NIA NIH HHS / AG / AG015453-05S2; United States / NINDS NIH HHS / NS / R01 NS033249-12; United States / NIA NIH HHS / AG / AG013741-08; United States / NIMH NIH HHS / MH / R01 MH065465-03; United States / NIMH NIH HHS / MH / MH065465-05; United States / NIA NIH HHS / AG / P01 AG015453-05S1; United Kingdom / Wellcome Trust / / ; United States / NINDS NIH HHS / NS / NS033249-13; United States / NIA NIH HHS / AG / AG021975-03; United States / NIMH NIH HHS / MH / MH065465-04; United States / NIA NIH HHS / AG / R01 AG021975; United States / NINDS NIH HHS / NS / R01 NS033249-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Furans; 0 / Inflammation Mediators; 0 / Interleukin-1beta; 0 / Peptide Fragments; 0 / Tumor Necrosis Factor-alpha; 0 / amyloid beta-protein (1-42); 162011-83-8 / 3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl)phenyl)-2(5H)-furanone; 57Y76R9ATQ / Naproxen; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone; WK2XYI10QM / Ibuprofen
  • [Other-IDs] NLM/ NIHMS57155; NLM/ PMC2628581
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9. Velez D, Hinojar-Gutierrez A, Nam-Cha S, Acevedo-Barbera A: Laryngeal plasmacytoma presenting as amyloid tumour: a case report. Eur Arch Otorhinolaryngol; 2007 Aug;264(8):959-61
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  • [Title] Laryngeal plasmacytoma presenting as amyloid tumour: a case report.
  • Immunohistochemical studies showed that the tumour cells of the plasmacytoma were monoclonal (lambda-restricted).
  • The amyloid deposits were also shown to be reactive with lambda immunoglobulin light chain, suggesting the pathogenetic relationship between the plasmacytoma and amyloid deposition in the larynx.
  • The majority of the cases reported of amyloid deposition with plasmacytoma, the lesions were found in the nasopharynx, in contrast to our case in which the lesions were sited in the larynx and with the peculiarity of being multiples.
  • Moreover, amyloid and plasmacytoma were clearly delimitated and the amyloid tissue was more extensive than the tumour tissue.

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  • (PMID = 17431662.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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10. Kang MS, Park MS, Kwon SW, Ma SA, Cho DY, Kim DY, Kim Y: Amyloid-producing odontogenic tumour (calcifying epithelial odontogenic tumour) in the mandible of a Bengal tiger (Panthera tigris tigris). J Comp Pathol; 2006 Feb-Apr;134(2-3):236-40

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  • [Title] Amyloid-producing odontogenic tumour (calcifying epithelial odontogenic tumour) in the mandible of a Bengal tiger (Panthera tigris tigris).
  • A prominent feature of this tumour consisted of abundant nodular deposits of congophilic amyloid-like material with partial mineralization (Liesegang rings).
  • Immunohistochemically, the neoplastic cells and the amyloid-like material were positive for pancytokeratin and negative for vimentin.
  • The findings supported the diagnosis of an amyloid-producing odontogenic tumour (APOT), also known as calcifying epithelial odontogenic tumour in man and animals.
  • [MeSH-minor] Amyloid / metabolism. Animals. Biomarkers, Tumor / metabolism. Fatal Outcome. Immunohistochemistry / veterinary. Keratins / metabolism

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  • (PMID = 16540113.001).
  • [ISSN] 0021-9975
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid; 0 / Biomarkers, Tumor; 68238-35-7 / Keratins
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11. Samandouras G, Teddy PJ, Cadoux-Hudson T, Ansorge O: Amyloid in neurosurgical and neurological practice. J Clin Neurosci; 2006 Feb;13(2):159-67
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  • [Title] Amyloid in neurosurgical and neurological practice.
  • The amyloidoses are a diverse group of diseases characterized by the deposition of specific proteins with distinct affinity to the dye Congo red, collectively called amyloid.
  • The amyloid may be distributed in different organs with a remarkable diversity.
  • A tropism of amyloid proteins to the neural tissue produces certain patterns of central nervous system diseases: cerebral amyloid angiopathy, a substrate of spontaneous intracerebral haemorrhage; mature neuritic plaques found in Alzheimer disease and a subset of prion diseases; a topographically restricted accumulation of extracellular proteins giving rise to tumour-mimicking masses, the amyloidomas; and finally, spinal extradural amyloid collections that occasionally are found in the context of rheumatoid arthritis.
  • In this review article we present original illustrative cases of amyloid diseases of the central nervous system that may be encountered in neurosurgical and neurological practice.
  • [MeSH-major] Amyloid / metabolism. Amyloidosis / surgery. Amyloidosis / therapy
  • [MeSH-minor] Animals. Cerebral Amyloid Angiopathy / pathology. Cerebral Amyloid Angiopathy / surgery. Cerebral Amyloid Angiopathy / therapy. Humans. Plaque, Amyloid / pathology

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  • (PMID = 16403633.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Amyloid
  • [Number-of-references] 36
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12. Cuesta A, Zambrano A, Royo M, Pascual A: The tumour suppressor p53 regulates the expression of amyloid precursor protein (APP). Biochem J; 2009 Mar 15;418(3):643-50
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  • [Title] The tumour suppressor p53 regulates the expression of amyloid precursor protein (APP).
  • The expression of the APP (amyloid precursor protein), which plays a key role in the development of AD (Alzheimer's disease), is regulated by a variety of cellular mediators in a cell-dependent manner.
  • [MeSH-major] Amyloid beta-Protein Precursor / biosynthesis. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Animals. Camptothecin / pharmacology. Cell Line, Tumor. Chromatin Immunoprecipitation. DNA / drug effects. Electrophoretic Mobility Shift Assay. Gene Expression Regulation, Neoplastic. Humans. Mice. Neuroblastoma / metabolism. Promoter Regions, Genetic / physiology. Proto-Oncogene Proteins c-mdm2 / metabolism. Rats. Sp1 Transcription Factor / metabolism

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  • (PMID = 19049493.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Sp1 Transcription Factor; 0 / Tumor Suppressor Protein p53; 9007-49-2 / DNA; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2; XT3Z54Z28A / Camptothecin
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13. Wang R, Chadalavada K, Wilshire J, Kowalik U, Hovinga KE, Geber A, Fligelman B, Leversha M, Brennan C, Tabar V: Glioblastoma stem-like cells give rise to tumour endothelium. Nature; 2010 Dec 09;468(7325):829-33
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  • [Title] Glioblastoma stem-like cells give rise to tumour endothelium.
  • Yet the mechanisms of angiogenesis and the origin of tumour endothelial cells remain poorly defined.
  • Here we demonstrate that a subpopulation of endothelial cells within glioblastomas harbour the same somatic mutations identified within tumour cells, such as amplification of EGFR and chromosome 7.
  • Extensive in vitro and in vivo lineage analyses, including single cell clonal studies, further show that a subpopulation of the CD133(+) stem-like cell fraction is multipotent and capable of differentiation along tumour and endothelial lineages, possibly via an intermediate CD133(+)/CD144(+) progenitor cell.
  • The findings are supported by genetic studies of specific exons selected from The Cancer Genome Atlas, quantitative FISH and comparative genomic hybridization data that demonstrate identical genomic profiles in the CD133(+) tumour cells, their endothelial progenitor derivatives and mature endothelium.
  • Exposure to the clinical anti-angiogenesis agent bevacizumab or to a γ-secretase inhibitor as well as knockdown shRNA studies demonstrate that blocking VEGF or silencing VEGFR2 inhibits the maturation of tumour endothelial progenitors into endothelium but not the differentiation of CD133(+) cells into endothelial progenitors, whereas γ-secretase inhibition or NOTCH1 silencing blocks the transition into endothelial progenitors.
  • The lineage plasticity and capacity to generate tumour vasculature of the putative cancer stem cells within glioblastoma are novel findings that provide new insight into the biology of gliomas and the definition of cancer stemness, as well as the mechanisms of tumour neo-angiogenesis.
  • [MeSH-minor] AC133 Antigen. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Animals. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antigens, CD / metabolism. Bevacizumab. Cadherins / deficiency. Cadherins / metabolism. Cell Line, Tumor. Cell Lineage. Chromosome Aberrations. Coculture Techniques. Female. Glycoproteins / metabolism. Humans. In Situ Hybridization, Fluorescence. Integrin beta4 / metabolism. Male. Mice. Mice, Inbred NOD. Mice, SCID. Peptides / metabolism. Receptor, Notch1 / deficiency. Receptor, Notch1 / genetics. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • [CommentIn] Nat Rev Cancer. 2011 Jan;11(1):4 [21218530.001]
  • [CommentIn] Nat Rev Neurosci. 2011 Jan;12(1):3 [21218567.001]
  • [CommentIn] Nature. 2010 Dec 9;468(7325):770-1 [21150987.001]
  • (PMID = 21102433.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE24244/ GSE24446/ GSE24452/ GSE24557/ GSE24558
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 Antigen; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Cadherins; 0 / Glycoproteins; 0 / Integrin beta4; 0 / PROM1 protein, human; 0 / Peptides; 0 / Prom1 protein, mouse; 0 / Receptor, Notch1; 0 / Vascular Endothelial Growth Factor A; 0 / cadherin 5; 2S9ZZM9Q9V / Bevacizumab; EC 3.4.- / Amyloid Precursor Protein Secretases
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14. Rowan MJ, Klyubin I, Wang Q, Hu NW, Anwyl R: Synaptic memory mechanisms: Alzheimer's disease amyloid beta-peptide-induced dysfunction. Biochem Soc Trans; 2007 Nov;35(Pt 5):1219-23
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  • [Title] Synaptic memory mechanisms: Alzheimer's disease amyloid beta-peptide-induced dysfunction.
  • There is growing evidence that mild cognitive impairment in early AD (Alzheimer's disease) may be due to synaptic dysfunction caused by the accumulation of non-fibrillar, oligomeric Abeta (amyloid beta-peptide), long before widespread synaptic loss and neurodegeneration occurs.
  • Here, we summarize experiments that investigated whether certain putative receptors for Abeta, the alphav integrin extracellular cell matrix-binding protein and the cytokine TNFalpha (tumour necrosis factor alpha) type-1 death receptor mediate Abeta oligomer-induced inhibition of LTP (long-term potentiation).
  • [MeSH-major] Alzheimer Disease / physiopathology. Amyloid beta-Peptides / physiology. Synapses / physiology

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  • (PMID = 17956317.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Cell Adhesion Molecules
  • [Number-of-references] 50
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15. Hartig W, Leifsson PS, Nielsen OL: Immunohistochemical identification of amyloid, using an anti-human serum amyloid P component (SAP) antibody, is possible in ruminants but not in dogs and cats. J Vet Med A Physiol Pathol Clin Med; 2005 Nov;52(9):447-53
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  • [Title] Immunohistochemical identification of amyloid, using an anti-human serum amyloid P component (SAP) antibody, is possible in ruminants but not in dogs and cats.
  • Amyloid consists primarily of the amyloid fibrils but also of the amyloid P component (AP).
  • This component, which is identical with the serum counterpart (SAP), is found in all types of human amyloid, and immunohistochemical identification of AP has been proposed as an adjunct to the universal, type-independent diagnosis of human amyloidosis.
  • In the present study of animal amyloidosis, we compared the amyloid-specific Congo red stain with an immunohistochemical protocol using an anti-human SAP antibody for the identification of amyloid in formalin fixed tissue samples.
  • The species and types of amyloidoses investigated were: (i) seven cows, one yak (Bos grunniens), and one sheep affected with amyloidosis of presumed AA type, (ii) one dog with a pancreatic endocrine tumour producing amyloid of presumed AIAPP type, (iii) two cats with presumed AIAPP-amyloidosis of the islets of Langerhans, one cat with presumed AA-amyloidosis, and one cat with an amyloid-producing odontogenic tumour.
  • Intense immunostaining co-localized with amyloid, identified by its congophilia and green birefringence, using a protocol without any antigen retrieval in each of the seven cows, the yak and the sheep.
  • The method seemed more sensitive in the ruminants than the Congo red stain, but was unable to detect amyloid in the dog and the cats regardless of the application of various antigen retrieval protocols.
  • However, specific identification of amyloid still rests on the Congo red method or similar histochemical techniques.
  • [MeSH-major] Amyloidosis / veterinary. Ruminants. Serum Amyloid P-Component / immunology. Staining and Labeling / veterinary
  • [MeSH-minor] Amyloid / analysis. Animals. Antibodies. Cats. Cattle. Coloring Agents. Congo Red. Dogs. Histocytochemistry / veterinary. Humans. Immunohistochemistry / veterinary. Retrospective Studies. Sheep. Species Specificity

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  • (PMID = 16268955.001).
  • [ISSN] 0931-184X
  • [Journal-full-title] Journal of veterinary medicine. A, Physiology, pathology, clinical medicine
  • [ISO-abbreviation] J Vet Med A Physiol Pathol Clin Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Amyloid; 0 / Antibodies; 0 / Coloring Agents; 0 / Serum Amyloid P-Component; 3U05FHG59S / Congo Red
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16. Apaydin R, Gürbüz Y, Bayramgürler D, Bilen N: Cytokeratin contents of basal cell carcinoma, epidermis overlying tumour, and associated stromal amyloidosis: an immunohistochemical study. Amyloid; 2005 Mar;12(1):41-7
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  • [Title] Cytokeratin contents of basal cell carcinoma, epidermis overlying tumour, and associated stromal amyloidosis: an immunohistochemical study.
  • We investigated the expression of CKs immunohistochemically in basal cell carcinomas (BCCs), epidermis overlying tumour, and skin tumor-associated amyloidosis (STA).
  • In BCCs without STA, CK1-8, CK14 and CK17 antibodies were expressed by tumour tissue in all biopsy specimens.
  • In the BCCs with STA, tumour tissue was immunoreactive always with CK1-8 and CK17 antibodies, and commonly immunoreactive with anti-CK 14 antibody.
  • In the epidermis overlying tumour tissue, there was positive immunoreactivity with anti-CK 1-8, CK 5/6/18, CK 10 and CK 14 antibodies in all biopsy specimens.
  • Weak positivity and a few number of CKs were shown in STA when compared with those of BCC and epidermis overlying tumour tissue expressing the more variable CKs.

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  • (PMID = 16076610.001).
  • [ISSN] 1350-6129
  • [Journal-full-title] Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
  • [ISO-abbreviation] Amyloid
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 68238-35-7 / Keratins
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17. Vissers YL, von Meyenfeldt MF, Luiking YC, Dejong CH, Buurman WA, Deutz NE: Presence of tumour inhibits the normal post-operative response in arginine and NO production in non-cachectic mice. Clin Sci (Lond); 2007 May;112(10):527-32
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  • [Title] Presence of tumour inhibits the normal post-operative response in arginine and NO production in non-cachectic mice.
  • We have described recently that cancer patients have low plasma arginine concentrations, even without weight loss being present, suggesting that decreased arginine availability may be a specific feature of the presence of tumour.
  • SAP (serum amyloid P component) concentrations were measured to assess the acute-phase response.
  • In healthy FVB mice, laparotomy significantly increased whole-body arginine production (from 42+/-3 to 54+/-3 nmol x 10 g(-1) of carcass weight x min(-1)), NO production (from 1.1+/-0.1 to 1.4+/-0.2 nmol x 10 g(-1) of carcass weight x min(-1)) and levels of SAP (from 4+/-1 to 115+/-23 ng/ml), whereas in all MCA tumour-bearing mice baseline values of arginine metabolism and SAP concentration were already elevated and the response to laparotomy was absent.
  • In conclusion, MCA tumour-bearing mice had a disturbed post-operative metabolic response, as evidenced by attenuated post-operative arginine and NO production, concomitant with an attenuated acute-phase response.
  • [MeSH-minor] Animals. Biomarkers / blood. Male. Mice. Mice, Inbred Strains. Postoperative Period. Random Allocation. Serum Amyloid P-Component / analysis

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  • (PMID = 17212586.001).
  • [ISSN] 1470-8736
  • [Journal-full-title] Clinical science (London, England : 1979)
  • [ISO-abbreviation] Clin. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Serum Amyloid P-Component; 31C4KY9ESH / Nitric Oxide; 94ZLA3W45F / Arginine
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18. Tobinick E: Tumour necrosis factor modulation for treatment of Alzheimer's disease: rationale and current evidence. CNS Drugs; 2009 Sep;23(9):713-25
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  • [Title] Tumour necrosis factor modulation for treatment of Alzheimer's disease: rationale and current evidence.
  • Tumour necrosis factor (TNF), a key regulator of varied physiological mechanisms in multiple organ systems, is an immune signalling molecule produced by glia, neurons, macrophages and other immune cells.
  • TNF may also play a role in endothelial and microvascular dysfunction in AD, and in amyloidogenesis and amyloid-induced memory dysfunction in AD.
  • [MeSH-major] Alzheimer Disease / drug therapy. Drug Delivery Systems. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Brain / metabolism. Brain / physiopathology. Etanercept. Humans. Immunoglobulin G / administration & dosage. Immunoglobulin G / pharmacology. Immunoglobulin G / therapeutic use. Receptors, Tumor Necrosis Factor / administration & dosage. Receptors, Tumor Necrosis Factor / therapeutic use. Risk Factors. Synaptic Transmission

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  • (PMID = 19689163.001).
  • [ISSN] 1179-1934
  • [Journal-full-title] CNS drugs
  • [ISO-abbreviation] CNS Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
  • [Number-of-references] 117
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19. Fogarty MP, McCormack RM, Noonan J, Murphy D, Gowran A, Campbell VA: A role for p53 in the beta-amyloid-mediated regulation of the lysosomal system. Neurobiol Aging; 2010 Oct;31(10):1774-86
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  • [Title] A role for p53 in the beta-amyloid-mediated regulation of the lysosomal system.
  • Beta-amyloid accumulates around neurons in Alzheimer's disease and is thought to contribute to the neurodegenerative process.
  • This study examined the role of the tumour suppressor protein, p53, in the neurodegenerative pathway, with focus on the interaction of p53 with the lysosomal system. beta-Amyloid increased expression of p53 and its transcription target, Bax, in cultured cortical neurons.
  • These effects of beta-amyloid were abolished by the p53 inhibitor, pifithrin-alpha, and siRNA-mediated knockdown of p53, demonstrating that p53 is a critical regulator of lysosomal integrity and the induction of cathepsin-L protease activity.
  • We conclude that p53 associates with the lysosome to regulate a lysosomal branch of the apoptotic cascade which contributes to beta-amyloid-mediated neurodegeneration.
  • [MeSH-major] Alzheimer Disease / metabolism. Amyloid beta-Peptides / metabolism. Lysosomes / metabolism. Tumor Suppressor Protein p53 / metabolism. bcl-2-Associated X Protein / metabolism

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  • [Copyright] (c) 2008 Elsevier Inc. All rights reserved.
  • (PMID = 19059678.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Benzothiazoles; 0 / Phosphoproteins; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / pifithrin; 3FPU23BG52 / Toluene; EC 3.4.22.15 / Cathepsin L
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20. Tutar E, Onat AM, Aydin A, Kervancioğlu S, Buyukhatipoglu H, Inan G, Pehlivan Y: Amyloid tumor of the breast mimicking breast carcinoma. South Med J; 2008 Feb;101(2):199-201
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  • [Title] Amyloid tumor of the breast mimicking breast carcinoma.
  • Amyloid tumors of the breast are extremely rare.
  • Amyloid involvement of the breast has no specific diagnostic features on mammography; on occasion, this causes diagnostic challenges.
  • In this paper, the case of a 58-year-old woman with an amyloid tumor of the breast, which developed secondary to long-standing rheumatoid arthritis, is presented.

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  • (PMID = 18364625.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Hiratsuka S, Watanabe A, Sakurai Y, Akashi-Takamura S, Ishibashi S, Miyake K, Shibuya M, Akira S, Aburatani H, Maru Y: The S100A8-serum amyloid A3-TLR4 paracrine cascade establishes a pre-metastatic phase. Nat Cell Biol; 2008 Nov;10(11):1349-55
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  • [Title] The S100A8-serum amyloid A3-TLR4 paracrine cascade establishes a pre-metastatic phase.
  • Here, we show that serum amyloid A (SAA) 3, which is induced in pre-metastatic lungs by S100A8 and S100A9, has a role in the accumulation of myeloid cells and acts as a positive-feedback regulator for chemoattractant secretion.
  • This inflammation-like state accelerated the migration of primary tumour cells to lung tissues, but this was suppressed by the inhibition of either TLR4 or SAA3.
  • [MeSH-major] Calgranulin A / metabolism. Paracrine Communication. Serum Amyloid A Protein / metabolism. Toll-Like Receptor 4 / metabolism

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  • (PMID = 18820689.001).
  • [ISSN] 1476-4679
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calgranulin A; 0 / Calgranulin B; 0 / NF-kappa B; 0 / Recombinant Fusion Proteins; 0 / S100 Proteins; 0 / S100a8 protein, mouse; 0 / Saa3 protein, mouse; 0 / Serum Amyloid A Protein; 0 / Tlr4 protein, mouse; 0 / Toll-Like Receptor 4; EC 1.13.12.- / Luciferases; EC 2.5.1.18 / Glutathione Transferase
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22. Song C, Shen Y, Yamen E, Hsu K, Yan W, Witting PK, Geczy CL, Freedman SB: Serum amyloid A may potentiate prothrombotic and proinflammatory events in acute coronary syndromes. Atherosclerosis; 2009 Feb;202(2):596-604
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  • [Title] Serum amyloid A may potentiate prothrombotic and proinflammatory events in acute coronary syndromes.
  • AIMS: Elevated serum amyloid A (SAA) levels, like C-reactive protein (CRP), predict coronary events.
  • This study examined SAA induction of TF and tumour necrosis factor-alpha (TNF) in PBMC from patients with CAD and in monocytoid THP-1 cells.
  • [MeSH-major] Acute Coronary Syndrome / immunology. Acute Coronary Syndrome / metabolism. Serum Amyloid A Protein / metabolism. Thrombosis / immunology. Thrombosis / metabolism
  • [MeSH-minor] Aged. Angina Pectoris / immunology. Angina Pectoris / metabolism. C-Reactive Protein / metabolism. Cell Line. Cells, Cultured. Cholesterol, HDL / metabolism. Humans. Leukocytes, Mononuclear / cytology. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. RNA, Messenger / metabolism. Thromboplastin / genetics. Thromboplastin / metabolism. Tumor Necrosis Factor-alpha / metabolism. Vasculitis / immunology. Vasculitis / metabolism

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  • (PMID = 18571179.001).
  • [ISSN] 1879-1484
  • [Journal-full-title] Atherosclerosis
  • [ISO-abbreviation] Atherosclerosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cholesterol, HDL; 0 / RNA, Messenger; 0 / SAA1 protein, human; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; 9007-41-4 / C-Reactive Protein; 9035-58-9 / Thromboplastin
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23. Hermey G, Sjøgaard SS, Petersen CM, Nykjaer A, Gliemann J: Tumour necrosis factor alpha-converting enzyme mediates ectodomain shedding of Vps10p-domain receptor family members. Biochem J; 2006 Apr 15;395(2):285-93
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  • [Title] Tumour necrosis factor alpha-converting enzyme mediates ectodomain shedding of Vps10p-domain receptor family members.
  • Except for sorCS2, shedding of the receptors was dramatically reduced in mutant CHO cells (CHO-M2) devoid of active TACE (tumour necrosis factor alpha-converting enzyme), demonstrating that this enzyme accounts for most sheddase activity.
  • Purified shed sorLA bound several ligands similarly to the entire luminal domain of the receptor, including PDGF-BB (platelet-derived growth factor-BB) and amyloid-beta precursor protein.

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  • (PMID = 16393139.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Vesicular Transport; 0 / LDL-Receptor Related Proteins; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / Membrane Transport Proteins; 0 / Nerve Tissue Proteins; 0 / Protein Isoforms; 0 / Receptors, Cell Surface; 0 / Receptors, LDL; 0 / Receptors, Neuropeptide; 0 / SORCS1 protein, human; 0 / SORCS2 protein, human; 0 / SORL1 protein, human; 0 / SorCS3 protein, human; 0 / Vesicular Transport Proteins; 0 / sortilin; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
  • [Other-IDs] NLM/ PMC1422770
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24. Niemi K, Baumann MH, Kovanen PT, Eklund KK: Serum amyloid A (SAA) activates human mast cells which leads into degradation of SAA and generation of an amyloidogenic SAA fragment. Biochim Biophys Acta; 2006 Apr;1762(4):424-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum amyloid A (SAA) activates human mast cells which leads into degradation of SAA and generation of an amyloidogenic SAA fragment.
  • Serum amyloid A (SAA) is a precursor for the amyloid A in AA type of amyloidosis.
  • Distribution of mast cells in tissues is similar to the distribution of amyloid deposits in secondary AA-amyloidosis.
  • Human mast cell line (HMC-1) cells were cultured with recombinant human apoSAA (rhSAA), and the production of tumour necrosis factor (TNF)-alpha and interleukin (IL)-1 beta was determined by ELISA.
  • [MeSH-major] Amyloid / metabolism. Mast Cells / physiology. Peptide Fragments / metabolism. Serum Amyloid A Protein / physiology
  • [MeSH-minor] Cell Degranulation. Cells, Cultured. Chymases. Histamine Release. Humans. Interleukin-1 / biosynthesis. Recombinant Proteins / metabolism. Serine Endopeptidases / metabolism. Tryptases. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 16483749.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid; 0 / Interleukin-1; 0 / Peptide Fragments; 0 / Recombinant Proteins; 0 / Serum Amyloid A Protein; 0 / TNF protein, human; 0 / Tumor Necrosis Factor-alpha; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.39 / Chymases; EC 3.4.21.59 / Tryptases
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25. Perry ME, Stirling A, Hunter JA: Effect of etanercept on serum amyloid A protein (SAA) levels in patients with AA amyloidosis complicating inflammatory arthritis. Clin Rheumatol; 2008 Jul;27(7):923-5
Hazardous Substances Data Bank. Etanercept .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of etanercept on serum amyloid A protein (SAA) levels in patients with AA amyloidosis complicating inflammatory arthritis.
  • We assessed changes in serum amyloid A protein (SAA) levels during treatment with etanercept in AA amyloidosis complicating inflammatory arthritis.
  • In seven out of nine patients the median SAA level during etanercept treatment was lower than levels before anti-tumour necrosis factor therapy.
  • Etanercept therapy was associated with a fall in SAA levels in seven of nine patients, five of whom achieved levels which might be expected to be associated with stable or regressing amyloid deposits.
  • [MeSH-major] Amyloidosis / drug therapy. Immunoglobulin G / therapeutic use. Receptors, Tumor Necrosis Factor / therapeutic use. Serum Amyloid A Protein / metabolism. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 18379834.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
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26. Tammam J, Ware C, Efferson C, O'Neil J, Rao S, Qu X, Gorenstein J, Angagaw M, Kim H, Kenific C, Kunii K, Leach KJ, Nikov G, Zhao J, Dai X, Hardwick J, Scott M, Winter C, Bristow L, Elbi C, Reilly JF, Look T, Draetta G, Van der Ploeg L, Kohl NE, Strack PR, Majumder PK: Down-regulation of the Notch pathway mediated by a gamma-secretase inhibitor induces anti-tumour effects in mouse models of T-cell leukaemia. Br J Pharmacol; 2009 Nov;158(5):1183-95

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down-regulation of the Notch pathway mediated by a gamma-secretase inhibitor induces anti-tumour effects in mouse models of T-cell leukaemia.
  • Here we study GSI's effect on tumour and normal cellular processes to optimize dosing regimens for anti-tumour efficacy.
  • KEY RESULTS: Three days of >70% Notch pathway inhibition was sufficient to provide an anti-tumour effect and was well tolerated.
  • Anti-tumour efficacy was associated with cell cycle arrest and apoptosis that was in part due to Notch-dependent regulation of mitochondrial homeostasis.
  • CONCLUSIONS AND IMPLICATIONS: Intermittent but potent inhibition of Notch signalling is sufficient for anti-tumour efficacy in these T-ALL models.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Cyclic S-Oxides / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Receptor, Notch1 / physiology. Thiadiazoles / pharmacology
  • [MeSH-minor] Amyloid beta-Peptides / blood. Animals. Apoptosis. Cell Differentiation. Cell Line, Tumor. Colon / cytology. Colon / drug effects. Down-Regulation. Drug Administration Schedule. Humans. Intestinal Mucosa / cytology. Intestinal Mucosa / drug effects. Membrane Potential, Mitochondrial / drug effects. Mice. Mice, Nude. Mitochondrial Proteins / biosynthesis. Mitochondrial Proteins / genetics. Neoplasm Transplantation. Peptide Fragments / blood. Signal Transduction. Transplantation, Heterologous

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  • (PMID = 19775282.001).
  • [ISSN] 1476-5381
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Antineoplastic Agents; 0 / Cyclic S-Oxides; 0 / MRK 003; 0 / Mitochondrial Proteins; 0 / Peptide Fragments; 0 / Receptor, Notch1; 0 / Thiadiazoles; 0 / amyloid beta-protein (1-40); EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2782329
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27. Paret C, Schön Z, Szponar A, Kovacs G: Inflammatory protein serum amyloid A1 marks a subset of conventional renal cell carcinomas with fatal outcome. Eur Urol; 2010 May;57(5):859-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inflammatory protein serum amyloid A1 marks a subset of conventional renal cell carcinomas with fatal outcome.
  • As the metastatic conventional RCC is practically incurable, there is a need for markers to estimate the tumour aggressiveness.
  • MEASUREMENTS: Serum amyloid A 1 (SAA1) was found to be upregulated in conventional RCCs and it has been analysed by quantitative RT-PCR and immunohistochemistry on TMAs to establish the correlation between SAA1 protein expression and patient survival by uni and multivariate analysis.
  • The effect of SAA1 on tumour cell behaviour in vitro has also been examined by invasion assay and zymography.
  • Stimulation of conventional RCC cell lines with recombinant SAA1 increased the expression of metalloproteinase (MMP)-9 and the invasive potential of tumour cells.
  • [MeSH-major] Carcinoma, Renal Cell / chemistry. Kidney Neoplasms / chemistry. Serum Amyloid A Protein / analysis

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  • [Copyright] Copyright © 2009. Published by Elsevier B.V.
  • [CommentIn] Eur Urol. 2010 May;57(5):866 [19747759.001]
  • (PMID = 19747761.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers; 0 / SAA1 protein, human; 0 / Serum Amyloid A Protein
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28. Arvidsson Y, Andersson E, Bergström A, Andersson MK, Altiparmak G, Illerskog AC, Ahlman H, Lamazhapova D, Nilsson O: Amyloid precursor-like protein 1 is differentially upregulated in neuroendocrine tumours of the gastrointestinal tract. Endocr Relat Cancer; 2008 Jun;15(2):569-81
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amyloid precursor-like protein 1 is differentially upregulated in neuroendocrine tumours of the gastrointestinal tract.
  • High expression of a number of genes was found including amyloid precursor-like protein 1 (APLP1).
  • Quantitative real-time PCR and western blot analysis demonstrated higher expression of APLP1 in carcinoid metastases relative to primary tumours indicating a role of APLP1 in tumour dissemination.
  • Cellular localization of APLP1, APLP2 and amyloid precursor protein (APP) in carcinoid cells (GOT1) by confocal microscopy demonstrated partial co-localization with synaptophysin.
  • This suggests that the APP family of proteins is transported to the cell membrane by synaptic microvesicles and that they may influence tumour cell adhesion and invasiveness.
  • Identification of APLP1 in NE tumours offers a novel target for treatment and may also serve as a tumour-specific marker.
  • [MeSH-major] Amyloid beta-Protein Precursor / genetics. Carcinoid Tumor / genetics. Gastrointestinal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Liver Neoplasms / genetics
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Line, Tumor. Endosomes / metabolism. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / metabolism. Nuclear Proteins / metabolism. Oligonucleotide Array Sequence Analysis. Synaptic Vesicles / metabolism. Up-Regulation / physiology

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  • (PMID = 18430897.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / APBB1 protein, human; 0 / APLP1 protein, human; 0 / APLP2 protein, human; 0 / Amyloid beta-Protein Precursor; 0 / Biomarkers, Tumor; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins
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29. Serdar A, Basak D, Sercan G, Ali V: Solitary amyloid tumor of the tongue base. Int J Otolaryngol; 2009;2009:515068

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solitary amyloid tumor of the tongue base.
  • The purpose of this article is to present a rare case of localized, solitary amyloid tumor of tongue base and emphasize some of the characteristic features of challenging clinical and histopathologic diagnosis.
  • In this paper, we focused on the clinical and pathological specifications of this rare tumor, so any unnecessary examinations or measures may be spared.
  • Negative staining of amyloid material with AAC and osseous metaplasia noted in the histopathologic examination may not be thought as definite criteria for localized amyloidosis, but a supporter of localized, solitary amyloid tumor diagnosis.

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  • (PMID = 20107570.001).
  • [ISSN] 1687-921X
  • [Journal-full-title] International journal of otolaryngology
  • [ISO-abbreviation] Int J Otolaryngol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2809435
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30. Jiang H, Liu CX, Feng JB, Wang P, Zhao CP, Xie ZH, Wang Y, Xu SL, Zheng CY, Bi JZ: Granulocyte colony-stimulating factor attenuates chronic neuroinflammation in the brain of amyloid precursor protein transgenic mice: an Alzheimer's disease mouse model. J Int Med Res; 2010 Jul-Aug;38(4):1305-12
MedlinePlus Health Information. consumer health - Alzheimer's Disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Granulocyte colony-stimulating factor attenuates chronic neuroinflammation in the brain of amyloid precursor protein transgenic mice: an Alzheimer's disease mouse model.
  • Mice transgenic for the V171I mutant amyloid precursor protein (APP) were injected subcutaneously with G-CSF 50 μg/kg per day or phosphate-buffered saline (PBS; control group) for 7 days, and wild-type C57/BL6 mice were injected with PBS daily for 7 days.
  • Levels of α7 nAChR protein were significantly increased and levels of interleukin-1β, tumour necrosis factor-α and nuclear factor-κB (NF-κB) protein were significantly decreased in the brain of APP transgenic mice in response to G-CSF.
  • [MeSH-major] Alzheimer Disease / pathology. Amyloid beta-Protein Precursor / genetics. Brain / pathology. Granulocyte Colony-Stimulating Factor / therapeutic use. Inflammation / drug therapy
  • [MeSH-minor] Animals. Chronic Disease. Disease Models, Animal. Fluorescent Antibody Technique. Humans. Interleukin-1beta / metabolism. Mice. Mice, Inbred C57BL. Mice, Transgenic. NF-kappa B / metabolism. Receptors, Nicotinic / metabolism. Tumor Necrosis Factor-alpha / metabolism. alpha7 Nicotinic Acetylcholine Receptor

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  • (PMID = 20926003.001).
  • [ISSN] 0300-0605
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Chrna7 protein, human; 0 / Chrna7 protein, mouse; 0 / Interleukin-1beta; 0 / NF-kappa B; 0 / Receptors, Nicotinic; 0 / Tumor Necrosis Factor-alpha; 0 / alpha7 Nicotinic Acetylcholine Receptor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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31. Cho WC, Yip TT, Cheng WW, Au JS: Serum amyloid A is elevated in the serum of lung cancer patients with poor prognosis. Br J Cancer; 2010 Jun 8;102(12):1731-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum amyloid A is elevated in the serum of lung cancer patients with poor prognosis.
  • RESULTS: A differential protein with m/z 11.6 kDa was detected and identified as an isoform of human serum amyloid A (SAA).
  • CONCLUSION: There are several functions of the SAA protein, described in the context of inflammation, that are compatible with the mechanism of tumour invasion and metastasis.
  • [MeSH-major] Biomarkers, Tumor / blood. Lung Neoplasms / blood. Serum Amyloid A Protein / metabolism

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  • (PMID = 20502455.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Serum Amyloid A Protein
  • [Other-IDs] NLM/ PMC2883701
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32. Dhamija B, Hassan MF, Thambinayagam H, Moore A, Adams W, Hilton D: Intracranial Aspergillus infection associated with an amyloid tumor and lymphoma. Skull Base; 2008 Nov;18(6):405-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intracranial Aspergillus infection associated with an amyloid tumor and lymphoma.
  • We illustrate the case in a patient who developed right-sided visual disturbance and facial paresthesia, where radiological diagnosis was meningioma but histopathology revealed an amyloid tumor with synchronous aspergillus infection and lymphoma at the same site.

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  • (PMID = 19412411.001).
  • [ISSN] 1531-5010
  • [Journal-full-title] Skull base : official journal of North American Skull Base Society ... [et al.]
  • [ISO-abbreviation] Skull Base
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2637077
  • [Keywords] NOTNLM ; Intracranial aspergillosis / amyloid / lymphoma / meningioma / skull base
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33. Lotz M, Ebert S, Esselmann H, Iliev AI, Prinz M, Wiazewicz N, Wiltfang J, Gerber J, Nau R: Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2 and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation in primary mouse microglial cell cultures. J Neurochem; 2005 Jul;94(2):289-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2 and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation in primary mouse microglial cell cultures.
  • The interaction of endogenous and exogenous stimulators of innate immunity was examined in primary cultures of mouse microglial cells and macrophages after application of defined Toll-like receptor (TLR) agonists [lipopolysaccharide (LPS) (TLR4), the synthetic lipopeptide Pam3Cys-Ser-Lys4 (Pam3Cys) (TLR2) and single-stranded unmethylated CpG-DNA (CpG) (TLR9)] alone and in combination with amyloid beta peptide (Abeta) 1-40.
  • Co-administration of Abeta1-40 with LPS or Pam3Cys led to an additive release of nitric oxide (NO) and tumour necrosis factor alpha (TNF-alpha).
  • [MeSH-major] Amyloid beta-Peptides / pharmacology. DNA-Binding Proteins / antagonists & inhibitors. Inflammation / physiopathology. Lipopolysaccharides / pharmacology. Lipoproteins / pharmacology. Microglia / drug effects. Peptide Fragments / pharmacology. Receptors, Cell Surface / antagonists & inhibitors. Receptors, Immunologic / agonists

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  • (PMID = 15998280.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / CpG-DNA, E coli; 0 / Cytokines; 0 / DNA, Bacterial; 0 / DNA-Binding Proteins; 0 / Lectins; 0 / Lipopolysaccharides; 0 / Lipoproteins; 0 / Nitrites; 0 / Peptide Fragments; 0 / Receptors, Cell Surface; 0 / Receptors, Immunologic; 0 / Tlr2 protein, mouse; 0 / Tlr4 protein, mouse; 0 / Tlr9 protein, mouse; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4; 0 / Toll-Like Receptor 9; 0 / amyloid beta-protein (1-40); 112208-00-1 / N-palmitoyl-S-(2,3-bis(palmitoyloxy)propyl)cysteinyl-seryl-lysyl-lysyl-lysyl-lysine
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34. van Es JH, de Geest N, van de Born M, Clevers H, Hassan BA: Intestinal stem cells lacking the Math1 tumour suppressor are refractory to Notch inhibitors. Nat Commun; 2010;1:18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intestinal stem cells lacking the Math1 tumour suppressor are refractory to Notch inhibitors.
  • [MeSH-minor] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Animals. Cell Differentiation / drug effects. Cell Differentiation / genetics. Dibenzazepines / pharmacology. Goblet Cells / cytology. Goblet Cells / metabolism. Immunohistochemistry. In Situ Hybridization. In Vitro Techniques. Mice. Receptors, Notch / genetics. Receptors, Notch / metabolism

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  • (PMID = 20975679.001).
  • [ISSN] 2041-1723
  • [Journal-full-title] Nature communications
  • [ISO-abbreviation] Nat Commun
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Atoh1 protein, mouse; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Dibenzazepines; 0 / Receptors, Notch; 0 / dibenzazepine; EC 3.4.- / Amyloid Precursor Protein Secretases
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35. Walter M, Heinze C, Steiner T, Pilchowski R, von Eggeling F, Wunderlich H, Junker K: Immunochemotherapy-associated protein patterns in tumour tissue and serum of patients with metastatic renal cell carcinoma. Arch Physiol Biochem; 2010 Oct-Dec;116(4-5):197-207
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunochemotherapy-associated protein patterns in tumour tissue and serum of patients with metastatic renal cell carcinoma.
  • Caveolin-1 (CAV-1) and plasminogen activator inhibitor 1 (PAI-1) were identified in tissue; serum amyloid A (SAA) and transthyretin (TTR) were found in serum.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Renal Cell / blood. Carcinoma, Renal Cell / immunology. Carcinoma, Renal Cell / therapy. Caveolin 1 / analysis. Electrophoresis, Gel, Two-Dimensional / methods. Kidney Neoplasms / blood. Kidney Neoplasms / immunology. Kidney Neoplasms / therapy. Neoplasm Proteins. Plasminogen Activator Inhibitor 1 / analysis. Prealbumin / analysis. Protein Array Analysis. Serum Amyloid A Protein / analysis. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization / methods. Treatment Outcome

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  • (PMID = 20836751.001).
  • [ISSN] 1744-4160
  • [Journal-full-title] Archives of physiology and biochemistry
  • [ISO-abbreviation] Arch. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Caveolin 1; 0 / Neoplasm Proteins; 0 / Plasminogen Activator Inhibitor 1; 0 / Prealbumin; 0 / Serum Amyloid A Protein
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36. Molloy ES, Singhal AB, Calabrese LH: Tumour-like mass lesion: an under-recognised presentation of primary angiitis of the central nervous system. Ann Rheum Dis; 2008 Dec;67(12):1732-5
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  • [Title] Tumour-like mass lesion: an under-recognised presentation of primary angiitis of the central nervous system.
  • A higher percentage (13 of 45; 29%) was seen in the amyloid-related angiitis subset.
  • Poorer outcomes were reported in the amyloid group, with five deaths.
  • Of the non-amyloid group, better outcomes were seen in the group treated with corticosteroids and cyclophosphamide as compared with the group treated with corticosteroids alone.
  • Biopsy evidence of angiitis is required for diagnosis; specimens should routinely be stained for amyloid.

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  • (PMID = 18625623.001).
  • [ISSN] 1468-2060
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / P01NS035611; United States / NINDS NIH HHS / NS / P50NS051343; United States / NINDS NIH HHS / NS / R01NS051412; United States / NINDS NIH HHS / NS / R01NS38477
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Number-of-references] 34
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37. Small DH: Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression? Trends Mol Med; 2008 Mar;14(3):103-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Accumulation of beta-amyloid protein (Abeta) in the brain is a key feature of Alzheimer's disease (AD).
  • Recent studies indicate that brain-derived neurotrophic factor, tumour necrosis factor-alpha and alpha7 nicotinic acetylcholine receptors (alpha7 nAChRs) regulate synaptic scaling in the AD brain.
  • [MeSH-minor] Amyloid beta-Peptides / metabolism. Animals. Dementia / physiopathology. Disease Progression. Homeostasis. Humans. Mice. Mice, Transgenic. Models, Biological

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  • (PMID = 18262842.001).
  • [ISSN] 1471-4914
  • [Journal-full-title] Trends in molecular medicine
  • [ISO-abbreviation] Trends Mol Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides
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38. Endres K, Fahrenholz F: Upregulation of the alpha-secretase ADAM10--risk or reason for hope? FEBS J; 2010 Apr;277(7):1585-96
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A decade ago, a disintegrin and metalloproteinase 10 (ADAM10) was identified as an alpha-secretase and as a key proteinase in the processing of the amyloid precursor protein.
  • Initially, ADAM10 was suggested to be an enzyme, shaping the extracellular matrix by cleavage of collagen type IV, or to be a tumour necrosis factor alpha convertase.
  • In a relatively short time, a wide variety of additional substrates (with amyloid precursor protein probably being the most prominent) has been identified and the search is still ongoing.
  • [MeSH-major] ADAM Proteins / biosynthesis. Amyloid Precursor Protein Secretases / biosynthesis. Gene Expression Regulation. Membrane Proteins / biosynthesis
  • [MeSH-minor] Alzheimer Disease / metabolism. Amyloid beta-Protein Precursor / chemistry. Animals. Collagen Type IV / metabolism. Extracellular Matrix / metabolism. Humans. Mice. Mice, Transgenic. Models, Biological. Neurodegenerative Diseases / metabolism. Protein Structure, Tertiary. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20136654.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Collagen Type IV; 0 / Membrane Proteins; 0 / Tumor Necrosis Factor-alpha; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 protein, human
  • [Number-of-references] 122
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39. Paltrinieri S: The feline acute phase reaction. Vet J; 2008 Jul;177(1):26-35
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  • It begins with the release of interleukin (IL)-1, IL-6 and tumour necrosis factor (TNF)-alpha from inflammatory cells.
  • The major APPs are serum amyloid A and alpha(1)-acid glycoprotein (AGP), which both increase a few hours after the inflammatory stimulus and remain elevated for as long as the inflammation persists.
  • [MeSH-minor] Animals. Biomarkers / blood. Cats. Feline Infectious Peritonitis / blood. Feline Infectious Peritonitis / diagnosis. Serum Amyloid A Protein / analysis. Tumor Necrosis Factor-alpha / blood. Tumor Necrosis Factor-alpha / metabolism

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  • [CommentIn] Vet J. 2008 Jul;177(1):6-7 [18294886.001]
  • (PMID = 17686640.001).
  • [ISSN] 1090-0233
  • [Journal-full-title] Veterinary journal (London, England : 1997)
  • [ISO-abbreviation] Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / Biomarkers; 0 / Cytokines; 0 / Immunoglobulins; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 89
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40. van der Hilst JC, Simon A, Drenth JP: Hereditary periodic fever and reactive amyloidosis. Clin Exp Med; 2005 Oct;5(3):87-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Familial Mediterranean fever (FMF) is the most frequent entity within this group of disorders which further consists of hyperimmunoglobulinaemia D and periodic fever syndrome (HIDS), tumour necrosis factor receptor-associated periodic syndrome (TRAPS) and cryopyrin-associated periodic syndrome (CAPS).
  • This is caused by deposition of fibrils that consist of the proteolytically cleaved acutephase protein serum amyloid A (SAA).
  • [MeSH-minor] Carrier Proteins / genetics. Humans. Hypergammaglobulinemia / genetics. Immunoglobulin D / genetics. Prognosis. Receptors, Tumor Necrosis Factor / genetics. Serum Amyloid A Protein / metabolism

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  • (PMID = 16284730.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Immunoglobulin D; 0 / NLRP3 protein, human; 0 / Receptors, Tumor Necrosis Factor; 0 / Serum Amyloid A Protein
  • [Number-of-references] 167
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41. Papassotiriou I, Alexiou VG, Tsironi M, Skenderi K, Spanos A, Falagas ME: Severe aseptic inflammation caused by long distance running (246 km) does not increase procalcitonin. Eur J Clin Invest; 2008 Apr;38(4):276-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Serum interleukin-6, serum amyloid A protein, C-reactive protein, tumour necrosis factor-alpha and procalcitonin concentrations were determined.
  • RESULTS: Serum interleukin-6, serum amyloid A protein and C-reactive protein were dramatically increased after the end of the race (150-, 116- and 10,470- fold increase of the mean values, respectively).
  • Tumour necrosis factor-alpha measurements revealed no significant changes.
  • [MeSH-minor] Adult. Humans. Interleukin-6 / metabolism. Middle Aged. Serum Amyloid A Protein / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • [CommentIn] Eur J Clin Invest. 2008 Oct;38(10):784-5 [18837805.001]
  • (PMID = 18339008.001).
  • [ISSN] 1365-2362
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Protein Precursors; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; 56645-65-9 / procalcitonin; 9007-12-9 / Calcitonin; 9007-41-4 / C-Reactive Protein
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42. Notebaert S, Carlsen H, Janssen D, Vandenabeele P, Blomhoff R, Meyer E: In vivo imaging of NF-kappaB activity during Escherichia coli-induced mammary gland infection. Cell Microbiol; 2008 Jun;10(6):1249-58
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This systemic reaction was confirmed by increased circulating levels of the acute phase protein serum amyloid A, tumour necrosis factor-alpha and interleukin-6.
  • [MeSH-minor] Animals. Epithelium / metabolism. Female. Immunohistochemistry. Interleukin-6 / metabolism. Liver / metabolism. Luciferases / genetics. Mice. Mice, Transgenic. Microscopy, Fluorescence. Serum Amyloid A Protein / metabolism. Transcription Factor RelA / isolation & purification. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18241210.001).
  • [ISSN] 1462-5822
  • [Journal-full-title] Cellular microbiology
  • [ISO-abbreviation] Cell. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / NF-kappa B; 0 / Rela protein, mouse; 0 / Serum Amyloid A Protein; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; EC 1.13.12.- / Luciferases
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43. Oprica M, Hjorth E, Spulber S, Popescu BO, Ankarcrona M, Winblad B, Schultzberg M: Studies on brain volume, Alzheimer-related proteins and cytokines in mice with chronic overexpression of IL-1 receptor antagonist. J Cell Mol Med; 2007 Jul-Aug;11(4):810-25
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  • Effects on brain morphology and brain levels of the AD-related proteins beta-amyloid precursor protein (APP) and presenilin 1(PS1), as well as the levels of IL-1beta, IL-6 and tumour necrosis factor-alpha (TNF-alpha) were analysed in homozygotic and heterozygotic mice and wild type (WT) controls, of both genders and of young (30-40 days) and adult (13-14 months) age.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Brain / metabolism. Brain / pathology. Cytokines / metabolism. Interleukin 1 Receptor Antagonist Protein / metabolism. Presenilin-1 / metabolism

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  • (PMID = 17760842.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Cytokines; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Presenilin-1
  • [Other-IDs] NLM/ PMC3823259
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44. Davenport CM, Sevastou IG, Hooper C, Pocock JM: Inhibiting p53 pathways in microglia attenuates microglial-evoked neurotoxicity following exposure to Alzheimer peptides. J Neurochem; 2010 Jan;112(2):552-63
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • Following activation with chromogranin A (100 nM), or beta-amyloid(25-35), (10 microM), microglia became apoptotic.
  • Regulating p53 pathways modulated microglial inducible nitric oxide synthase expression and tumour necrosis factor alpha secretion.
  • [MeSH-major] Amyloid beta-Peptides / pharmacology. Microglia / drug effects. Microglia / metabolism. Peptide Fragments / pharmacology. Signal Transduction / drug effects. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adjuvants, Immunologic / pharmacology. Animals. Animals, Newborn. Apoptosis / drug effects. Benzothiazoles / pharmacology. Cells, Cultured. Cerebellum / cytology. Chromogranin A / pharmacology. Drug Interactions. Enzyme-Linked Immunosorbent Assay / methods. Lithium Chloride / pharmacology. Neurons / drug effects. Neurons / metabolism. Polysaccharides / pharmacology. Rats. Rats, Wistar. Time Factors. Toluene / analogs & derivatives. Toluene / pharmacology. Transcription Factor CHOP / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19895660.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Amyloid beta-Peptides; 0 / Benzothiazoles; 0 / Chromogranin A; 0 / Peptide Fragments; 0 / Polysaccharides; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 0 / amyloid beta-protein (25-35); 0 / pifithrin; 147336-12-7 / Transcription Factor CHOP; 3FPU23BG52 / Toluene; G4962QA067 / Lithium Chloride
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45. Freund-Levi Y, Hjorth E, Lindberg C, Cederholm T, Faxen-Irving G, Vedin I, Palmblad J, Wahlund LO, Schultzberg M, Basun H, Eriksdotter Jönhagen M: Effects of omega-3 fatty acids on inflammatory markers in cerebrospinal fluid and plasma in Alzheimer's disease: the OmegAD study. Dement Geriatr Cogn Disord; 2009;27(5):481-90
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  • The inflammatory markers interleukin (IL)-6, tumour necrosis factor-alpha and soluble interleukin-1 receptor type II (sIL-1RII) were analysed in CSF and plasma at baseline and at 6 months.
  • The AD markers tau-protein, hyperphosphorylated tau-protein and beta-amyloid (Abeta(1-42)) were assessed in CSF.
  • [MeSH-minor] Aged. Amyloid beta-Peptides / blood. Apolipoproteins E / genetics. Biomarkers / blood. Biomarkers / cerebrospinal fluid. C-Reactive Protein / cerebrospinal fluid. Cytokines / blood. Dietary Supplements. Double-Blind Method. Female. Genotype. Humans. Male. Neuropsychological Tests. tau Proteins / blood

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  • (PMID = 19439966.001).
  • [ISSN] 1421-9824
  • [Journal-full-title] Dementia and geriatric cognitive disorders
  • [ISO-abbreviation] Dement Geriatr Cogn Disord
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Apolipoproteins E; 0 / Biomarkers; 0 / Cytokines; 0 / Fatty Acids, Omega-3; 0 / tau Proteins; 9007-41-4 / C-Reactive Protein
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46. Li LY, Yang M, Gao X, Zhang HB, Li JF, Xu WF, Lin Z, Zhou XL: Prospective comparison of five mediators of the systemic response after high-intensity focused ultrasound and targeted cryoablation for localized prostate cancer. BJU Int; 2009 Oct;104(8):1063-7
The Lens. Cited by Patents in .

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  • The extent of the systemic response to surgery-induced tissue trauma was measured by assessing the levels of acute-phase markers tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-10, C-reactive protein (CRP) and serum amyloid A (SAA), at all sampling times in all patients.
  • [MeSH-minor] Aged. C-Reactive Protein / metabolism. Epidemiologic Methods. Humans. Interleukin-10. Interleukin-6 / metabolism. Male. Middle Aged. Serum Amyloid A Protein / metabolism. Treatment Outcome. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19298406.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Comparative Study; Controlled Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 9007-41-4 / C-Reactive Protein
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47. Oyasiji T, Yood S: Jejunal Amyloidoma - a rare cause of gastrointestinal bleeding. Cases J; 2009;2:9100

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We report a case of localized amyloid tumor of the jejunum which presented with abdominal pain and gastrointestinal bleeding.
  • We reviewed the pathophysiologic process that precipitates bleeding in this rare tumor.
  • All with a view to add to the growing evidence on this rare tumor which will facilitate accurate diagnosis and management.

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  • [Other-IDs] NLM/ PMC2803897
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48. Edgell T, Martin-Roussety G, Barker G, Autelitano DJ, Allen D, Grant P, Rice GE: Phase II biomarker trial of a multimarker diagnostic for ovarian cancer. J Cancer Res Clin Oncol; 2010 Jul;136(7):1079-88
The Lens. Cited by Patents in .

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  • A multivariate classification model was developed that incorporated five biomarkers of ovarian cancer, CA-125; C-reactive protein (CRP); serum amyloid A (SAA); interleukin 6 (IL-6); and interleukin 8 (IL-8) from a modelling cohort (n = 179).
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / blood. C-Reactive Protein / analysis. Case-Control Studies. Cohort Studies. Female. Humans. Interleukin-6 / blood. Interleukin-8 / blood. Middle Aged. Multivariate Analysis. Retrospective Studies. Sensitivity and Specificity. Serum Amyloid A Protein / analysis. Young Adult

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  • (PMID = 20082099.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Serum Amyloid A Protein; 9007-41-4 / C-Reactive Protein
  • [Other-IDs] NLM/ PMC2874491
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49. Gao WM, Kuick R, Orchekowski RP, Misek DE, Qiu J, Greenberg AK, Rom WN, Brenner DE, Omenn GS, Haab BB, Hanash SM: Distinctive serum protein profiles involving abundant proteins in lung cancer patients based upon antibody microarray analysis. BMC Cancer; 2005;5:110
The Lens. Cited by Patents in .

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  • Proteins that exhibited higher abundances in the lung cancer samples relative to the control samples included C-reactive protein (CRP; a 13.3 fold increase), serum amyloid A (SAA; a 2.0 fold increase), mucin 1 and alpha-1-antitrypsin (1.4 fold increases).
  • At a cutoff where all 56 of the non-tumor samples were correctly classified, 15/24 lung tumor patient sera were correctly classified.
  • [MeSH-minor] Antibodies / chemistry. Antibodies, Neoplasm / chemistry. Blotting, Western. C-Reactive Protein / biosynthesis. Case-Control Studies. Collodion / chemistry. Electrophoresis, Polyacrylamide Gel. Humans. Mass Spectrometry / methods. Microarray Analysis / methods. Mucins / biosynthesis. Pulmonary Disease, Chronic Obstructive / metabolism. Serum Amyloid A Protein / biosynthesis. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. alpha 1-Antitrypsin / biosynthesis

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  • (PMID = 16117833.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antibodies, Neoplasm; 0 / Blood Proteins; 0 / Mucins; 0 / Serum Amyloid A Protein; 0 / alpha 1-Antitrypsin; 9004-70-0 / Collodion; 9007-41-4 / C-Reactive Protein
  • [Other-IDs] NLM/ PMC1198221
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50. Westra J, Bijzet J, Doornbos-van der Meer B, van Rijswijk MH, Limburg PC: Differential influence of p38 mitogen activated protein kinase (MAPK) inhibition on acute phase protein synthesis in human hepatoma cell lines. Ann Rheum Dis; 2006 Jul;65(7):929-35
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  • METHODS: The effects of p38 MAPK inhibition on APP production and mRNA expression in four human hepatoma cell lines was investigated, after stimulation with interleukin (IL)6 and/or IL1beta or tumour necrosis factor alpha.
  • Serum amyloid A (SAA) was produced in all four lines.
  • [MeSH-minor] Analysis of Variance. Blotting, Western / methods. C-Reactive Protein / biosynthesis. Cell Line, Tumor. Complement C3 / biosynthesis. Fibrinogen / biosynthesis. Humans. Immunization. Interleukin-1 / pharmacology. MAP Kinase Signaling System / drug effects. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor / biosynthesis. Serum Amyloid A Protein / biosynthesis. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16269426.001).
  • [ISSN] 0003-4967
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / Complement C3; 0 / Imidazoles; 0 / Interleukin-1; 0 / Pyridines; 0 / RNA, Messenger; 0 / RWJ 67657; 0 / STAT3 Transcription Factor; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; 9001-32-5 / Fibrinogen; 9007-41-4 / C-Reactive Protein; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1798216
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51. Maheshwari AV, Muro-Cacho CA, Kransdorf MJ, Temple HT: Soft-tissue amyloidoma of the extremities: a case report and review of literature. Skeletal Radiol; 2009 Mar;38(3):287-92
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  • The least common presentation of an amyloid deposition is as a discrete mass called amyloidoma or amyloid tumor.

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  • (PMID = 19050870.001).
  • [ISSN] 0364-2348
  • [Journal-full-title] Skeletal radiology
  • [ISO-abbreviation] Skeletal Radiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 29
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52. Murai T, Miyauchi T, Yanagida T, Sako Y: Epidermal growth factor-regulated activation of Rac GTPase enhances CD44 cleavage by metalloproteinase disintegrin ADAM10. Biochem J; 2006 Apr 1;395(1):65-71
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  • Invasive tumour cells, such as gliomas, frequently express EGF (epidermal growth factor) receptor at a high level and they exhibit enhanced cell migration in response to EGF.
  • We reported previously that tumour cell migration is associated with ectodomain cleavage of CD44, the major adhesion molecule that is implicated in tumour invasion and metastasis, and that the cleavage is enhanced by ligation of CD44.
  • These results indicate that EGF induces ADAM10-mediated CD44 cleavage through Rac1 and mitogen-activated protein kinase activation, and thereby promotes tumour cell migration and invasion.
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Cell Line, Tumor. Cell Movement / drug effects. Cell Surface Extensions / drug effects. Cell Surface Extensions / metabolism. Enzyme Activation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Mitogen-Activated Protein Kinases / metabolism. Pseudopodia / drug effects. Pseudopodia / metabolism. Tumor Cells, Cultured

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  • (PMID = 16390331.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Disintegrins; 0 / Membrane Proteins; 62229-50-9 / Epidermal Growth Factor; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 protein, human; EC 3.6.5.2 / rac1 GTP-Binding Protein
  • [Other-IDs] NLM/ PMC1409701
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53. Gao S, Krogdahl A, Sørensen JA, Kousted TM, Dabelsteen E, Andreasen PA: Overexpression of protease nexin-1 mRNA and protein in oral squamous cell carcinomas. Oral Oncol; 2008 Mar;44(3):309-13
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  • Whilst there are numerous studies of the occurrence and functions of PAI-1 in cancer, a possible tumour biological role of PN-1 has been almost totally neglected.
  • We found that the average PN-1 mRNA level in tumours and normal tissues was significantly different, being increased up to 13 fold in tumour samples compared with the average level in normal tissues.
  • We hypothesise that PN-1 may have a tumour biological function similar to that of PAI-1.
  • [MeSH-major] Amyloid beta-Protein Precursor / analysis. Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / chemistry. Gene Expression Regulation, Neoplastic. Mouth Neoplasms / chemistry. Receptors, Cell Surface / analysis

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  • (PMID = 17468036.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Biomarkers, Tumor; 0 / Protease Nexins; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / SERPINE2 protein, human; 0 / Serpin E2
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54. Okuda I, Ubara Y, Takaichi K, Kitajima I, Motoi N, Hara S, Kokubo T: Genital beta2-microglobulin amyloidoma in a long-term dialysis patient. Am J Kidney Dis; 2006 Sep;48(3):e35-9
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  • We present the case of a 58-year-old Japanese woman with a huge amyloid tumor in the genital region.
  • From 1989 to 1991, carpal tunnel decompression was performed surgically, and beta(2)-microglobulin (beta2MG)-amyloid deposition was found in the wrists.
  • A biopsy specimen of the mass obtained by using a transvaginal approach showed material that was positive for beta2MG-amyloid immunohistologically.

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  • (PMID = 16931206.001).
  • [ISSN] 1523-6838
  • [Journal-full-title] American journal of kidney diseases : the official journal of the National Kidney Foundation
  • [ISO-abbreviation] Am. J. Kidney Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / beta 2-Microglobulin
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55. Cheng JY, Fong KS, Cheah ES, Choo CT: Lacrimal gland amyloidosis. Ophthal Plast Reconstr Surg; 2006 Jul-Aug;22(4):306-8
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  • This report describes two patients with amyloid tumor of the lacrimal gland.

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  • (PMID = 16855510.001).
  • [ISSN] 0740-9303
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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56. Bisceglia M, Spagnolo D, Galliani C, Fisher C, Suster S, Kazakov DV, Cooper K, Michal M: Tumoral, quasitumoral and pseudotumoral lesions of the superficial and somatic soft tissue: new entities and new variants of old entities recorded during the last 25 years. Part XII: appendix. Pathologica; 2006 Aug;98(4):239-98

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  • Detailed clinicomorphological and differential diagnostic features of approximately sixty entities were chosen on the basis of their clinical significance and morphologic distinctiveness.
  • The series included fibrous and myofibroblastic tumors (e.g. solitary fibrous tumor, high grade classic and pigmented dermatofibrosarcoma protuberans, inflammatory myofibroblastic tumor and myofibrosarcomas), fibromyxoid and fibrohistiocytic neoplasms (e.g., Evans' tumor, phosphaturic mesenchymal tumor, inflammatory myxohyaline tumor), special adipocytic/vascular/and smooth muscle lesions (e.g., chondroid lipoma, Dabska's tumor, ST hemangioblastoma, lipoleiomyosarcoma), epithelioid mesenchymal malignancies of diverse lineages (e.g., epithelioid liposarcoma, proximal-type epithelioid sarcoma, neuroendocrine extraskeletal chondromyxoid sarcoma), ST Ewing's tumor and peripheral nerve sheath tumors (perineuriomas and pigmented and rosetting tumors of the schwannoma/neurofibroma group), extranodal dendritic or histiocytic proliferative processes (follicular dendritic cell sarcoma, Rosai-Dorfman disease, Castleman's disease, and plexiform xanthomatous tumor), and tumors with myoepithelial differentiation.
  • The section devoted to selected pseudotumoral entities considered representatives of the hamartoma group (neural fibrolipomatous hamartoma, ectopic hamartomatous thymoma, rudimentary meningocele), metabolic diseases (amyloid tumor, nephrogenic fibrosing dermopathy, tophaceous pseudogout, pseudoinfiltrative parathyromatosis), stromal tissue reactions to trauma (fibroosseous pseudotumors of digits) and infections (bacillary angiomatosis), and normal organs (glomus coccygeum).

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  • (PMID = 17175794.001).
  • [ISSN] 0031-2983
  • [Journal-full-title] Pathologica
  • [ISO-abbreviation] Pathologica
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 272
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57. Gutwein P, Schramme A, Sinke N, Abdel-Bakky MS, Voss B, Obermüller N, Doberstein K, Koziolek M, Fritzsche F, Johannsen M, Jung K, Schaider H, Altevogt P, Ludwig A, Pfeilschifter J, Kristiansen G: Tumoural CXCL16 expression is a novel prognostic marker of longer survival times in renal cell cancer patients. Eur J Cancer; 2009 Feb;45(3):478-89
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  • Our immunohistochemical analysis on tissue microarray of renal cancer samples of 104 patients revealed that ADAM10 correlated significantly with tumour stage, pathological nodal status, M status and lymphangiosis carcinomatosa.
  • Importantly, high levels of CXCL16 expression in renal cancer tissue correlated with better survival of patients, and CXCL16 correlated inversely to the tumour stage.
  • [MeSH-major] ADAM Proteins / metabolism. Amyloid Precursor Protein Secretases / metabolism. Carcinoma, Renal Cell / metabolism. Chemokines, CXC / metabolism. Kidney Neoplasms / metabolism. Membrane Proteins / metabolism. Neoplasm Proteins / metabolism. Receptors, Chemokine / metabolism. Receptors, Scavenger / metabolism. Receptors, Virus / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / genetics. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / genetics. Humans. Immunohistochemistry. Male

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  • (PMID = 19070478.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CXCL16 protein, human; 0 / CXCR6 protein, human; 0 / Chemokines, CXC; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Receptors, Chemokine; 0 / Receptors, Scavenger; 0 / Receptors, Virus; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 protein, human
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58. Holland DB, Bojar RA, Farrar MD, Holland KT: Differential innate immune responses of a living skin equivalent model colonized by Staphylococcus epidermidis or Staphylococcus aureus. FEMS Microbiol Lett; 2009 Jan;290(2):149-55
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  • There was upregulation in gene expression of many skin defence factors including Toll-like receptor 2, beta defensin 4, properdin, PTX3, proinflammatory cytokines tumour necrosis factor-alpha, IL-1 alpha, IL-1 beta, IL-17C, IL-20, IL-23A and chemokines IL-8, CCL4, CCL5, CCL20 and CCL27.
  • [MeSH-minor] Adult. C-Reactive Protein / genetics. C-Reactive Protein / immunology. Cells, Cultured. Cytokines / genetics. Cytokines / immunology. Defensins / genetics. Defensins / immunology. Fibroblasts / immunology. Fibroblasts / microbiology. Gene Expression. Humans. Keratinocytes / immunology. Keratinocytes / microbiology. Models, Biological. Serum Amyloid P-Component / genetics. Serum Amyloid P-Component / immunology

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  • (PMID = 19054079.001).
  • [ISSN] 1574-6968
  • [Journal-full-title] FEMS microbiology letters
  • [ISO-abbreviation] FEMS Microbiol. Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Defensins; 0 / Serum Amyloid P-Component; 148591-49-5 / PTX3 protein; 9007-41-4 / C-Reactive Protein
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59. Alberti L, Gilardini L, Zulian A, Micheletto G, Peri G, Doni A, Mantovani A, Invitti C: Expression of long pentraxin PTX3 in human adipose tissue and its relation with cardiovascular risk factors. Atherosclerosis; 2009 Feb;202(2):455-60
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  • We investigated (a) PTX3 expression and secretion in subcutaneous adipose tissue (SAT) and omental visceral adipose tissue (VAT) obtained from 21 obese (37.4+/-8.15 yr) and 10 normal weight subjects (43.7+/-11.07 yr) and (b) the relationships of adipose PTX3 with tumour necrosis factor alpha (TNFalpha) and adiponectin expression and with cardiometabolic risk factors.
  • [MeSH-major] Atherosclerosis / epidemiology. Atherosclerosis / genetics. C-Reactive Protein / genetics. Intra-Abdominal Fat / physiology. Serum Amyloid P-Component / genetics

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  • (PMID = 18571180.001).
  • [ISSN] 1879-1484
  • [Journal-full-title] Atherosclerosis
  • [ISO-abbreviation] Atherosclerosis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / ADIPOQ protein, human; 0 / Adiponectin; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / Lipids; 0 / Serum Amyloid P-Component; 148591-49-5 / PTX3 protein; 9007-41-4 / C-Reactive Protein
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60. van Es JH, van Gijn ME, Riccio O, van den Born M, Vooijs M, Begthel H, Cozijnsen M, Robine S, Winton DJ, Radtke F, Clevers H: Notch/gamma-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells. Nature; 2005 Jun 16;435(7044):959-63
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  • The inhibitor also induced goblet cell differentiation in adenomas in mice carrying a mutation of the Apc tumour suppressor gene.
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Animals. Aspartic Acid Endopeptidases. Cell Differentiation / drug effects. DNA-Binding Proteins / deficiency. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Dibenzazepines / pharmacology. Female. Genes, APC. Immunoglobulin J Recombination Signal Sequence-Binding Protein. Male. Mice. Mice, Inbred C57BL. Nuclear Proteins / deficiency. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Phenotype. Receptors, Notch. Signal Transduction / drug effects


61. Mambole A, Baruch D, Nusbaum P, Bigot S, Suzuki M, Lesavre P, Fukuda M, Halbwachs-Mecarelli L: The cleavage of neutrophil leukosialin (CD43) by cathepsin G releases its extracellular domain and triggers its intramembrane proteolysis by presenilin/gamma-secretase. J Biol Chem; 2008 Aug 29;283(35):23627-35
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  • [Title] The cleavage of neutrophil leukosialin (CD43) by cathepsin G releases its extracellular domain and triggers its intramembrane proteolysis by presenilin/gamma-secretase.
  • The highly negatively charged membrane sialoglycoprotein leukosialin, CD43, is shed during neutrophil activation.
  • This is generally thought to enhance cell adhesion.
  • We here describe two novel consequences of this shedding, during neutrophil activation by phorbol esters or by chemoattractants after TNF-alpha priming.
  • CD43 proteolysis was investigated by Western blotting, using a polyclonal antibody to CD43 intracellular domain.
  • Our data emphasize the importance of a juxtamembranous cleavage of about 50% of membrane CD43 molecules by cathepsin G.
  • Indeed, it is inhibited by alpha1-antichymotrypsin and cathepsin G inhibitor I and is reproduced by exogenous purified cathepsin G.
  • The resulting membrane-anchored C-terminal fragment, CD43-CTF, becomes susceptible to presenilin/gamma-secretase, which releases CD43 intracytoplasmic domain: preincubation with three different gamma-secretase inhibitors, before PMN treatment by agonists or by purified cathepsin G, results in the accumulation of CD43-CTF.
  • Because CD43 binds E-selectin, we also investigated the effect of the soluble extracellular domain CD43s, released by cathepsin G juxtamembranous cleavage, on neutrophil adhesion to endothelial cells.
  • A recombinant CD43s-Fc fusion protein inhibited neutrophil E selectindependent adhesion to endothelial cells under flow conditions, while it had no effect on neutrophil static adhesion.
  • We thus propose that, in addition to its potential pro-adhesive role, CD43 proteolysis results in: (i) the release, by cathepsin G, of CD43 extracellular domain, able to inhibit the adhesion of flowing neutrophils on endothelial cells and thus to participate to the natural control of inflammation;.
  • (ii) the release and/or the clearance, by presenilin/gamma-secretase, of CD43 intracellular domain, thereby regulating CD43-mediated signaling.

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  • (PMID = 18586676.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA033000; United States / NCI NIH HHS / CA / CA 33000
  • [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, CD43; 0 / E-Selectin; 0 / Presenilins; 0 / Protease Inhibitors; 0 / UN1 sialoglycoprotein, human; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Cathepsins; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.20 / CTSG protein, human; EC 3.4.21.20 / Cathepsin G
  • [Other-IDs] NLM/ PMC2527098
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62. Marron MB, Singh H, Tahir TA, Kavumkal J, Kim HZ, Koh GY, Brindle NP: Regulated proteolytic processing of Tie1 modulates ligand responsiveness of the receptor-tyrosine kinase Tie2. J Biol Chem; 2007 Oct 19;282(42):30509-17
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Amyloid Precursor Protein Secretases / metabolism. Carcinogens / pharmacology. Cells, Cultured. Enzyme Activation / drug effects. Enzyme Activation / physiology. Humans. Ligands. Phorbol Esters / pharmacology. Proteasome Endopeptidase Complex / metabolism. RNA Interference. Vascular Endothelial Growth Factor A / pharmacology

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  • (PMID = 17728252.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United Kingdom / British Heart Foundation / / BHF/ PG/03/094/15787; United Kingdom / British Heart Foundation / / BHF/ PG/05/028/18599
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANGPT1 protein, human; 0 / Angiopoietin-1; 0 / Carcinogens; 0 / Ligands; 0 / Phorbol Esters; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor, TIE-1; EC 2.7.10.1 / Receptor, TIE-2; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2270410; NLM/ UKMS1570
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63. Andersson CX, Fernandez-Rodriguez J, Laos S, Baeckström D, Haass C, Hansson GC: Shedding and gamma-secretase-mediated intramembrane proteolysis of the mucin-type molecule CD43. Biochem J; 2005 Apr 15;387(Pt 2):377-84
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Animals. Antigens, CD43. Cell Line. Endopeptidases. Gene Expression. Humans. Membrane Proteins / genetics. Membrane Proteins / metabolism. Mutagenesis, Site-Directed. Plasmids. Presenilin-1. Protein Processing, Post-Translational. Protein Structure, Tertiary. Recombinant Proteins

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  • (PMID = 15540986.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD43; 0 / Membrane Proteins; 0 / PSEN1 protein, human; 0 / Presenilin-1; 0 / Recombinant Proteins; 0 / Sialoglycoproteins; 0 / UN1 sialoglycoprotein, human; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human
  • [Other-IDs] NLM/ PMC1134965
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64. Markert E, Gruber-Moesenbacher U, Porubsky C, Popper HH: Lung osteoma--a new benign lung lesion. Virchows Arch; 2006 Jul;449(1):117-20
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  • Tumors with osseous elements can be found, such as hamartoma and amyloid tumor, and reactive lesions such as osseous metaplasia.
  • A 39-year-old male patient was treated for multiple myeloma and got a bone marrow transplantation 2 years and a few months before he presented with a solitary well-circumscribed tumor in the right middle lobe.
  • The tumor presented with a fibrous capsule and consisted of mature bone trabecules.
  • Within the tumor, fatty tissue was seen.
  • No amyloid deposition, no immature epithelial tubules as in hamartomas, and no normal lung structure as in osseous metaplasia were seen.
  • This tumor might have been induced by circulating stem cells; however, due to autologous bona marrow transplantation, this cannot be proven.
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Bone Marrow Transplantation. Diagnosis, Differential. Hamartoma / diagnosis. Humans. Immunohistochemistry. Male. Multiple Myeloma / pathology. Multiple Myeloma / therapy. Osteonectin / analysis

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  • (PMID = 16639606.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Osteonectin
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65. Lendeckel U, Kohl J, Arndt M, Carl-McGrath S, Donat H, Röcken C: Increased expression of ADAM family members in human breast cancer and breast cancer cell lines. J Cancer Res Clin Oncol; 2005 Jan;131(1):41-8
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  • CONCLUSION: The results of this study suggest that ADAMs are differentially expressed in human breast cancer and are capable of modulating tumour cell growth.
  • [MeSH-major] Biomarkers, Tumor / analysis. Breast Neoplasms / chemistry. Membrane Glycoproteins / analysis. Metalloendopeptidases / analysis
  • [MeSH-minor] ADAM Proteins. Adult. Aged. Aged, 80 and over. Amyloid Precursor Protein Secretases. Carcinoma, Ductal, Breast / chemistry. Carcinoma, Lobular / chemistry. Cell Line, Tumor. Cell Proliferation. Disintegrins / analysis. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Membrane Proteins / analysis. Middle Aged. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • (PMID = 15565459.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Disintegrins; 0 / Membrane Glycoproteins; 0 / Membrane Proteins; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM 12 protein; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAM15 protein, human; EC 3.4.24.- / ADAM9 protein, human; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.- / tumor necrosis factor-alpha convertase; EC 3.4.24.81 / ADAM10 protein, human
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66. Willeke F, Assad A, Findeisen P, Schromm E, Grobholz R, von Gerstenbergk B, Mantovani A, Peri S, Friess HH, Post S, von Knebel Doeberitz M, Schwarzbach MH: Overexpression of a member of the pentraxin family (PTX3) in human soft tissue liposarcoma. Eur J Cancer; 2006 Oct;42(15):2639-46
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  • We hypothesised that genes downstream of FUS/CHOP might serve as attractive candidates for novel tumour associated antigens.
  • [MeSH-major] C-Reactive Protein / metabolism. Liposarcoma / genetics. Neoplasm Proteins / metabolism. Serum Amyloid P-Component / metabolism

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  • (PMID = 16959485.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / Serum Amyloid P-Component; 0 / TLS-CHOP fusion protein, human; 147336-12-7 / Transcription Factor CHOP; 148591-49-5 / PTX3 protein; 9007-41-4 / C-Reactive Protein
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67. Junker K, von Eggeling F, Müller J, Steiner T, Schubert J: [Identification of biomarkers and therapeutic targets for renal cell cancer using ProteinChip technology]. Urologe A; 2006 Mar;45(3):305-6, 308, 310-12 passim
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  • In order to understand tumour biology in its complexity, it is necessary to investigate the proteomics in addition to the DNA and RNA level.
  • Several proteins have been identified, i.e. serum amyloid alpha (SAA).
  • Analysis of tumour tissues leads to a better understanding of tumour biology and provides the basis for differential classification and evaluation of prognosis.

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  • (PMID = 16491405.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 31
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68. Li HX, Hwang BY, Laxmikanthan G, Blaber SI, Blaber M, Golubkov PA, Ren P, Iverson BL, Georgiou G: Substrate specificity of human kallikreins 1 and 6 determined by phage display. Protein Sci; 2008 Apr;17(4):664-72
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • KLK6 is overexpressed in breast and ovarian cancer tissues and has been shown to cleave peptide derived from human myelin protein and Abeta amyloid peptide in vitro.

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  • (PMID = 18359858.001).
  • [ISSN] 1469-896X
  • [Journal-full-title] Protein science : a publication of the Protein Society
  • [ISO-abbreviation] Protein Sci.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM079686-01A1; United States / NINDS NIH HHS / NS / 1R15NS057771-01; United States / NIGMS NIH HHS / GM / R01 GM073089; United States / NINDS NIH HHS / NS / R15 NS057771; United States / NIGMS NIH HHS / GM / R01GM079686; United States / NIGMS NIH HHS / GM / R01 GM065551; United States / NIGMS NIH HHS / GM / R01 GM079686; United States / NIGMS NIH HHS / GM / GM079686-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Peptide Library; EC 3.4.21.- / KLK6 protein, human; EC 3.4.21.- / Kallikreins; EC 3.4.21.35 / Tissue Kallikreins
  • [Other-IDs] NLM/ PMC2271166
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69. Weber MA, Schnyder-Candrian S, Schnyder B, Quesniaux V, Poli V, Stewart CL, Ryffel B: Endogenous leukemia inhibitory factor attenuates endotoxin response. Lab Invest; 2005 Feb;85(2):276-84
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These findings correlated with 10-fold higher tumour necrosis factor-alpha (TNFalpha) and interleukin-6 (IL-6) serum levels and reduced IL-10 production in LIF-/- mice in response to LPS.
  • [MeSH-minor] Acute-Phase Reaction / etiology. Animals. Cells, Cultured. Down-Regulation. Galactosamine / administration & dosage. Galactosamine / pharmacology. Interleukin-10 / blood. Leukemia Inhibitory Factor. Lipopolysaccharides / toxicity. Liver / pathology. Lung / pathology. Macrophages / drug effects. Macrophages / physiology. Mice. Mice, Inbred BALB C. Mice, Knockout. RNA, Messenger / analysis. Serum Amyloid A Protein / analysis. Spleen / pathology. Time Factors. Tumor Necrosis Factor-alpha / analysis. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 15702085.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endotoxins; 0 / Interleukin-6; 0 / Leukemia Inhibitory Factor; 0 / Lif protein, mouse; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 7535-00-4 / Galactosamine
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70. Huang W, Li LB, Han L, Zhang H, Yang YZ: [Screening of TACE peptide inhibitors from a phage display random 15-peptide library by recombinant TACE ecotodomain]. Sheng Wu Gong Cheng Xue Bao; 2005 Jan;21(1):30-5

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  • Tumour necrosis factor-alpha converting enzyme (TACE) is the major protease responsible for processing proTNF from membrane-anchored precursor into secreted TNF-alpha.
  • [MeSH-major] ADAM Proteins / antagonists & inhibitors. ADAM Proteins / biosynthesis. Amyloid Precursor Protein Secretases. Peptide Library
  • [MeSH-minor] Animals. Humans. Mice. Peptides / chemistry. Recombinant Proteins / biosynthesis. Recombinant Proteins / genetics. Tumor Necrosis Factor-alpha

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  • (PMID = 15859325.001).
  • [ISSN] 1000-3061
  • [Journal-full-title] Sheng wu gong cheng xue bao = Chinese journal of biotechnology
  • [ISO-abbreviation] Sheng Wu Gong Cheng Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Peptide Library; 0 / Peptides; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
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71. Onorati M, Ambrosio MR, Mourmouras V, Mastrogiulio MG, Rocca BJ: Primary linitis plastica of the right colon. Pathologica; 2009 Apr;101(2):85-8

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  • This case is of interest for three reasons: the site of origin in the right colon (80% of cases reported develop distally to the splenic flexure), a biopsy previously taken from the mucosa demonstrated the presence of a signet ring cell carcinoma (endoscopic biopsies do not provide a conclusive diagnosis in the majority of cases reported) and hyaline with sparse amyloid nodules were detected in the extensive, dense fibrous tissue intermingled with tumour cells.

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  • (PMID = 19886554.001).
  • [ISSN] 0031-2983
  • [Journal-full-title] Pathologica
  • [ISO-abbreviation] Pathologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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72. Wilhelm K, Darinskas A, Noppe W, Duchardt E, Mok KH, Vukojević V, Schleucher J, Morozova-Roche LA: Protein oligomerization induced by oleic acid at the solid-liquid interface--equine lysozyme cytotoxic complexes. FEBS J; 2009 Aug;276(15):3975-89
The Lens. Cited by Patents in .

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  • The properties of ELOA were characterized using NMR, spectroscopic methods and atomic force microscopy, and showed similarity with both amyloid oligomers and the complexes with oleic acid and its structural homologous protein alpha-lactalbumin, known as human alpha-lactalbumin made lethal for tumour cells (HAMLET).
  • Similar to amyloid oligomers, ELOA also interacts with thioflavin-T dye, shows a spherical morphology, assembles into ring-shaped structures, as monitored by atomic force microscopy, and exerts a toxic effect in cells.
  • Studies of well-populated ELOA shed light on the nature of the amyloid oligomers and HAMLET complexes, suggesting that they constitute one large family of cytotoxic proteinaceous species.

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  • (PMID = 19594832.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytotoxins; 0 / Fluorescent Dyes; 0 / HAMLET complex, human; 0 / Oleic Acids; 9013-90-5 / Lactalbumin; EC 3.2.1.17 / Muramidase
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73. Mahmoudi M, Curzen N, Gallagher PJ: Atherogenesis: the role of inflammation and infection. Histopathology; 2007 Apr;50(5):535-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Prospective epidemiological studies have unequivocally demonstrated increased vascular risk in individuals with elevated levels of (i) cytokines such as interleukin-6 and tumour necrosis factor-alpha, (ii) cell adhesion molecules such as intercellular adhesion molecule-1 and P-selectin, and (iii) acute-phase proteins such as C-reactive protein, fibrinogen and serum amyloid A.

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  • (PMID = 17394488.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 98
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74. Wozny W, Schroer K, Schwall GP, Poznanović S, Stegmann W, Dietz K, Rogatsch H, Schaefer G, Huebl H, Klocker H, Schrattenholz A, Cahill MA: Differential radioactive quantification of protein abundance ratios between benign and malignant prostate tissues: cancer association of annexin A3. Proteomics; 2007 Jan;7(2):313-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The most differentially abundant proteins between cancer and benign samples were isopeptidase T, serum amyloid P (SAP), annexin A3 (ANXA3) and mitochondrial enoyl coenzyme-A hydratase.
  • ANXA3 is present in healthy epithelial cells, exhibits strong staining in precancerous prostatic intraepithelial neoplasia, and is relatively less abundant in individual tumour cells of increasing Gleason pattern (GP), despite exhibiting higher overall tissue abundance in tumours.
  • Strongly staining single cells, possibly phagocytes, were interspersed in highly dedifferentiated GP5 tumour areas among tumour cells without measurable ANXA3.
  • Results are discussed focussing on the potential implications for tumour tissues.
  • [MeSH-major] Annexin A3 / metabolism. Biomarkers, Tumor. Prostatic Hyperplasia / metabolism. Prostatic Neoplasms / metabolism. Radioisotopes


75. Stoeck A, Keller S, Riedle S, Sanderson MP, Runz S, Le Naour F, Gutwein P, Ludwig A, Rubinstein E, Altevogt P: A role for exosomes in the constitutive and stimulus-induced ectodomain cleavage of L1 and CD44. Biochem J; 2006 Feb 1;393(Pt 3):609-18
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Calcium influx augmented the release of exosomes containing functionally active forms of ADAM10 (a disintegrin and metalloprotease 10) and ADAM17 [TACE (tumour necrosis factor a-converting enzyme)] as well as CD44 and L1 cytoplasmic cleavage fragments.
  • [MeSH-minor] ADAM Proteins / genetics. ADAM Proteins / metabolism. Amyloid Precursor Protein Secretases. Cell Line, Tumor. Gene Expression Regulation. Humans. Membrane Proteins / genetics. Membrane Proteins / metabolism. Protein Structure, Tertiary. RNA Interference

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  • (PMID = 16229685.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Membrane Proteins; 0 / Neural Cell Adhesion Molecule L1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase; EC 3.4.24.81 / ADAM10 protein, human
  • [Other-IDs] NLM/ PMC1360713
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76. Bioulac-Sage P, Laumonier H, Rullier A, Cubel G, Laurent C, Zucman-Rossi J, Balabaud C: Over-expression of glutamine synthetase in focal nodular hyperplasia: a novel easy diagnostic tool in surgical pathology. Liver Int; 2009 Mar;29(3):459-65

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND AND AIMS: Glutamine synthetase (GS) is a useful marker in tumour liver pathology, including hepatocellular adenomas and nodules in cirrhosis.
  • In case of uncertainty, particularly with hepatocellular adenoma, additional immunostainings including liver fatty acid-binding protein, serum amyloid A and beta-catenin were performed.
  • In comparison, hepatocellular adenoma staining was completely different, even in cases of fibrotic bands due to tumour remodelling related to necrosis or haemorrhage.

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  • (PMID = 18803590.001).
  • [ISSN] 1478-3231
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; EC 6.3.1.2 / Glutamate-Ammonia Ligase
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77. Hermeyer K, Kühn M, Kuchelmeister K, Laik C, Baumgärtner W, Wohlsein P: Multiple cutaneous ganglioneuromas in a dog. Vet Dermatol; 2007 Oct;18(5):360-4
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  • The first tumour cell population showed histomorphological characteristics of mature ganglion cells; the second featured small, spindle-shaped tumour cells with scant cytoplasm.
  • Both neoplastic cell components expressed vimentin, neurofilament protein, pan-neuronal neurofilament, amyloid-precursor protein and chromogranin A.
  • In addition, the spindle-shaped tumour cells were positive for 2', 3'-cyclicnucleotide 3'-phosphodiesterase.

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  • (PMID = 17845625.001).
  • [ISSN] 0959-4493
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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78. Jones LN, Sinclair RD, Carver J, Ecroyd H, Lui Y, Bennett LE: Bioprospecting keratinous materials. Int J Trichology; 2010 Jan;2(1):47-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The published literature reports multiple examples of proline-rich peptides with productive bio-activity in models of human disease including tumour formation, hypertension control and Alzheimer's disease.
  • A bio-assay of determining inhibition of early stage amyloid aggregation involved using a model fibril-forming protein - reduced and carboxymethylated bovine K-casein (RCMk-CN) and quantitation of fibril development with the amyloid-specific fluorophore, Thioflavin T (ThT).

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  • (PMID = 21188026.001).
  • [ISSN] 0974-9241
  • [Journal-full-title] International journal of trichology
  • [ISO-abbreviation] Int J Trichology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3002413
  • [Keywords] NOTNLM ; Bioactive peptides / bioprospecting / keratin
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79. Juanes PP, Ferreira L, Montero JC, Arribas J, Pandiella A: N-terminal cleavage of proTGFalpha occurs at the cell surface by a TACE-independent activity. Biochem J; 2005 Jul 1;389(Pt 1):161-72

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In vivo treatment with the hydroxamate-based metalloprotease inhibitors BB3103 or TAPI-2 (tumour necrosis factor-alpha protease inhibitor 2) reversibly induced accumulation of forms of proTGFalpha that included the N-terminal extension.
  • Experiments of proTGFalpha expression and maturation in cells deficient in TACE (tumour-necrosis-factor-alpha-converting enzyme) activity indicated that this protease was dispensable for N-terminal processing of proTGFalpha in vivo, but was required for regulated cleavage at the C-terminus.
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Animals. Aspartic Acid Endopeptidases. CHO Cells. Cricetinae. Dose-Response Relationship, Drug. Endopeptidases / metabolism. Endoplasmic Reticulum / metabolism. HeLa Cells. Humans. Hydroxamic Acids / pharmacology. Protease Inhibitors / pharmacology. Protein Processing, Post-Translational / drug effects

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  • (PMID = 15777285.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydroxamic Acids; 0 / Protease Inhibitors; 0 / Protein Precursors; 0 / Transforming Growth Factor alpha; 0 / protransforming growth factor alpha; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
  • [Other-IDs] NLM/ PMC1184548
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80. Riedle S, Kiefel H, Gast D, Bondong S, Wolterink S, Gutwein P, Altevogt P: Nuclear translocation and signalling of L1-CAM in human carcinoma cells requires ADAM10 and presenilin/gamma-secretase activity. Biochem J; 2009 Jun 15;420(3):391-402
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Overexpression promotes tumour-cell invasion and motility, growth in nude mice and tumour metastasis.
  • However, little is known about its mechanism in tumour cells.
  • [MeSH-major] ADAM Proteins / metabolism. Amyloid Precursor Protein Secretases / metabolism. Cell Nucleus / metabolism. Membrane Proteins / metabolism. Neural Cell Adhesion Molecule L1 / metabolism. Presenilins / metabolism. Signal Transduction
  • [MeSH-minor] Active Transport, Cell Nucleus. Animals. Binding Sites / genetics. CHO Cells. Cell Line. Cell Line, Tumor. Cricetinae. Cricetulus. Female. Flow Cytometry. Humans. Lysosome-Associated Membrane Glycoproteins / metabolism. Membrane Microdomains / metabolism. Microscopy, Fluorescence. Ovarian Neoplasms / genetics. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / pathology. RNA, Small Interfering / genetics. Receptors, Retinoic Acid / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Transfection

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  • (PMID = 19260824.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / LAMP1 protein, human; 0 / Lysosome-Associated Membrane Glycoproteins; 0 / Membrane Proteins; 0 / Neural Cell Adhesion Molecule L1; 0 / Presenilins; 0 / RNA, Small Interfering; 0 / Receptors, Retinoic Acid; 0 / retinoic acid binding protein II, cellular; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 protein, human
  • [Other-IDs] NLM/ PMC2782312
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81. Selzer-Plon J, Bornholdt J, Friis S, Bisgaard HC, Lothe IM, Tveit KM, Kure EH, Vogel U, Vogel LK: Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis. BMC Cancer; 2009 Jun 25;9:201
MedlinePlus Health Information. consumer health - Colorectal Cancer.

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  • BACKGROUND: Clinical trials where cancer patients were treated with protease inhibitors have suggested that the serine protease, prostasin, may act as a tumour suppressor.
  • [MeSH-minor] Aged. Alternative Splicing. Amyloid beta-Protein Precursor / biosynthesis. Cohort Studies. Female. Humans. Male. Middle Aged. Protease Nexins. Protein Isoforms. Proteinase Inhibitory Proteins, Secretory / biosynthesis. RNA, Messenger / metabolism. Receptors, Cell Surface / biosynthesis. Serpin E2

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  • (PMID = 19555470.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Protease Nexins; 0 / Protein Isoforms; 0 / Proteinase Inhibitory Proteins, Secretory; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / SERPINE2 protein, human; 0 / SPINT1 protein, human; 0 / Serpin E2; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / prostasin
  • [Other-IDs] NLM/ PMC2717118
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82. Mannello F: New implications of the proteolytic balance between matrix metalloproteinases and their tissue inhibitors in migraine with and without aura. Clin Chim Acta; 2009 Nov;409(1-2):1-3
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  • Uncontrolled or inappropriate expression/activity of MMPs contributes to different pathologic conditions, including inflammation, tumour growth, cancer cell invasion and infection diseases.
  • However, an alteration of the MMP/TIMP balance is thought to be a key feature of the pathology of many inflammatory, degenerative and malignant neurological diseases; their pathogenesis is correlated to the detrimental effects of altered MMP/TIMP expression, leading to breakdown of the blood-brain barrier (BBB), demyelination, cytokine production and propagation of inflammatory response, deposition of amyloid proteins, tumor invasion and metastasis).

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  • (PMID = 19632213.001).
  • [ISSN] 1873-3492
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases
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83. Maciel CM, Junqueira M, Paschoal ME, Kawamura MT, Duarte RL, Carvalho Mda G, Domont GB: Differential proteomic serum pattern of low molecular weight proteins expressed by adenocarcinoma lung cancer patients. J Exp Ther Oncol; 2005;5(1):31-8
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  • Based on the assumption that proteins can emanate from tumour to serum, we investigated whether serum low molecular weight proteins (LMW) can discriminate lung cancer patients from healthy donors.
  • Results of 2D-E/ MALDI-TOF showed five up regulated proteins (immunoglobulin lambda chain, transthyretin monomer, haptoglobin-alfa 2 and two isoforms of serum amyloid protein) and one down regulated (fragment of apolipoprotein A-I) in patients.

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  • (PMID = 16416599.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Proteins; EC 3.4.21.4 / Trypsin
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84. Janot MS, Kersting S, Chromik AM, Tannapfel A, Uhl W: [Amyloidosis of the small intestine following whipple operation is a rare cause of chronic ileus and has to be considered as differential diagnosis]. Zentralbl Chir; 2010 Aug;135(4):345-9
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • INTRODUCTION: When patients who underwent a Whipple operation because of a tumour of the pancreas develop symptoms of chronic ileus several months after surgery, the most common cause is a relapse of tumour growth or a peritoneal carcinomatosis.
  • Surprisingly, the intraoperative situs did not show any tumour growth.
  • Diffuse amyloid deposits were found on the small intestine.
  • Surgeons have to keep in mind that amyloidosis is a possible differential diagnosis in addition to relapse of tumour growth and peritoneal carcinomatosis in these patients.

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  • [Copyright] Georg Thieme Verlag Stuttgart ˙ New York.
  • (PMID = 20464655.001).
  • [ISSN] 1438-9592
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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85. Caescu CI, Jeschke GR, Turk BE: Active-site determinants of substrate recognition by the metalloproteinases TACE and ADAM10. Biochem J; 2009 Oct 23;424(1):79-88
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  • The metalloproteinases TACE [tumour necrosis factor alpha-converting enzyme; also known as ADAM17 (a disintegrin and metalloproteinase 17)] and ADAM10 are the primary enzymes responsible for catalysing release of membrane-anchored proteins from the cell surface in metazoan organisms.

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  • (PMID = 19715556.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / R21 RR022859; United States / NCRR NIH HHS / RR / RR022859-02; United States / NCRR NIH HHS / RR / R21 RR022859-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factors; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase; EC 3.4.24.81 / Adam10 protein, mouse
  • [Other-IDs] NLM/ NIHMS152772; NLM/ PMC2774824
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86. Calbo E, Alsina M, Rodríguez-Carballeira M, Lite J, Garau J: The impact of time on the systemic inflammatory response in pneumococcal pneumonia. Eur Respir J; 2010 Mar;35(3):614-8
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  • At admission, vital signs, time from onset of pneumonia symptoms and circulating levels of C-reactive protein (CRP), serum amyloid A (SAA), tumour necrosis factor (TNF)-alpha, and interleukin (IL)-1beta, IL-6, IL-8, IL-10 and IL-1ra were recorded.

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  • (PMID = 19608588.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / Cytokines
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87. Bannerman DD, Springer HR, Paape MJ, Kauf AC, Goff JP: Evaluation of breed-dependent differences in the innate immune responses of Holstein and Jersey cows to Staphylococcus aureus intramammary infection. J Dairy Res; 2008 Aug;75(3):291-301
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  • The following parameters of the innate immune response were evaluated: acute phase protein synthesis of serum amyloid A and lipopolysaccharide-binding protein; total and differential circulating white blood cell counts; milk somatic cell counts; mammary vascular permeability; milk N-acetyl-beta-d-glucosaminidase (NAGase) activity; and production of the cytokines, interferon (IFN)-gamma, interleukin (IL)-12, tumour growth factor(TGF)-alpha, and TGF-beta1.

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  • (PMID = 18680613.001).
  • [ISSN] 0022-0299
  • [Journal-full-title] The Journal of dairy research
  • [ISO-abbreviation] J. Dairy Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
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88. Hill AL, Lowes DA, Webster NR, Sheth CC, Gow NA, Galley HF: Regulation of pentraxin-3 by antioxidants. Br J Anaesth; 2009 Dec;103(6):833-9
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  • METHODS: Human endothelial cells were cultured with lipopolysaccharide 2 microg ml(-1), peptidoglycan G 20 microg ml(-1), tumour necrosis factor (TNF) alpha 10 ng ml(-1), interleukin-1 (IL-1) beta 20 ng ml(-1), or killed Candida albicans yeast cells plus either N-acetylcysteine (NAC) 25 mM, trolox 100 mM, or idebenone 1 microM.

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  • (PMID = 19864306.001).
  • [ISSN] 1471-6771
  • [Journal-full-title] British journal of anaesthesia
  • [ISO-abbreviation] Br J Anaesth
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Biomarkers; 0 / Inflammation Mediators; 0 / Lipid Peroxides; 0 / Serum Amyloid P-Component; 148591-49-5 / PTX3 protein; 9007-41-4 / C-Reactive Protein
  • [Other-IDs] NLM/ PMC2777941
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89. Bierhaus A, Nawroth PP: Multiple levels of regulation determine the role of the receptor for AGE (RAGE) as common soil in inflammation, immune responses and diabetes mellitus and its complications. Diabetologia; 2009 Nov;52(11):2251-63
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  • Its biological activity seems to be mainly dependent on the presence of its various ligands, including AGE, S100-calcium binding protein/calgranulins, high-mobility group protein 1, amyloid-beta-peptides and the family of beta-sheet fibrils, all known to be elevated in chronic metabolic, malignant and inflammatory diseases.
  • RAGE-mediated persistent cell activation is of pivotal importance in various experimental and clinical settings, including diabetes and its complications, neurodegeneration, ageing, tumour growth, and autoimmune and infectious inflammatory disease.

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  • (PMID = 19636529.001).
  • [ISSN] 1432-0428
  • [Journal-full-title] Diabetologia
  • [ISO-abbreviation] Diabetologia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Advanced Glycosylation End Product-Specific Receptor; 0 / Glycosylation End Products, Advanced; 0 / Leukocyte L1 Antigen Complex; 0 / Receptors, Immunologic
  • [Number-of-references] 108
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90. Llamas Moya S, Boyle LA, Lynch PB, Arkins S: Age-related changes in pro-inflammatory cytokines, acute phase proteins and cortisol concentrations in neonatal piglets. Neonatology; 2007;91(1):44-8
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  • This study evaluated the plasma concentrations of the pro-inflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), the acute phase proteins C-reactive protein (CRP), serum amyloid A (SAA) and haptoglobin (Hp), as well as cortisol during the first week of postnatal life in piglets.

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  • (PMID = 17344651.001).
  • [ISSN] 1661-7800
  • [Journal-full-title] Neonatology
  • [ISO-abbreviation] Neonatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / Cytokines; 0 / Inflammation Mediators; WI4X0X7BPJ / Hydrocortisone
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91. Byrne FR, Morony S, Warmington K, Geng Z, Brown HL, Flores SA, Fiorino M, Yin SL, Hill D, Porkess V, Duryea D, Pretorius JK, Adamu S, Manoukian R, Danilenko DM, Sarosi I, Lacey DL, Kostenuik PJ, Senaldi G: CD4+CD45RBHi T cell transfer induced colitis in mice is accompanied by osteopenia which is treatable with recombinant human osteoprotegerin. Gut; 2005 Jan;54(1):78-86
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  • CD4+CD45RBHi T cell recipients also had a bone marrow inflammatory cell infiltrate expressing tumour necrosis factor alpha which was unaffected by treatment with Fc-OPG.
  • [MeSH-minor] Animals. Bone Density / drug effects. CD4-Positive T-Lymphocytes / transplantation. Female. Intestine, Large / pathology. Mice. Mice, SCID. Osteoblasts / pathology. Osteoclasts / pathology. Osteoprotegerin. Parathyroid Hormone / blood. Receptors, Tumor Necrosis Factor. Recombinant Proteins / therapeutic use. Serum Amyloid A Protein / metabolism. T-Lymphocyte Subsets / transplantation. Weight Loss

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  • (PMID = 15591508.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / Osteoprotegerin; 0 / Parathyroid Hormone; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Proteins; 0 / Serum Amyloid A Protein; 0 / TNFRSF11B protein, human; 0 / Tnfrsf11b protein, mouse
  • [Other-IDs] NLM/ PMC1774360
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92. Bioulac-Sage P, Balabaud C, Zucman-Rossi J: Subtype classification of hepatocellular adenoma. Dig Surg; 2010;27(1):39-45
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  • There is an overexpression of the inflammatory proteins serum amyloid A and C-reactive protein in tumour hepatocytes both at mRNA and protein levels.
  • [MeSH-minor] Biomarkers, Tumor / analysis. Female. Hepatocyte Nuclear Factor 1 / genetics. Histocytochemistry. Humans. beta Catenin / genetics

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20357450.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / beta Catenin; 126548-29-6 / Hepatocyte Nuclear Factor 1
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93. Clapperton M, Bishop SC, Glass EJ: Innate immune traits differ between Meishan and Large White pigs. Vet Immunol Immunopathol; 2005 Apr 8;104(3-4):131-44

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  • Monocyte phagocytosis of E. coli was significantly less than that of neutrophils in both breeds but the function of Meishan monocytes as measured by phagocytosis and tumour necrosis factor alpha (TNFalpha) release did not differ from that of Large White monocytes.
  • Levels of acute phase proteins also differed between the breeds with a significantly higher proportion of Meishans having elevated serum amyloid A levels.
  • [MeSH-minor] Acute-Phase Proteins / immunology. Animals. Escherichia coli / immunology. Female. Flow Cytometry / veterinary. Leukocyte Count / veterinary. Lymphocyte Count / veterinary. Lymphocyte Subsets / immunology. Male. Monocytes / immunology. Neutrophils / immunology. Phagocytosis / immunology. Respiratory Burst / immunology. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 15734534.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / Tumor Necrosis Factor-alpha
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94. Davis PA, Mussap M, Pagnin E, Bertipaglia L, Savica V, Semplicini A, Calò LA: Early markers of inflammation in a high angiotensin II state--results of studies in Bartter's/Gitelman's syndromes. Nephrol Dial Transplant; 2006 Jun;21(6):1697-701
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  • METHODS: We evaluated the plasma levels of inflammation-associated markers, C-reactive protein (CRP), serum amyloid A (SAA), vascular cell adhesion molecules (VCAM) and intercellular adhesion molecules (ICAM), and the inflammation-related cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) using immunonephelometric and ELISA-based assays.
  • [MeSH-minor] Acute-Phase Proteins / analysis. Adolescent. Adult. Biomarkers / blood. Case-Control Studies. Female. Humans. Male. Middle Aged. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16574683.001).
  • [ISSN] 0931-0509
  • [Journal-full-title] Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • [ISO-abbreviation] Nephrol. Dial. Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / Biomarkers; 0 / Tumor Necrosis Factor-alpha; 11128-99-7 / Angiotensin II
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95. Brocker CN, Vasiliou V, Nebert DW: Evolutionary divergence and functions of the ADAM and ADAMTS gene families. Hum Genomics; 2009 Oct;4(1):43-55
The Lens. Cited by Patents in .

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  • Membrane-anchored ADAM proteins are best known for their role in activating zymogens--including tumour necrosis factor-alpha, epidermal growth factor (EGF) and amyloid precursor protein (APP).

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  • (PMID = 19951893.001).
  • [ISSN] 1479-7364
  • [Journal-full-title] Human genomics
  • [ISO-abbreviation] Hum. Genomics
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES06096; United States / NEI NIH HHS / EY / R01 EY11490
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.24.- / ADAM Proteins
  • [Other-IDs] NLM/ PMC3500187
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96. Zampieri N, Chao MV: Mechanisms of neurotrophin receptor signalling. Biochem Soc Trans; 2006 Aug;34(Pt 4):607-11
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  • Regulation of cell survival decisions and neuronal plasticity by neurotrophins are mediated by two classes of receptors, Trks (tropomyosin receptor kinases) and p75, the first discovered member of the tumour necrosis factor receptor superfamily.
  • Like amyloid precursor protein and Notch, p75 is a substrate for gamma-secretase cleavage.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Cell Line. Humans. Ligands. NF-kappa B / metabolism. Protein Binding. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. Receptor, trkA / genetics. Receptor, trkA / metabolism. Receptor-Interacting Protein Serine-Threonine Kinase 2. TNF Receptor-Associated Factor 6 / genetics. TNF Receptor-Associated Factor 6 / metabolism. Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / genetics. Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / metabolism

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  • (PMID = 16856873.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Ligands; 0 / NF-kappa B; 0 / Receptor, Nerve Growth Factor; 0 / TNF Receptor-Associated Factor 6; 0 / Tumor Necrosis Factor Receptor-Associated Peptides and Proteins; EC 2.7.10.1 / Receptor, trkA; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / RIPK2 protein, human; EC 2.7.11.1 / Receptor-Interacting Protein Serine-Threonine Kinase 2
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97. Ryska A, Cap J, Vaclavikova E, Dvorakova S, Bendlova B, Hovorkova E, Kohout A: Paraganglioma-like medullary thyroid carcinoma: fine needle aspiration cytology features with histological correlation. Cytopathology; 2009 Jun;20(3):188-94
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  • The tumour cells showed significant nuclear atypia with occasional bizarre and/or binucleated cells.
  • Polygonal or triangular cells, amyloid and azurophillic cytoplasmic granules were absent in both cases.

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  • (PMID = 18631354.001).
  • [ISSN] 1365-2303
  • [Journal-full-title] Cytopathology : official journal of the British Society for Clinical Cytology
  • [ISO-abbreviation] Cytopathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-ret
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98.