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1. Kostakis GC, Papadogeorgakis N, Koumaki V, Kamakari S, Koumaki D, Alexandridis C: Absence of hotspot mutations in exons 9 and 20 of the PIK3CA gene in human oral squamous cell carcinoma in the Greek population. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2010 May;109(5):e53-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Absence of hotspot mutations in exons 9 and 20 of the PIK3CA gene in human oral squamous cell carcinoma in the Greek population.
  • Recent studies have reported high frequencies of somatic hotspot mutations in the phosphatidylinositol-3 kinase catalytic alpha (PIK3CA) gene, which encodes for one of these kinases, in several human solid tumors, including oral squamous cell carcinoma (OSCC).
  • STUDY DESIGN: Eighty-six formalin-fixed and paraffin-embedded primary tumor specimens were analyzed by direct genomic DNA sequencing.
  • RESULTS: No hotspot mutations were detected in any of the samples.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Squamous Cell / enzymology. Exons / genetics. Mouth Neoplasms / enzymology. Mutation / genetics. Phosphatidylinositol 3-Kinases / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Cytosine. Female. Gingival Neoplasms / enzymology. Gingival Neoplasms / genetics. Greece. Guanine. Humans. Introns / genetics. Male. Mandibular Neoplasms / enzymology. Mandibular Neoplasms / genetics. Middle Aged. Mouth Mucosa / pathology. Neoplasm Staging. Polymerase Chain Reaction. Polymorphism, Genetic / genetics. Sequence Analysis, DNA. Thymine. Tongue Neoplasms / enzymology. Tongue Neoplasms / genetics. Young Adult

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  • [Copyright] Copyright (c) 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20416519.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 5Z93L87A1R / Guanine; 8J337D1HZY / Cytosine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; QR26YLT7LT / Thymine
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2. Wang YA, Shen K, Ishida Y, Wang Y, Kakizuka A, Brooks SC: Induction of murine leukemia and lymphoma by dominant negative retinoic acid receptor alpha. Mol Carcinog; 2005 Dec;44(4):252-61
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  • [Title] Induction of murine leukemia and lymphoma by dominant negative retinoic acid receptor alpha.
  • Acute promyelocytic leukemia (APL) is invariably associated with chromosomal translocation to retinoic acid receptor alpha (RARalpha) locus.
  • It was thought that the fusion protein PML-RARalpha acts as a double dominant negative mutant to inhibit the PML and RARalpha signaling.
  • In an attempt to study the physiological role of retinoic acid in mammary gland development, we created a transgenic model system expressing a dominant negative RARalpha under the regulation of murine mammary tumor viral promoter.
  • Retinoic acid blocked tumor development ex vivo through induction of apoptosis.
  • Thus, our results suggested that disruption of RARalpha signaling was the first essential step in the development of APL in vivo.
  • [MeSH-major] Gene Expression Regulation / physiology. Genes, Dominant. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Receptors, Retinoic Acid / genetics
  • [MeSH-minor] Acute Disease. Animals. Apoptosis. Cell Proliferation. Female. Humans. Male. Mammary Tumor Virus, Mouse / genetics. Mice. Mice, Transgenic. Survival Rate. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 16273555.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NCI NIH HHS / CA / R01 CA89526
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin
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3. Shen R, Tao L, Xu Y, Chang S, Van Brocklyn J, Gao JX: Reversibility of aberrant global DNA and estrogen receptor-alpha gene methylation distinguishes colorectal precancer from cancer. Int J Clin Exp Pathol; 2009;2(1):21-33
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  • [Title] Reversibility of aberrant global DNA and estrogen receptor-alpha gene methylation distinguishes colorectal precancer from cancer.
  • Recently we have identified a new type of cancer cell called precancerous stem cells (pCSCs) and proposed that cancer may arise from a lengthy development process of tumor initiating cells (TICs) --> pCSCs --> cancer stem cells (CSCs) --> cancer, which is in parallel to histological changes of hyperplasia (TICs) --> precancer (pCSCs) --> carcinoma (CSCs/cancer cells), accompanied by clonal evolutionary epigenetic and genetic alterations.
  • In this study, we investigated whether aberrant DNA methylation can be used as a biomarker for the differentiation between premalignant and malignant lesions in the colorectum.
  • The profile of global DNA and estrogen receptor (ER)-alpha gene methylation during cancer development was determined by analysis of 5-methylcytosine (5-MeC) using immunohistochemical (IHC) staining, dot blot analysis or a quantitative gene methylation assay (QGMA).
  • Herein we show that global DNA hypomethylation and ER-alpha gene hypermethylation are progressively enhanced from hyperplastic polyps (HPs) --> adenomatous polyps (APs) --> adenomatous carcinoma (AdCa).
  • In normal colorectal mucosa, while global DNA methylation was not affected by aging, ER-alpha gene methylation was significantly increased with aging.
  • Taken together, reversibility of aberrant global DNA and ER-alpha gene methylation distinguishes colorectal precancer from cancer.

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  • [Cites] Clin Immunol. 2006 Dec;121(3):274-85 [16945588.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):293-7 [10667579.001]
  • [Cites] N Engl J Med. 2006 Aug 31;355(9):873-84 [16943400.001]
  • [Cites] J Natl Cancer Inst. 2006 May 17;98(10):665-7 [16705118.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4542-6 [16618783.001]
  • [Cites] Br J Cancer. 2006 Feb 27;94(4):593-8 [16421593.001]
  • [Cites] Dis Colon Rectum. 2006 Jan;49(1):113-24; discussion 124-5 [16362805.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S4-11 [16341240.001]
  • [Cites] Nucleic Acids Res. 2005;33(21):6823-36 [16326863.001]
  • [Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1330-8 [16174854.001]
  • [Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1317-9 [16174847.001]
  • [Cites] Curr Gastroenterol Rep. 2005 Oct;7(5):389-95 [16168238.001]
  • [Cites] Biochem Soc Trans. 2005 Aug;33(Pt 4):709-11 [16042580.001]
  • [Cites] Oncol Rep. 2005 Apr;13(4):559-83 [15756426.001]
  • [Cites] Anal Chem. 2004 Nov 15;76(22):6829-32 [15538812.001]
  • [Cites] PLoS One. 2008;3(2):e1652 [18286204.001]
  • [Cites] Cancer Biomark. 2007;3(3):153-61 [17611306.001]
  • [Cites] Crit Rev Oncog. 2006 Dec;12(3-4):273-87 [17425506.001]
  • [Cites] PLoS One. 2007;2(3):e293 [17356702.001]
  • [Cites] Clin Cancer Res. 2006 Nov 15;12(22):6626-36 [17121881.001]
  • [Cites] Int J Colorectal Dis. 1997;12(5):267-71 [9401839.001]
  • [Cites] Adv Cancer Res. 1998;72:141-96 [9338076.001]
  • [Cites] Endoscopy. 1997 Sep;29(7):626-31 [9360872.001]
  • [Cites] Nat Genet. 1994 Aug;7(4):536-40 [7951326.001]
  • [Cites] Age Ageing. 1993 Jul;22(4):260-4 [8213330.001]
  • [Cites] Cancer Res. 1988 Mar 1;48(5):1159-61 [3342396.001]
  • [Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]
  • [Cites] Carcinogenesis. 2004 Oct;25(10):1917-23 [15205357.001]
  • [Cites] Semin Oncol. 2004 Apr;31(2 Suppl 7):12-21 [15252926.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Jul;287(1):G7-17 [15194558.001]
  • [Cites] Clin Gastroenterol Hepatol. 2004 Jan;2(1):1-8 [15017625.001]
  • [Cites] N Engl J Med. 2004 Mar 4;350(10):991-1004 [14999111.001]
  • [Cites] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):29-39 [15000147.001]
  • [Cites] Mol Carcinog. 2004 Feb;39(2):79-84 [14750212.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4878-81 [12941809.001]
  • [Cites] Ann N Y Acad Sci. 2003 Mar;983:213-9 [12724226.001]
  • [Cites] Ann N Y Acad Sci. 2003 Mar;983:84-100 [12724214.001]
  • [Cites] Ann N Y Acad Sci. 2003 Mar;983:28-42 [12724210.001]
  • [Cites] Surg Clin North Am. 2002 Oct;82(5):891-904 [12507199.001]
  • [Cites] Endoscopy. 2003 Jan;35(1):27-35 [12510223.001]
  • [Cites] Gastroenterology. 2002 Sep;123(3):862-76 [12198712.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2002;3:101-28 [12142355.001]
  • [Cites] Cell Mol Life Sci. 2002 May;59(5):821-31 [12088282.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] Climacteric. 2002 Mar;5(1):3-14 [11974557.001]
  • [Cites] Ann Pharmacother. 2001 Dec;35(12):1638-43 [11793634.001]
  • [Cites] Genome Res. 2002 Jan;12(1):153-7 [11779840.001]
  • [Cites] J Pathol. 2001 Sep;195(1):111-34 [11568897.001]
  • [Cites] Hum Mol Genet. 2001 Apr;10(7):687-92 [11257100.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5040-4 [11016626.001]
  • [Cites] Gut. 2006 Oct;55(10):1467-74 [16469793.001]
  • (PMID = 18830381.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; DNA methylation / Precancer / cancer progression / colorectal cancer / epigenetic / estrogen receptor-α / nonsteroidal anti-inflammatory drugs / tumor initiation
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4. Li MY, Yuan H, Ma LT, Kong AW, Hsin MK, Yip JH, Underwood MJ, Chen GG: Roles of peroxisome proliferator-activated receptor-alpha and -gamma in the development of non-small cell lung cancer. Am J Respir Cell Mol Biol; 2010 Dec;43(6):674-83
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  • [Title] Roles of peroxisome proliferator-activated receptor-alpha and -gamma in the development of non-small cell lung cancer.
  • Peroxisome proliferator-activated receptor (PPAR)-α and PPARγ participate in cell proliferation and apoptosis.
  • The roles of PPARα and -γ were investigated in the development of pulmonary tumors induced in the adult A/J mouse by treatment with 4-(methylnitrosamino)-l-(3-pyridyl)-lbutanone (NNK).
  • Compared with the normal lung tissues, PPARγ expression was much higher in the NNK-induced lung tumor tissues.
  • Along with the alteration of PPARγ and its endogenous ligands, the level of PPARα and its activity were increased in the NNK-induced mouse lung tumors.
  • Treatment of mice with the synthetic PPARγ ligand, pioglitazone, significantly inhibited the formation of mouse lung tumors induced by NNK.
  • Our study demonstrated that the reduction of endogenous PPARγ ligands and increased PPARα occurred before the formation of lung tumors, indicating that the molecular changes play a role in lung carcinogenesis.
  • The results suggest that the enhancement of PPARγ activity with its ligands, and the suppression of PPARα with its inhibitors, may prevent the formation of lung tumors, as well as accelerate the therapy of lung cancer.
  • Our findings may also reveal the possibility of using the level of endogenous PPARγ ligands and the activities of PPARγ or PPARα as tumor markers for lung cancer.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. PPAR alpha / metabolism. PPAR gamma / metabolism. Precancerous Conditions / pathology
  • [MeSH-minor] Animals. Disease Progression. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hydroxyeicosatetraenoic Acids / metabolism. Ligands. Linoleic Acids / metabolism. Lipid Metabolism / drug effects. Lipid Metabolism / genetics. Male. Mice. Nitrosamines. Retinoid X Receptor alpha / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Thiazolidinediones / pharmacology. Transcription, Genetic / drug effects

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  • (PMID = 20081051.001).
  • [ISSN] 1535-4989
  • [Journal-full-title] American journal of respiratory cell and molecular biology
  • [ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hydroxyeicosatetraenoic Acids; 0 / Ligands; 0 / Linoleic Acids; 0 / Nitrosamines; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Retinoid X Receptor alpha; 0 / Thiazolidinediones; 5204-88-6 / 13-hydroxy-9,11-octadecadienoic acid; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 73945-47-8 / 15-hydroxy-5,8,11,13-eicosatetraenoic acid; X4OV71U42S / pioglitazone
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5. Blank C, Brown I, Kacha AK, Markiewicz MA, Gajewski TF: ICAM-1 contributes to but is not essential for tumor antigen cross-priming and CD8+ T cell-mediated tumor rejection in vivo. J Immunol; 2005 Mar 15;174(6):3416-20
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  • [Title] ICAM-1 contributes to but is not essential for tumor antigen cross-priming and CD8+ T cell-mediated tumor rejection in vivo.
  • ICAM-1 has been described to provide both adhesion and costimulatory functions during T cell activation.
  • In the setting of antitumor immunity, ICAM-1/LFA-1 interactions could be important at the level of T cell priming by APCs in draining lymph nodes as well as for transendothelial migration and tumor cell recognition at the tumor site.
  • To determine the contribution of ICAM-1 to tumor rejection in vivo, we performed adoptive transfer of 2C TCR-transgenic/RAG2(-/-) T cells into TCRalpha(-/-) vs ICAM(-/-)/TCRalpha(-/-) recipient animals.
  • ICAM-1-deficient mice successfully rejected HTR.C tumors expressing Ld recognized by the 2C TCR, albeit with a kinetic delay.
  • Inasmuch as HTR.C tumor cells themselves express ICAM-1, a second model was pursued using B16-F10 melanoma cells that lack ICAM-1 expression.
  • These cells were transduced to express the SIYRYYGL peptide recognized by the 2C TCR in the context of Kb, which is cross-presented by APCs in H-2b mice in vivo.
  • These tumors also grew more slowly but were eventually rejected by the majority of ICAM-1(-/-)/TCRalpha(-/-) recipients.
  • Delayed rejection in ICAM-1(-/-) mice was associated with diminished T cell priming as assessed by ELISPOT.
  • In contrast, T cell penetration into the tumor was comparable in wild-type and ICAM-1(-/-) hosts, and adoptively transferred primed effector 2C cells rejected normally in ICAM-1(-/-) recipients.
  • Our results suggest that ICAM-1 contributes to but is not absolutely required for CD8+ T cell-mediated tumor rejection in vivo and dominantly acts at the level of priming rather than the effector phase of the antitumor immune response.
  • [MeSH-major] Antigens, Neoplasm. CD8-Positive T-Lymphocytes / immunology. Intercellular Adhesion Molecule-1 / immunology
  • [MeSH-minor] Adoptive Transfer. Animals. Antigen Presentation. Cell Line, Tumor. In Vitro Techniques. Mice. Mice, Knockout. Mice, Transgenic. Neoplasm Transplantation. Neoplasms, Experimental / immunology. Receptors, Antigen, T-Cell, alpha-beta / deficiency. Receptors, Antigen, T-Cell, alpha-beta / genetics

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  • (PMID = 15749875.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / 5 T32 GM07281; United States / NCI NIH HHS / CA / P01CA97296
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Receptors, Antigen, T-Cell, alpha-beta; 126547-89-5 / Intercellular Adhesion Molecule-1
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26. Villa-Bellosta R, Levi M, Sorribas V: Vascular smooth muscle cell calcification and SLC20 inorganic phosphate transporters: effects of PDGF, TNF-alpha, and Pi. Pflugers Arch; 2009 Oct;458(6):1151-61
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  • [Title] Vascular smooth muscle cell calcification and SLC20 inorganic phosphate transporters: effects of PDGF, TNF-alpha, and Pi.
  • Pi transport by vascular smooth muscle cells (VSMC) has been proposed to play an important role in the pathogenesis of vascular calcification.
  • In this study, we have determined the correlation between calcification induced by Pi, platelet-derived growth factor (PDGF)-BB, and tumor necrosis factor-alpha and Pi transport activity in primary cultures of rat aortic VSMC.
  • Only PDGF increased Pi transport when it was expressed per unit of DNA, as PDGF also increased total cell protein by 100%, while DNA content and number of cells were not modified.
  • PDGF increased the expression of the Pi transporter, Pit-1, but membrane protein biotinylation showed that Pit-1 abundance was not modified in the cell surface.
  • Immunofluorescence revealed that, under basal conditions, Pit-1 is only slightly expressed at the cell membrane, but strongly expressed inside the cell.
  • The intracellular signal colocalizes with endoplasmic reticulum (ER) markers, and PDGF increases Pit-1 expression in the ER but not the cell membrane.
  • In conclusion, Pi transport across the plasma membrane does not correlate directly with calcification, but the expression of Pit-1 in the ER opens new possibilities for the study of the pathogenesis of vascular calcification.
  • [MeSH-major] Muscle, Smooth, Vascular / metabolism. Phosphates / pharmacology. Platelet-Derived Growth Factor / pharmacology. Sodium-Phosphate Cotransporter Proteins, Type III / physiology. Tumor Necrosis Factor-alpha / pharmacology

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  • [Cites] Circ Res. 2005 Jul 22;97(2):105-14 [16037577.001]
  • [Cites] Thromb Haemost. 1999 Dec;82(6):1764-7 [10613667.001]
  • [Cites] J Bone Miner Res. 2002 Jul;17(7):1171-9 [12096831.001]
  • [Cites] Toxicol Appl Pharmacol. 2008 Oct 1;232(1):125-34 [18586044.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2009 May;29(5):761-6 [19213941.001]
  • [Cites] Circ Res. 2000 Sep 29;87(7):E10-7 [11009570.001]
  • [Cites] Connect Tissue Res. 1996;34(1):23-32 [8835845.001]
  • [Cites] Am J Physiol Cell Physiol. 2007 Aug;293(2):C606-20 [17494632.001]
  • [Cites] Br J Pharmacol. 2002 Jun;136(4):530-9 [12055131.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2007 May;27(5):1030-6 [17322102.001]
  • [Cites] Endocrinology. 2008 Apr;149(4):1646-53 [18174285.001]
  • [Cites] Toxicol In Vitro. 2007 Sep;21(6):1066-76 [17521863.001]
  • [Cites] Kidney Int. 2002 Nov;62(5):1724-31 [12371973.001]
  • [Cites] J Am Soc Nephrol. 2008 Feb;19(2):213-6 [18094365.001]
  • [Cites] Atherosclerosis. 2007 Nov;195(1):e65-75 [17412344.001]
  • [Cites] Ann N Y Acad Sci. 2007 Nov;1117:40-50 [18056036.001]
  • [Cites] Kidney Int. 2008 Feb;73(4):384-90 [18046319.001]
  • [Cites] Kidney Int. 2006 Apr;69(8):1464-70 [16531981.001]
  • [Cites] Circ Res. 2006 Apr 14;98(7):905-12 [16527991.001]
  • [Cites] Am J Physiol Renal Physiol. 2005 Jul;289(1):F154-65 [15769937.001]
  • [Cites] Atherosclerosis. 2008 Aug;199(2):271-7 [18179800.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2007 Dec;27(12):2589-96 [17932314.001]
  • [Cites] Kidney Int. 2008 Feb;73(4):456-64 [18046316.001]
  • [Cites] Circ Res. 2000 Nov 24;87(11):1055-62 [11090552.001]
  • [Cites] J Am Soc Nephrol. 2005 Feb;16(2):520-8 [15615819.001]
  • [Cites] Circ Res. 2004 Oct 1;95(7):671-6 [15459088.001]
  • [Cites] Circulation. 2005 May 10;111(18):2364-72 [15851600.001]
  • [Cites] Nephrol Dial Transplant. 2006 Apr;21(4):911-6 [16384827.001]
  • [Cites] Atherosclerosis. 2004 May;174(1):17-24 [15135246.001]
  • [Cites] Nephrol Dial Transplant. 2004 Sep;19(9):2387-93 [15252163.001]
  • [Cites] Circulation. 2000 Nov 21;102(21):2636-42 [11085968.001]
  • [Cites] Endocr J. 2007 Feb;54(1):103-12 [17135708.001]
  • [Cites] Am J Kidney Dis. 2001 Oct;38(4 Suppl 1):S34-7 [11576919.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Sep 26;374(3):553-8 [18655772.001]
  • (PMID = 19506901.001).
  • [ISSN] 1432-2013
  • [Journal-full-title] Pflugers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1 R01 DK066029
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Phosphates; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / Slc20a1 protein, rat; 0 / Sodium-Phosphate Cotransporter Proteins, Type III; 0 / Tumor Necrosis Factor-alpha; 1B56C968OA / becaplermin
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27. Studebaker AW, Storci G, Werbeck JL, Sansone P, Sasser AK, Tavolari S, Huang T, Chan MW, Marini FC, Rosol TJ, Bonafé M, Hall BM: Fibroblasts isolated from common sites of breast cancer metastasis enhance cancer cell growth rates and invasiveness in an interleukin-6-dependent manner. Cancer Res; 2008 Nov 1;68(21):9087-95
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  • [Title] Fibroblasts isolated from common sites of breast cancer metastasis enhance cancer cell growth rates and invasiveness in an interleukin-6-dependent manner.
  • Common sites of breast cancer metastasis include the lung, liver, and bone, and of these secondary metastatic sites, estrogen receptor alpha (ERalpha)-positive breast cancer often favors bone.
  • Within secondary organs, cancer cells would predictably encounter tissue-specific fibroblasts or their soluble factors, yet our understanding of how tissue-specific fibroblasts directly affect cancer cell growth rates and survival remains largely unknown.
  • Therefore, we tested the hypothesis that mesenchymal fibroblasts isolated from common sites of breast cancer metastasis provide a more favorable microenvironment with respect to tumor growth rates.
  • We found a direct correlation between the ability of breast, lung, and bone fibroblasts to enhance ERalpha-positive breast cancer cell growth and the level of soluble interleukin-6 (IL-6) produced by each organ-specific fibroblast, and fibroblast-mediated growth enhancement was inhibited by the removal or inhibition of IL-6.
  • Interestingly, mice coinjected with MCF-7 breast tumor cells and senescent skin fibroblasts, which secrete IL-6, developed tumors, whereas mice coinjected with presenescent skin fibroblasts that produce little to no IL-6 failed to form xenograft tumors.
  • We subsequently determined that IL-6 promoted growth and invasion of breast cancer cells through signal transducer and activator of transcription 3-dependent up-regulation of Notch-3, Jagged-1, and carbonic anhydrase IX.
  • These data suggest that tissue-specific fibroblasts and the factors they produce can promote breast cancer disease progression and may represent attractive targets for development of new therapeutics.

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  • (PMID = 18974155.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA109451; United States / NCI NIH HHS / CA / R01 CA109451; United States / NCI NIH HHS / CA / RC1 CA146381; United States / NCI NIH HHS / CA / P50 CA116199; United States / NCI NIH HHS / CA / CA-116199
  • [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 / Culture Media, Conditioned; 0 / Interleukin-6; 0 / STAT3 Transcription Factor
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28. Li YT, He B, Wang YZ: Exposure to cigarette smoke upregulates AP-1 activity and induces TNF-alpha overexpression in mouse lungs. Inhal Toxicol; 2009 Jun;21(7):641-7
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  • [Title] Exposure to cigarette smoke upregulates AP-1 activity and induces TNF-alpha overexpression in mouse lungs.
  • Cigarette smoke-triggered inflammation is important in the pathophysiology of chronic obstructive pulmonary disease, and involves overexpression of many proinflammatory genes.
  • Transcription factors regulating expression of inflammatory mediators may play a key role in characterizing the disease.
  • The levels of inflammatory mediators tumor necrosis factor (TNF)-alpha, interleukin(IL)-6, and IL-8 in bronchoalveolar lavage fluid (BALF) were measured using enzyme-linked immunosorbent assay (ELISA).
  • Compared to the control group, smoke exposure induced a notable increase in TNF-alpha in BALF.
  • These data demonstrated that subacute smoke-triggered lung inflammation was accompanied by inflammatory cell influx, AP-1 activation, and proinflammatory gene overexpression in mouse lungs.
  • [MeSH-major] Gene Expression Regulation / physiology. Lung / metabolism. Smoking / metabolism. Transcription Factor AP-1 / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis. Up-Regulation / physiology

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  • (PMID = 19235541.001).
  • [ISSN] 1091-7691
  • [Journal-full-title] Inhalation toxicology
  • [ISO-abbreviation] Inhal Toxicol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Inflammation Mediators; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha
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29. Yang DI, Chen S, Ezekiel UR, Xu J, Wu Y, Hsu CY: Antisense RNA to inducible nitric oxide synthase reduces cytokine-mediated brain endothelial cell death. Ann N Y Acad Sci; 2005 May;1042:439-47
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  • [Title] Antisense RNA to inducible nitric oxide synthase reduces cytokine-mediated brain endothelial cell death.
  • We test whether inhibition of inducible nitric oxide synthase (iNOS) can exert a cytoprotective effect on cerebral endothelial cells upon stimulation by pro-inflammatory cytokines.
  • Mouse brain endothelial cells were stably transfected to express an antisense RNA against iNOS driven by an endothelium-specific von Willebrand factor (vWF) promoter.
  • Upon stimulation with tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma), antisense transfectants showed less iNOS enzymatic activity with less nitric oxide (NO) when compared to the sense control cells.
  • Correspondingly, the antisense cells showed a reduced LDH release and less cytosolic content of oligonucleosomes.
  • These findings establish a cell-specific antisense strategy and confirm the cytotoxic role of iNOS expression in cultured cerebral endothelial cells.
  • [MeSH-major] Brain / cytology. Brain / metabolism. Cytokines / pharmacology. Endothelial Cells / cytology. Endothelial Cells / metabolism. Nitric Oxide Synthase Type II / metabolism. RNA, Antisense / genetics
  • [MeSH-minor] Animals. Cell Death / drug effects. Cell Line. Mice

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  • (PMID = 15965090.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Antisense; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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30. Birraux J, Kirby JA, Thomason JM, Taylor JJ: The effect of cyclosporin on cell division and apoptosis in human oral keratinocytes. J Periodontal Res; 2006 Aug;41(4):297-302
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  • [Title] The effect of cyclosporin on cell division and apoptosis in human oral keratinocytes.
  • The objective of the present study was to investigate the effects of CsA on the growth of oral epithelial cells in vitro and to test the hypothesis that CsA influences apoptosis in these cells.
  • MATERIAL AND METHODS: Cyclosporin was cocultured with an immortalized normal human oral keratinocyte cell line (HOK-16B), an epitheloid cervical carcinoma cell line (HeLa) and primary oral keratinocytes.
  • Cell division was quantified using a CyQUANT kit.
  • Apoptosis was induced using tumour necrosis factor-alpha (TNF-alpha) and assayed by analysis of caspase-3 activity.
  • RESULTS: CsA exhibited a dose- and time-dependent inhibition of cell division in all three keratinocyte cell cultures.
  • Significantly, HOK-16B cells treated with high doses of CsA (10 alphag/ml) did not recover their proliferative capacity 3 d after withdrawal of CsA, indicating that CsA-induced inhibition of growth is not temporary.
  • Concentrations of CsA that inhibited cell division (1 microg/ml) did not have any effect on constitutive or TNF-alpha -induced apoptosis or Bcl-2 expression in HOK-16B cells.
  • CONCLUSION: CsA inhibits oral epithelial cell division and this effect is not associated with changes in apoptosis in these cells.
  • The action of CsA on oral epithelial cells may be associated with a long-lasting stress signal, which might account for some of the pathological effects of this drug.
  • [MeSH-minor] Caspase 3. Caspases / metabolism. Cell Line, Transformed. Cell Proliferation / drug effects. HeLa Cells. Humans. Proto-Oncogene Proteins c-bcl-2 / biosynthesis

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  • (PMID = 16827723.001).
  • [ISSN] 0022-3484
  • [Journal-full-title] Journal of periodontal research
  • [ISO-abbreviation] J. Periodont. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Proto-Oncogene Proteins c-bcl-2; 83HN0GTJ6D / Cyclosporine; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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31. Zhao YF, Feng DD, Chen C: Contribution of adipocyte-derived factors to beta-cell dysfunction in diabetes. Int J Biochem Cell Biol; 2006;38(5-6):804-19
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  • [Title] Contribution of adipocyte-derived factors to beta-cell dysfunction in diabetes.
  • In addition to serving as an energy reservoir, the adipocyte has been characterized as an endocrine cell, secreting many bioactive factors which influence energy homeostasis.
  • Being overweight, with excessive adipose tissue, is considered to be part of the pathogenesis of type 2 diabetes.
  • Insulin resistance and beta-cell dysfunction are two major pathophysiological changes seen in type 2 diabetes.
  • In addition to inducing insulin resistance in insulin-responsive tissues, adipocyte-derived factors play an important role in the pathogenesis of beta-cell dysfunction.
  • Leptin, free fatty acids, adiponectin, tumor necrosis factor-alpha and interleukin-6 are all produced and secreted by adipocytes, and may directly influence aspects of beta-cell function, including insulin synthesis and secretion, insulin cell survival and apoptosis.
  • During the progression from normal weight to obesity and on to overt diabetes, the adipocyte-derived factors contribute to the occurrence and development of beta-cell dysfunction and type 2 diabetes.
  • [MeSH-major] Adipocytes / physiology. Diabetes Mellitus / physiopathology. Insulin-Secreting Cells / drug effects
  • [MeSH-minor] Adiponectin / physiology. Animals. Fatty Acids, Nonesterified / physiology. Humans. Interleukin-6 / physiology. Leptin / physiology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 16378747.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Fatty Acids, Nonesterified; 0 / Interleukin-6; 0 / Leptin; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 155
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32. Moll R, Sievers E, Hämmerling B, Schmidt A, Barth M, Kuhn C, Grund C, Hofmann I, Franke WW: Endothelial and virgultar cell formations in the mammalian lymph node sinus: endothelial differentiation morphotypes characterized by a special kind of junction (complexus adhaerens). Cell Tissue Res; 2009 Jan;335(1):109-41
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  • [Title] Endothelial and virgultar cell formations in the mammalian lymph node sinus: endothelial differentiation morphotypes characterized by a special kind of junction (complexus adhaerens).
  • The lymph node sinus are channel structures of unquestionable importance in immunology and pathology, specifically in the filtering of the lymph, the transport and processing of antigens, the adhesion and migration of immune cells, and the spread of metastatic cancer cells.
  • Our knowledge of the cell and molecular biology of the sinus-forming cells is still limited, and the origin and biological nature of these cells have long been a matter of debate.
  • Here, we review the relevant literature and present our own experimental results, in particular concerning molecular markers of intercellular junctions and cell differentiation.
  • We show that both the monolayer cells lining the sinus walls and the intraluminal virgultar cell meshwork are indeed different morphotypes of the same basic endothelial cell character, as demonstrated by the presence of a distinct spectrum of general and lymphatic endothelial markers, and we therefore refer to these cells as sinus endothelial/virgultar cells (SEVCs).
  • These cells are connected by unique adhering junctions, termed complexus adhaerentes, characterized by the transmembrane glycoprotein VE-cadherin, combined with the desmosomal plaque protein desmoplakin, several adherens junction plaque proteins including alpha- and beta-catenin and p120 catenin, and components of the tight junction ensemble, specifically claudin-5 and JAM-A, and the plaque protein ZO-1.
  • Overall, the SEVC system might be considered as a local and specific modification of the general lymphatic vasculature system.
  • Finally, physiological and pathological alterations of the SEVC system will be presented, and the possible value of the molecular markers described in histological diagnoses of autochthonous lymph node tumors will be discussed.
  • [MeSH-major] Adherens Junctions / metabolism. Desmosomes / metabolism. Endothelial Cells / metabolism. Lymph Nodes / metabolism. Lymphatic Vessels / metabolism. Tight Junctions / metabolism
  • [MeSH-minor] Animals. Antigens, Differentiation. Biological Transport. Cell Adhesion. Cell Differentiation. Cell Movement. Cytoskeletal Proteins / metabolism. Humans. Lymph / metabolism. Membrane Glycoproteins / metabolism. Neoplasm Metastasis. Neoplasms / metabolism. Neoplasms / pathology

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  • (PMID = 19015886.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Cytoskeletal Proteins; 0 / Membrane Glycoproteins
  • [Number-of-references] 202
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33. Liu R, Li Z, Bai S, Zhang H, Tang M, Lei Y, Chen L, Liang S, Zhao YL, Wei Y, Huang C: Mechanism of cancer cell adaptation to metabolic stress: proteomics identification of a novel thyroid hormone-mediated gastric carcinogenic signaling pathway. Mol Cell Proteomics; 2009 Jan;8(1):70-85
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  • [Title] Mechanism of cancer cell adaptation to metabolic stress: proteomics identification of a novel thyroid hormone-mediated gastric carcinogenic signaling pathway.
  • To determine the mechanism of adaptation to metabolic stress in cancer cells, we used gastric cancer as a model system to reveal the potential signaling pathways involved.
  • Two-dimensional polyacrylamide gel electrophoresis coupled with ESI-Q-TOF MS/MS analysis was used to identify differentially expressed proteins between gastric tumor tissues and the corresponding noncancerous tissues.
  • T(3)-induced expression of HIF1-alpha and vascular endothelial growth factor was further verified using a gastric cancer cell line and in vivo mouse model.
  • Because the early accumulation of HIF1-alpha was found to be independent of de novo transcription, we also found that the cytosolic cascade phosphatidylinositol 3-kinase/Akt pathway sensitive to T(3) stimulus was involved.
  • Furthermore we demonstrated that T(3)-induced overexpression of HIF1-alpha was mediated by fumarate accumulation and could be enhanced by fumarate hydratase inactivation but inhibited by 2-oxoglutarate.
  • These results provide evidence for alteration of metabolic proteins and dysfunction of thyroid hormone regulation in gastric tumors, and a novel thyroid hormone-mediated tumorigenic signaling pathway is proposed.
  • Our findings are considered a significant step toward a better understanding of adaptations to metabolic stress in gastric carcinogenesis.
  • [MeSH-major] Adaptation, Physiological. Proteomics. Signal Transduction. Stomach Neoplasms / metabolism. Stress, Physiological. Thyroid Hormones / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Citrates / metabolism. Electrophoresis, Gel, Two-Dimensional. Fumarate Hydratase / metabolism. Fumarates / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Mass Spectrometry. Mice. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Reproducibility of Results. Triiodothyronine / metabolism. Up-Regulation / drug effects. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18723843.001).
  • [ISSN] 1535-9484
  • [Journal-full-title] Molecular & cellular proteomics : MCP
  • [ISO-abbreviation] Mol. Cell Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Citrates; 0 / Fumarates; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Neoplasm Proteins; 0 / Thyroid Hormones; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 06LU7C9H1V / Triiodothyronine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 4.2.1.2 / Fumarate Hydratase
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34. Choi IY, Kim SJ, Jeong HJ, Park SH, Song YS, Lee JH, Kang TH, Park JH, Hwang GS, Lee EJ, Hong SH, Kim HM, Um JY: Hesperidin inhibits expression of hypoxia inducible factor-1 alpha and inflammatory cytokine production from mast cells. Mol Cell Biochem; 2007 Nov;305(1-2):153-61
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  • [Title] Hesperidin inhibits expression of hypoxia inducible factor-1 alpha and inflammatory cytokine production from mast cells.
  • The citrus unshiu peel has been used traditionally as a medicine to improve bronchial and asthmatic conditions or cardiac and blood circulation in Korea, China, and Japan.
  • Here, we report the effects of citrus unshiu peel water extract (CPWE) on the phorbol myristate acetate (PMA)+calcium ionophore A23187-induced hypoxia-inducible factor-1alpha (HIF-1alpha) activation and inflammatory cytokine production from the human mast cell line, HMC-1 cells.
  • CPWE and hesperidin inhibited the PMA+A23187-induced HIF-1alpha expression and the subsequent production of vascular endothelial growth factor (VEGF).
  • We also show that the increased cytokines interleukin (IL)-1beta, IL-8, and tumor necrosis factor (TNF)-alpha level was significantly inhibited by treatment of CPWE or hesperidin.
  • In the present study, we report that CPWE and hesperidin are inhibitors of HIF-1alpha and cytokines on the mast cell-mediated inflammatory responses.
  • [MeSH-major] Cytokines / metabolism. Hesperidin / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Inflammation Mediators / metabolism. Mast Cells / drug effects. Mast Cells / metabolism
  • [MeSH-minor] Calcimycin / pharmacology. Cell Survival / drug effects. Cells, Cultured. Citrus / chemistry. Drugs, Chinese Herbal / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression / drug effects. HL-60 Cells. HeLa Cells. Humans. Ionophores / pharmacology. Tetradecanoylphorbol Acetate / pharmacology. Vascular Endothelial Growth Factor A / metabolism

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  • [Cites] Phytother Res. 2002 Dec;16(8):781-4 [12458489.001]
  • [Cites] Biochem Pharmacol. 2003 Jun 15;65(12):2065-71 [12787887.001]
  • [Cites] Int Immunopharmacol. 2005 Mar;5(3):461-83 [15683844.001]
  • [Cites] Am J Chin Med. 2005;33(1):87-94 [15844836.001]
  • [Cites] Arch Pharm Res. 1999 Dec;22(6):642-5 [10615874.001]
  • [Cites] Kidney Int. 1997 Feb;51(2):553-5 [9027737.001]
  • [Cites] J Immunol. 2002 Aug 1;169(3):1482-91 [12133975.001]
  • [Cites] Inflamm Res. 2000 Jul;49(7):355-60 [10959557.001]
  • [Cites] Agric Biol Chem. 1990 Nov;54(11):2961-6 [1368650.001]
  • [Cites] Mol Biotechnol. 2001 Oct;19(2):153-68 [11725485.001]
  • [Cites] J Pathol. 2005 Mar;205(4):530-6 [15714461.001]
  • [Cites] Mol Pharmacol. 2001 May;59(5):1216-24 [11306706.001]
  • [Cites] Ann N Y Acad Sci. 2002 Nov;973:448-53 [12485909.001]
  • [Cites] Planta Med. 2006 Apr;72(5):477-9 [16557465.001]
  • [Cites] J Agric Food Chem. 2004 Jun 2;52(11):3389-93 [15161203.001]
  • [Cites] J Biol Chem. 1995 Jan 20;270(3):1230-7 [7836384.001]
  • [Cites] Biol Reprod. 2004 Jun;70(6):1822-7 [14960485.001]
  • [Cites] Clin Exp Allergy. 1997 Sep;27(9):1060-6 [9678838.001]
  • [Cites] Am J Physiol Cell Physiol. 2001 Dec;281(6):C1971-7 [11698256.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Jul;314(1):27-34 [15784648.001]
  • [Cites] Biochem J. 2000 Aug 15;350 Pt 1:307-12 [10926858.001]
  • [Cites] Inflammation. 2003 Jun;27(3):129-35 [12875366.001]
  • [Cites] Bioorg Med Chem. 2007 May 15;15(10):3381-9 [17391969.001]
  • [Cites] Farmaco. 1994 Nov;40(11):709-12 [7832973.001]
  • [Cites] Plant Foods Hum Nutr. 2006 Jun;61(2):57-65 [16816988.001]
  • [Cites] J Biol Chem. 2001 Oct 26;276(43):39805-11 [11514583.001]
  • [Cites] Immunology. 1999 Oct;98(2):253-7 [10540224.001]
  • [Cites] Biochem J. 2006 Jun 15;396(3):517-27 [16533170.001]
  • [Cites] J Nutr. 2005 Apr;135(4):870-7 [15795449.001]
  • [Cites] Biol Pharm Bull. 2000 Mar;23(3):356-8 [10726895.001]
  • [Cites] Mech Ageing Dev. 2005 Dec;126(12):1284-91 [16140359.001]
  • [Cites] FASEB J. 2003 Nov;17 (14 ):2115-7 [12958148.001]
  • [Cites] Autoimmunity. 2005 Aug;38(5):359-67 [16227151.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5059-66 [11016629.001]
  • [Cites] Toxicology. 2006 Sep 21;226(2-3):152-60 [16919860.001]
  • [Cites] Int Immunopharmacol. 2006 Feb;6(2):122-32 [16399617.001]
  • [Cites] Z Naturforsch C. 2003 Jul-Aug;58(7-8):580-9 [12939048.001]
  • [Cites] Nutr Cancer. 2005;51(1):78-82 [15749633.001]
  • [Cites] Planta Med. 2005 Jan;71(1):24-7 [15678369.001]
  • [Cites] J Biol Chem. 2001 Apr 20;276(16):12645-53 [11278891.001]
  • [Cites] Reproduction. 2004 Mar;127(3):379-87 [15016957.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17 ):4873-80 [10987301.001]
  • [Cites] J Biol Chem. 1993 Oct 15;268(29):21513-8 [8408001.001]
  • [Cites] Mol Reprod Dev. 2004 Jun;68(2):198-204 [15095341.001]
  • (PMID = 17629775.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Drugs, Chinese Herbal; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Inflammation Mediators; 0 / Ionophores; 0 / Vascular Endothelial Growth Factor A; 37H9VM9WZL / Calcimycin; E750O06Y6O / Hesperidin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; NI40JAQ945 / Tetradecanoylphorbol Acetate
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35. Bigley NJ, Perymon H, Bowman GC, Hull BE, Stills HF, Henderson RA: Inflammatory cytokines and cell adhesion molecules in a rat model of decompression sickness. J Interferon Cytokine Res; 2008 Feb;28(2):55-63
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  • [Title] Inflammatory cytokines and cell adhesion molecules in a rat model of decompression sickness.
  • Early blood and tissue markers predictive of DCS include inflammatory cytokines and cell adhesion molecules (CAMs).
  • Increased levels of inflammatory cytokines, especially tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interferon-gamma (IFN-gamma), were detected in the circulation 6 h after decompression.
  • Compared with control animals maintained at 1 atmospheres absolute pressure ATA (101 kPascal), significant increases in expression of E-selectin, and L-selectin, as well as intercellular adhesion molecule-1 (ICAM-1), were observed immunohistochemically in the lungs and brains of the rats 6 h after exposure to 2 (203 kPascal), 3 (303 kPascal), or 4 (404 kPascal) ATA, followed by rapid decompression.
  • In contrast to the observations in brain, greater increases in expression of E-selectin and L-selectin around vessels and connective tissue were seen at 24 h after decompression in the quadriceps of rats exposed to either 3 or 4 ATA.
  • This study demonstrated that rapid decompression induces the release of mediators of inflammation and resulting tissue inflammation cascades, as well as a protective anti-inflammatory response.
  • [MeSH-major] Cell Adhesion Molecules / metabolism. Cytokines / metabolism. Decompression Sickness / immunology
  • [MeSH-minor] Animals. Brain / immunology. Disease Models, Animal. E-Selectin / metabolism. Female. Inflammation Mediators / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Interferon-gamma / blood. Interferon-gamma / metabolism. Interleukin-6 / blood. Interleukin-6 / metabolism. L-Selectin / metabolism. Lung / immunology. Muscle, Skeletal / immunology. Rats. Rats, Sprague-Dawley. Receptor, Adenosine A2A / metabolism. Tumor Necrosis Factor-alpha / blood. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18279101.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / E-Selectin; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Receptor, Adenosine A2A; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 126880-86-2 / L-Selectin; 82115-62-6 / Interferon-gamma
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36. Pasche S, Wenger B, Ischer R, Giazzon M, Angeloni S, Voirin G: Integrated optical biosensor for in-line monitoring of cell cultures. Biosens Bioelectron; 2010 Dec 15;26(4):1478-85
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  • [Title] Integrated optical biosensor for in-line monitoring of cell cultures.
  • An analytical detection platform was developed to evaluate the induced toxicity in cell cultures exposed to foreign agents like growth factors or nanoparticles.
  • Connecting a biosensing detection device to the cell culture flasks allows analyzing the composition of cell medium in real-time.
  • The analysis relies on the quantification of inflammatory cytokines released by cells into the cell culture medium, by means of solid-phase immunoassays analyzed with the wavelength interrogated optical sensing (WIOS) instrument.
  • A fluidic system for in situ measurements allows detecting cytokines in real-time, with a sensitivity of 1-100 ng/mL depending on the cytokine.
  • In addition, integration of an in-line optical absorbance measurement unit, in combination with the standard AB cell proliferation assay, provides information on the cell viability in the culture.
  • Fluidic connections between the cell culture flasks, the optical biosensor and the absorbance measurement unit simultaneously allow quantifying up to three cytokines (interleukin 8, interleukin 6 and the monocyte chemotactic protein), assessing cellular proliferation, and thus discriminating between naïve cells and cells exposed to foreign agents such as growth factors (tumor necrosis factor alpha) or nanoparticles.
  • [MeSH-major] Biosensing Techniques / instrumentation. Cell Culture Techniques / instrumentation. Computer Systems
  • [MeSH-minor] Cell Line. Cell Proliferation / drug effects. Cell Survival. Culture Media / analysis. Cytokines / analysis. Cytokines / biosynthesis. Humans. Immunoassay / methods. Nanoparticles / toxicity. Optical Processes. Spectrophotometry. Tumor Necrosis Factor-alpha / pharmacology

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  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20732803.001).
  • [ISSN] 1873-4235
  • [Journal-full-title] Biosensors & bioelectronics
  • [ISO-abbreviation] Biosens Bioelectron
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media; 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha
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37. Zhang W, Liu J, Wu Y, Xiao F, Wang Y, Wang R, Yang H, Wang G, Yang J, Deng H, Li J, Wen Y, Wei Y: Immunotherapy of hepatocellular carcinoma with a vaccine based on xenogeneic homologous alpha fetoprotein in mice. Biochem Biophys Res Commun; 2008 Nov 7;376(1):10-4
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  • [Title] Immunotherapy of hepatocellular carcinoma with a vaccine based on xenogeneic homologous alpha fetoprotein in mice.
  • alpha-Fetoprotein (AFP) is a diagnostic marker for the presence of hepatocellular carcinoma, and a potential target for immunotherapy.
  • In the present study, we used AFP as a model antigen to explore the feasibility of the immunotherapy of AFP-positive liver cancer by the breaking of immune tolerance against AFP in a cross-reaction between the xenogeneic homologues and self molecules.
  • Recombinant rat AFP was prepared as a vaccine, and mouse AFP was prepared as a control.
  • Both humoral and cellular immune responses may be responsible for the antitumor activity against AFP-positive tumor cells, and no marked side effects were observed in the immunized mice.
  • [MeSH-major] Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Carcinoma, Hepatocellular / therapy. Liver Neoplasms / therapy. alpha-Fetoproteins / immunology. alpha-Fetoproteins / therapeutic use
  • [MeSH-minor] Animals. Antibodies, Neoplasm / blood. Antibodies, Neoplasm / immunology. Cell Line, Tumor. Immune Tolerance. Immunotherapy / methods. Mice. Mice, Inbred C57BL. Rats. Recombinant Proteins / genetics. Recombinant Proteins / immunology. Recombinant Proteins / therapeutic use

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  • (PMID = 18725206.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Cancer Vaccines; 0 / Recombinant Proteins; 0 / alpha-Fetoproteins
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38. He C, Deng LF, Yang QM, Shen W, Feng W, Zhang Y, Zhu YP: [Experiment on induction of fibroblasts on 3-D cell-foam structures to express osteoblastic phenotype and its mechanism]. Zhonghua Wai Ke Za Zhi; 2006 Feb 15;44(4):271-4
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  • [Title] [Experiment on induction of fibroblasts on 3-D cell-foam structures to express osteoblastic phenotype and its mechanism].
  • OBJECTIVE: To study the feasibility of osteogenic phenotype expression by human skin fibroblasts induced in polyglycolic acid (PGA) foams and the effect of tumor necrosis factor-alpha (TNF-alpha) on the expression of bone morphogenetic protein (BMP) receptors.
  • The cell-PGA complexes were cultured in RCCS for 6 weeks, in the media of TNF-alpha (50 U/ml) and BMP-2 (0.1 microg/ml).
  • 1 d, 3 and 6 weeks later, cells and extracellular matrix were investigated by electron microscopic and histochemistry observation respectively.
  • Secretion of osteogenic markers were analyzed by biochemical methods. (2) Fibroblasts were seeded on the glass fragments or culture flasks and treated with TNF-alpha (50 U/ml) in different usage (one-time, all-time).
  • The RT-PCR method and the immunohistochemistry fluorescence staining were used to examine the influence of TNF-alpha on the mRNA expression and the protein expression of the type I BMP receptors at 2, 4, 6, 8 d after treatment.
  • RESULTS: Fibroblasts seeded on the PGA foams formed 3-dimensional matrix 3 weeks after seeding, which was demonstrated as osteo-tissue by tetracycline labeling and ARS staining.
  • Cells secreted much more bone-specific alkaline phosphatase (B-AKP) and osteocalcin (OCN) into supernatant than the cells that were cultured in the media without TNF-a and BMP2.
  • Eight days after all-time usage, the TNF-alpha (50 U/ml) increased the expression of the mRNA and protein of the type IB BMP receptor.
  • CONCLUSIONS: Fibroblasts on 3-D cell-foam structures can express osteoblastic phenotype under certain inducing conditions.
  • The numerous fibroblasts in body would be a promising resource for cell seeds candidate of tissue- engineered bone.
  • TNF-alpha provides the essential condition for BMP2's target effect on fibroblasts, and combined use of TNF-alpha and BMP2 is one of the regulating factors.
  • [MeSH-major] Bone Morphogenetic Protein Receptors, Type I / genetics. Bone Morphogenetic Protein Receptors, Type II / genetics. Bone Morphogenetic Proteins / pharmacology. Fibroblasts / cytology. Fibroblasts / drug effects. Transforming Growth Factor beta / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Bone Morphogenetic Protein 2. Cell Culture Techniques / methods. Cell Differentiation / drug effects. Cells, Cultured. Drug Synergism. Humans. Phenotype. Polyglycolic Acid

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  • (PMID = 16635375.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BMP2 protein, human; 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Proteins; 0 / TNF protein, human; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 26009-03-0 / Polyglycolic Acid; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type II
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39. Belyaev NN, Bogdanov AY, Savvulidi PG, Krasnoshtanov VK, Tleulieva RT, Alipov GK, Sekine I, Bae JS, Lee JB, Min YK, Yang HM: The Influence of Alpha-fetoprotein on Natural Suppressor Cell Activity and Ehrlich Carcinoma Growth. Korean J Physiol Pharmacol; 2008 Aug;12(4):193-7
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  • [Title] The Influence of Alpha-fetoprotein on Natural Suppressor Cell Activity and Ehrlich Carcinoma Growth.
  • The influence of alpha-fetoprotein (AFP) on the bone marrow (BM) natural suppressor (NS) cells of intact Ehrlich carcinoma -bearing CBA mice was studied.
  • Bone marrow NS cells were fractionated into three fractions by isopycnic centrifugation on percoll gradients: NS1 (rho=1.080 g/ml), NS2 (rho=1.090 g/ml) and NS3 (1.100>rho>1.090 g/ml).
  • These fractions were highly different in their sensitivity to known NS cell inductors (interleukin (IL)-2, IL-3 or histamine).
  • None of the NS fractions isolated from the intact mice spontaneously produced antiproliferative activity, however, they showed a high level of NS (antiproliferative and natural killer cell inhibitory) activity under the influence of AFP.
  • A single injection of AFP to intact mice led to an increase of spontaneous NS activity and the inhibition of natural killer cell activity.
  • NS activity, especially NS2, was increased in when tumor cells were subcutaneously inoculated three days after AFP injection.
  • In the AFP-treated mice, the tumor mass at 14 days was 60% larger than that in the untreated mice.
  • Our data confirmed that AFP is a tumor marker that can inhibit cancer immunity and plays a role in cancer pathogenesis.

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  • [Cites] J Immunol. 1986 Dec 1;137(11):3538-43 [2946763.001]
  • [Cites] Clin Exp Immunol. 1989 May;76(2):262-7 [2474394.001]
  • [Cites] Int J Cancer. 1989 Aug 15;44(2):307-14 [2527208.001]
  • [Cites] Cancer Res. 1987 Feb 15;47(4):936-42 [3802100.001]
  • [Cites] Exp Hematol. 1990 Aug;18(7):806-11 [2143138.001]
  • [Cites] J Natl Cancer Inst. 1983 Apr;70(4):735-8 [6187964.001]
  • [Cites] J Clin Lab Immunol. 1991 Apr;34(4):183-8 [1726567.001]
  • [Cites] J Immunol. 1995 Jul 1;155(1):15-26 [7541413.001]
  • [Cites] In Vivo. 1994 May-Jun;8(3):279-83 [7803704.001]
  • [Cites] Immunol Invest. 1993 Jul;22(5):329-39 [7691735.001]
  • [Cites] Cancer Immunol Immunother. 1992;35(1):14-8 [1535284.001]
  • [Cites] Cell Immunol. 1992 May;141(2):398-408 [1533570.001]
  • [Cites] Adv Exp Med Biol. 1995;383:255-69 [8644510.001]
  • (PMID = 19967055.001).
  • [ISSN] 2093-3827
  • [Journal-full-title] The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology
  • [ISO-abbreviation] Korean J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2788635
  • [Keywords] NOTNLM ; Alpha-fetoprotein (AFP) / Ehrlich carcinoma (EC) / Natural killer cells / Natural suppressor (NS) cells
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40. Taura M, Fukuda R, Suico MA, Eguma A, Koga T, Shuto T, Sato T, Morino-Koga S, Kai H: TLR3 induction by anticancer drugs potentiates poly I:C-induced tumor cell apoptosis. Cancer Sci; 2010 Jul;101(7):1610-7
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  • [Title] TLR3 induction by anticancer drugs potentiates poly I:C-induced tumor cell apoptosis.
  • Toll-like receptor 3 (TLR3) has gained recognition as a novel molecular target for cancer therapy because TLR3 activation by its synthetic ligand poly I:C directly causes tumor cell death.
  • Recently, we reported that tumor suppressor p53 increases the expression of TLR3 in several tumor cell lines.
  • Another study also showed that interferon-alpha (IFN-alpha) up-regulates TLR3 expression.
  • We thus hypothesized that various anticancer drugs such as p53-activating reagents and IFNs may potentiate poly I:C-induced tumor cell death through the up-regulation of TLR3 expression.
  • Here, we screened several anticancer drugs that, together with poly I:C, effectively cause tumor cell death in colon carcinoma HCT116 cells.
  • We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.
  • On the other hand, IFN-alpha increased poly I:C-induced apoptosis and the TLR3 mRNA level in HCT116 p53(+/+) and p53(-/-) cell lines.
  • Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells.
  • Considering that the p53 status in malignant cells is heterogeneous, this combination approach may provide a highly effective tumor therapy.
  • [MeSH-minor] Adenocarcinoma / genetics. Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line. Cell Line, Tumor. Colorectal Neoplasms / genetics. DNA Damage / drug effects. Fluorouracil / pharmacology. Humans. Interferon-alpha / pharmacology. Interferon-beta / pharmacology. Kidney. Lung Neoplasms / genetics. Mice

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  • (PMID = 20367642.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / TLR3 protein, human; 0 / Toll-Like Receptor 3; 24939-03-5 / Poly I-C; 77238-31-4 / Interferon-beta; U3P01618RT / Fluorouracil
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41. Sapey E, Wood AM, Ahmad A, Stockley RA: Tumor necrosis factor-{alpha} rs361525 polymorphism is associated with increased local production and downstream inflammation in chronic obstructive pulmonary disease. Am J Respir Crit Care Med; 2010 Jul 15;182(2):192-9
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  • [Title] Tumor necrosis factor-{alpha} rs361525 polymorphism is associated with increased local production and downstream inflammation in chronic obstructive pulmonary disease.
  • RATIONALE: Chronic obstructive pulmonary disease (COPD) has a genetic component, explaining susceptibility.
  • Tumor necrosis factor (TNF)-alpha polymorphisms have been associated with COPD, but it is unclear if genotype influences clinical phenotype, protein expression, and bioactivity.
  • OBJECTIVES: To determine if a functional polymorphism was important by assessing TNF-alpha expression and activity and its association with clinical severity over time.
  • TNF-alpha, its antagonists, and downstream mediators were measured in plasma and sputum.
  • To determine TNF-alpha bioactivity, IL-8 secretion from primary bronchial epithelial cells (PBECs) was measured, and neutrophil migration was assessed using sputum from both subject groups in the presence and absence of TNF-alpha antibody.
  • MEASUREMENTS AND MAIN RESULTS: Patients with polymorphism had more chronic bronchitis, a lower body mass index, and a greater annual decline in FEV(1) than patients with COPD without rs361525 polymorphism.
  • TNF-alpha concentrations were 100-fold higher in airway secretions from the patients with the rs361525 polymorphism, with no difference in TNF-alpha antagonists.
  • These effects could be abrogated by TNF-alpha antibody, demonstrating the bioactivity of TNF-alpha in lung secretions from this group.
  • CONCLUSIONS: This TNF-alpha polymorphism is associated with clinical features of disease including progression.
  • There is clear evidence of TNF-alpha overexpression and bioactivity with neutrophilic inflammation.
  • The polymorphism is likely to be a factor that influences a COPD disease phenotype and its progression.
  • [MeSH-major] Polymorphism, Genetic. Pulmonary Disease, Chronic Obstructive / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Aged. Body Mass Index. Bronchi / cytology. Bronchitis / epidemiology. Case-Control Studies. Cell Movement. Disease Progression. Epithelial Cells / metabolism. Female. Forced Expiratory Volume. Genotype. Humans. Interleukin-8 / metabolism. Interleukin-8 / secretion. Male. Middle Aged. Neutrophils / physiology. Peroxidase / metabolism. Phenotype. Severity of Illness Index. Sputum / metabolism

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  • (PMID = 20299531.001).
  • [ISSN] 1535-4970
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / Tumor Necrosis Factor-alpha; EC 1.11.1.7 / Peroxidase
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42. Bolick DT, Srinivasan S, Kim KW, Hatley ME, Clemens JJ, Whetzel A, Ferger N, Macdonald TL, Davis MD, Tsao PS, Lynch KR, Hedrick CC: Sphingosine-1-phosphate prevents tumor necrosis factor-{alpha}-mediated monocyte adhesion to aortic endothelium in mice. Arterioscler Thromb Vasc Biol; 2005 May;25(5):976-81
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  • [Title] Sphingosine-1-phosphate prevents tumor necrosis factor-{alpha}-mediated monocyte adhesion to aortic endothelium in mice.
  • Sphingosine-1-phosphate (S1P) is a sphingolipid that binds to G protein-coupled receptors on endothelial cells (ECs).
  • METHODS AND RESULTS: We injected C57BL/6J mice intravenously with tumor necrosis factor (TNF)-alpha in the presence and absence of the S1P1 receptor agonist SEW2871 and examined monocyte adhesion.
  • Aortas from TNF-alpha-injected mice had a 4-fold increase in the number of monocytes bound, whereas aortas from TNF-alpha plus SEW2871-treated mice had few monocytes bound (P<0.0001).
  • Using siRNA, we found that inhibiting the S1P1 receptor in vascular ECs blocked the ability of S1P to prevent monocyte-EC interactions in response to TNF-alpha.
  • We examined signaling pathways downstream of S1P1 and found that 100 nM S1P increased phosphorylation of Akt and decreased activation of c-jun.
  • CONCLUSIONS: Thus, we provide the first evidence that S1P signaling through the endothelial S1P1 receptor protects the vasculature against TNF-alpha-mediated monocyte-EC interactions in vivo.
  • [MeSH-major] Cell Adhesion / drug effects. Endothelium, Vascular / cytology. Lysophospholipids / pharmacology. Monocytes / cytology. Sphingosine / analogs & derivatives. Tumor Necrosis Factor-alpha / metabolism. Vasculitis / drug therapy
  • [MeSH-minor] Animals. Aorta / cytology. Aorta / immunology. Cells, Cultured. Chemokines / metabolism. E-Selectin / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Mice. Mice, Inbred C57BL. Oxadiazoles / pharmacology. Receptors, Lysosphingolipid / agonists. Receptors, Lysosphingolipid / metabolism. Signal Transduction / drug effects. Signal Transduction / immunology. Thiophenes / pharmacology. Vascular Cell Adhesion Molecule-1 / metabolism

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  • (PMID = 15761190.001).
  • [ISSN] 1524-4636
  • [Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology
  • [ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / F31 GM064101; United States / NIGMS NIH HHS / GM / R01 GM067958; United States / NHLBI NIH HHS / HL / R01 HL079621
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokines; 0 / E-Selectin; 0 / Lysophospholipids; 0 / Oxadiazoles; 0 / Receptors, Lysosphingolipid; 0 / SEW2871; 0 / Thiophenes; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 26993-30-6 / sphingosine 1-phosphate; NGZ37HRE42 / Sphingosine
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43. Doedens AL, Stockmann C, Rubinstein MP, Liao D, Zhang N, DeNardo DG, Coussens LM, Karin M, Goldrath AW, Johnson RS: Macrophage expression of hypoxia-inducible factor-1 alpha suppresses T-cell function and promotes tumor progression. Cancer Res; 2010 Oct 1;70(19):7465-75
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  • [Title] Macrophage expression of hypoxia-inducible factor-1 alpha suppresses T-cell function and promotes tumor progression.
  • T cells can inhibit tumor growth, but their function in the tumor microenvironment is often suppressed.
  • Many solid tumors exhibit abundant macrophage infiltration and low oxygen tension, yet how hypoxic conditions may affect innate immune cells and their role in tumor progression is poorly understood.
  • Targeted deletion of the hypoxia-responsive transcription factor hypoxia-inducible factor-1α (HIF-1α) in macrophages in a progressive murine model of breast cancer resulted in reduced tumor growth, although vascular endothelial growth factor-A levels and vascularization were unchanged.
  • Tumor-associated macrophages can suppress tumor-infiltrating T cells by several mechanisms, and we found that hypoxia powerfully augmented macrophage-mediated T-cell suppression in vitro in a manner dependent on macrophage expression of HIF-1α.
  • Our findings link the innate immune hypoxic response to tumor progression through induction of T-cell suppression in the tumor microenvironment.

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  • [Copyright] © 2010 AACR.
  • [Cites] Trends Immunol. 2002 Nov;23(11):549-55 [12401408.001]
  • [Cites] J Immunol. 2002 Jan 15;168(2):689-95 [11777962.001]
  • [Cites] Cell. 2003 Mar 7;112(5):645-57 [12628185.001]
  • [Cites] J Immunol. 2003 May 15;170(10):5064-74 [12734351.001]
  • [Cites] Trends Immunol. 2003 Jun;24(6):302-6 [12810105.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] J Clin Invest. 2004 Jun;113(12):1734-42 [15199408.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5839-49 [15313928.001]
  • [Cites] J Exp Med. 1991 Mar 1;173(3):647-58 [1900079.001]
  • [Cites] J Surg Res. 1991 Apr;50(4):403-9 [2020192.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]
  • [Cites] J Immunol. 1993 Mar 1;150(5):2072-80 [8436836.001]
  • [Cites] J Immunol Methods. 1994 Sep 14;174(1-2):231-5 [8083527.001]
  • [Cites] Int J Cancer. 1995 Mar 3;60(5):660-7 [7860141.001]
  • [Cites] Eur J Immunol. 1995 Apr;25(4):1101-4 [7537672.001]
  • [Cites] Cancer Immunol Immunother. 1995 Nov;41(5):317-24 [8536278.001]
  • [Cites] J Exp Med. 1996 Apr 1;183(4):1323-9 [8666890.001]
  • [Cites] Mol Cell Biol. 1996 Sep;16(9):4604-13 [8756616.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Aug 14;225(2):485-8 [8753788.001]
  • [Cites] J Biol Chem. 1997 Feb 21;272(8):4959-63 [9030556.001]
  • [Cites] J Immunol. 1998 Jun 15;160(12):5729-34 [9637481.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1592-8 [10197634.001]
  • [Cites] Biochem J. 1999 Jun 1;340 ( Pt 2):549-53 [10333501.001]
  • [Cites] J Clin Invest. 2005 Jul;115(7):1806-15 [16007254.001]
  • [Cites] Nat Rev Immunol. 2005 Aug;5(8):641-54 [16056256.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):1123-31 [16424049.001]
  • [Cites] Immunology. 2006 Mar;117(3):386-95 [16476058.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1627-34 [16709924.001]
  • [Cites] J Clin Invest. 2006 Oct;116(10):2777-90 [17016559.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14895-900 [17003120.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1568-73 [17023580.001]
  • [Cites] Annu Rev Immunol. 2007;25:243-65 [17129181.001]
  • [Cites] Eur J Immunol. 2007 Apr;37(4):935-45 [17330821.001]
  • [Cites] Antioxid Redox Signal. 2007 Aug;9(8):1221-35 [17536958.001]
  • [Cites] Cancer Metastasis Rev. 2007 Jun;26(2):225-39 [17440684.001]
  • [Cites] J Immunol. 2007 Sep 1;179(5):2851-9 [17709499.001]
  • [Cites] Clin Cancer Res. 2007 Sep 15;13(18 Pt 1):5243-8 [17875751.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):903-7 [18026089.001]
  • [Cites] J Clin Invest. 2008 Jun;118(6):1991-2001 [18523649.001]
  • [Cites] Nature. 2008 Dec 11;456(7223):814-8 [18997773.001]
  • [Cites] Genes Dev. 2010 Mar 1;24(5):491-501 [20194441.001]
  • [Cites] Transgenic Res. 1999 Aug;8(4):265-77 [10621974.001]
  • [Cites] Cancer Res. 2000 Aug 1;60(15):4010-5 [10945599.001]
  • [Cites] J Exp Med. 2001 Mar 19;193(6):727-40 [11257139.001]
  • [Cites] Nature. 2001 Apr 26;410(6832):1107-11 [11323675.001]
  • [Cites] J Biol Chem. 2001 May 11;276(19):15881-5 [11278602.001]
  • [Cites] J Exp Med. 2001 Jun 4;193(11):1261-8 [11390433.001]
  • [Cites] J Immunol. 2001 Oct 15;167(8):4293-302 [11591752.001]
  • [Cites] J Immunother. 2001 Nov-Dec;24(6):431-46 [11759067.001]
  • [Cites] J Immunol. 2003 Jan 1;170(1):270-8 [12496409.001]
  • (PMID = 20841473.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA118165; United States / NCI NIH HHS / CA / R01 CA082515; United States / NCI NIH HHS / CA / R01 CA130980; United States / NIAID NIH HHS / AI / R01 AI072117; United States / NCI NIH HHS / CA / R01 CA118165; United States / NCI NIH HHS / CA / R01 CA130980-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse
  • [Other-IDs] NLM/ NIHMS226663; NLM/ PMC2948598
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44. Posypanova GA, Gorokhovets NV, Makarov VA, Savvateeva LV, Kireeva NN, Severin SE, Severin ES: Recombinant alpha-fetoprotein C-terminal fragment: the new recombinant vector for targeted delivery. J Drug Target; 2008 May;16(4):321-8
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  • [Title] Recombinant alpha-fetoprotein C-terminal fragment: the new recombinant vector for targeted delivery.
  • The specific receptor of alpha-fetoprotein (AFP) is a universal tumor marker, being expressed on the surface of many tumor cells, but not in normal human tissues.
  • AFP enters the cell by receptor-mediated endocytosis; its receptor-binding site is hypothetically localized in the third domain of AFP.
  • A recombinant C-terminal AFP fragment, which contains all the third and a part of the second domains of hAFP, was produced.
  • This AFP fragment was bound specifically to the AFP receptor on the surface of tumor cells and was accumulated by them with the same efficiency as the full-size hAFP.
  • Similar to hAFP, the recombinant C-terminal fragment inhibited the estradiol-induced growth of hormone-dependent MCF-7 cells in vitro.
  • Hence, the recombinant C-terminal AFP fragment can be used as a protein vector for the targeted delivery of cytostatic drugs to tumor cells.
  • [MeSH-major] Drug Carriers / pharmacology. alpha-Fetoproteins / pharmacology
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Bacteria / drug effects. Bacteria / genetics. Cell Line, Tumor. DNA, Complementary / biosynthesis. DNA, Complementary / genetics. Escherichia coli / metabolism. Estradiol / pharmacology. Female. Fluorescein-5-isothiocyanate. Fluorescent Dyes. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Microscopy, Fluorescence. Protein Folding. Receptors, Peptide / metabolism. Recombinant Proteins / pharmacology

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  • (PMID = 18446611.001).
  • [ISSN] 1061-186X
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Complementary; 0 / Drug Carriers; 0 / Fluorescent Dyes; 0 / Receptors, Peptide; 0 / Recombinant Proteins; 0 / alpha-Fetoproteins; 0 / alpha-fetoprotein receptor, human; 4TI98Z838E / Estradiol; I223NX31W9 / Fluorescein-5-isothiocyanate
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45. Unursaikhan S, Xu X, Zeng F, Zhang L: Antitumor activities of O-sulfonated derivatives of (1--&gt;3)-alpha-D-glucan from different Lentinus edodes. Biosci Biotechnol Biochem; 2006 Jan;70(1):38-46
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  • [Title] Antitumor activities of O-sulfonated derivatives of (1-->3)-alpha-D-glucan from different Lentinus edodes.
  • Four water-insoluble (1-->3)-alpha-D-glucans, coded L-II1, L-II2, L-II3 and L-II4, with different molecular weights were isolated from four kinds of fruiting bodies of Lentinus Edodes.
  • The four alpha-D-glucans were O-sulfonated to obtain derivatives (SL-II) having degrees of substitution (DS) from 0.9 to 2.1 respectively.
  • The structure of the samples was analyzed by infrared spectra, elemental analysis, and 13C NMR.
  • The weight-average molecular weight (Mw), radii of gyration (<s2>z1/2) and intrinsic viscosity ([eta]) of the native alpha-D-glucans and O-sulfonated derivatives were measured by size-exclusion chromatography combined with laser light scattering (SEC-LLS), LLS, and viscometry in 0.2 M aqueous NaCl and in dimethyl sulfoxide (DMSO) containing 0.25 M LiCl at 25 degrees C respectively.
  • The Mw values of the O-sulfonated derivatives were much lower than those of the native alpha-D-glucans.
  • The experimental results indicate that the O-sulfonated derivatives are water-soluble and exist as an expanded flexible chain in aqueous solution owing to intramolecular hydrogen bonding or interaction between charge groups.
  • The in vivo and in vitro antitumor activities of the native alpha-D-glucans and their O-sulfonated derivatives against solid tumor Sarcoma 180 cells were evaluated and compared.
  • The results reveal that the effect of O-sulfonation of the alpha-D-glucan on the improvement of their antitumor activities was considerable.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Magnetic Resonance Spectroscopy. Mice. Mice, Inbred BALB C. Molecular Weight. Spectroscopy, Fourier Transform Infrared. Viscosity

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  • (PMID = 16428819.001).
  • [ISSN] 0916-8451
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucans; 70FD1KFU70 / Sulfur; 9051-95-0 / alpha-1,3-glucan
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46. Brooksbank R, Woodiwiss AJ, Sliwa K, Badenhorst D, Deftereos D, Wadee AA, Essop MR, Sareli P, Norton GR: Endotoxin-independent white cell cytokine production in haemodynamically stable patients with idiopathic dilated cardiomyopathy. Cardiovasc J S Afr; 2005 Sep-Oct;16(5):260-5
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  • [Title] Endotoxin-independent white cell cytokine production in haemodynamically stable patients with idiopathic dilated cardiomyopathy.
  • INTRODUCTION: In heart failure, increased circulating white cell tumour necrosis factor-alpha production could be attributed to elevated plasma endotoxin concentrations or an increase in white cell sensitivity to endotoxin.
  • AIMS: To ascertain whether, in patients with IDC, circulating white cell TNF-alpha production is also mediated through endotoxin-independent mechanisms.
  • METHODS: Whole blood production of TNF-alpha, both with and without the presence of an endotoxin stimulus, was evaluated in 89 controls and in 60 patients with IDC in New York Heart Association functional class I, II or III heart failure and without evidence of oedema, reduced peripheral perfusion or elevated plasma endotoxin concentrations.
  • RESULTS: In patients compared to controls, IgG (p < 0.01) (IgG1 and IgG3), but not IgM concentrations were elevated, and plasma TNF-alpha and TGF-beta concentrations were raised (p < 0.001, p < 0.02 respectively).
  • In addition, endotoxin-free cultured whole blood TNF-alpha production (p < 0.0005) was increased.
  • Against a role for endotoxin-mediated pre-activation of white cells in patients, the sensitivity of white cells to endotoxin, as determined from the excitatory endotoxin concentration producing 50% maximal TNF-alpha production was unchanged.
  • Moreover, in favour of non-endotoxin-mediated white cell activation, the calcineurin inhibitor, cyclosporin-A, which did not alter endotoxin-induced TNF-alpha production, decreased TNF-alpha produced by unstimulated cultured cells in patients to values not significantly greater than those in controls.
  • CONCLUSIONS: We concluded that circulating white cell cytokine over-production can occur through both endotoxin- dependent and -independent mechanisms in IDC.
  • [MeSH-major] Cardiomyopathy, Dilated / blood. Endotoxins / pharmacology. Leukocytes / metabolism. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Female. Humans. Immunoglobulin G / blood. Immunoglobulin M / blood. In Vitro Techniques. Lymphotoxin-alpha / blood. Male. Middle Aged

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  • (PMID = 16307158.001).
  • [Journal-full-title] Cardiovascular journal of South Africa : official journal for Southern Africa Cardiac Society [and] South African Society of Cardiac Practitioners
  • [ISO-abbreviation] Cardiovasc J S Afr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] South Africa
  • [Chemical-registry-number] 0 / Endotoxins; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha
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47. Keslacy S, Tliba O, Baidouri H, Amrani Y: Inhibition of tumor necrosis factor-alpha-inducible inflammatory genes by interferon-gamma is associated with altered nuclear factor-kappaB transactivation and enhanced histone deacetylase activity. Mol Pharmacol; 2007 Feb;71(2):609-18
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  • [Title] Inhibition of tumor necrosis factor-alpha-inducible inflammatory genes by interferon-gamma is associated with altered nuclear factor-kappaB transactivation and enhanced histone deacetylase activity.
  • Airway smooth muscle (ASM) cells can act as effector cells in the initiation and/or perpetuation of airway inflammation in asthma by producing various inflammatory chemokines or cytokines.
  • Previous studies from our laboratory and others showed that the combination of tumor necrosis factor-alpha (TNFalpha) and interferon-gamma (IFNgamma) or endogenous IFNbeta results in a synergistic induction of various pro-inflammatory genes, including CD38 and regulated upon activation normal T-cell expressed and secreted (RANTES), in ASM cells.
  • [MeSH-major] Gene Expression Regulation / drug effects. Histone Deacetylases / metabolism. Inflammation / genetics. Interferon-gamma / pharmacology. NF-kappa B / genetics. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Cells, Cultured. Chemokine CCL11. Chemokines, CC / biosynthesis. Dose-Response Relationship, Drug. Drug Synergism. Humans. Interleukin-6 / biosynthesis. Interleukin-8 / biosynthesis. Myocytes, Smooth Muscle / cytology. Trachea / cytology. Transcriptional Activation

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  • (PMID = 17108260.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL064063
  • [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 / CCL11 protein, human; 0 / Chemokine CCL11; 0 / Chemokines, CC; 0 / Interleukin-6; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 3.5.1.98 / Histone Deacetylases
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48. Kelly K, Kittelson J, Franklin WA, Kennedy TC, Klein CE, Keith RL, Dempsey EC, Lewis M, Jackson MK, Hirsch FR, Bunn PA, Miller YE: A randomized phase II chemoprevention trial of 13-CIS retinoic acid with or without alpha tocopherol or observation in subjects at high risk for lung cancer. Cancer Prev Res (Phila); 2009 May;2(5):440-9
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  • [Title] A randomized phase II chemoprevention trial of 13-CIS retinoic acid with or without alpha tocopherol or observation in subjects at high risk for lung cancer.
  • We evaluated the effect of 13-cis retinoic acid (13-cis RA), with or without alpha tocopherol, as a lung cancer chemoprevention agent in a phase II randomized controlled clinical trial of adult subjects at high risk for lung cancer as defined by the presence of sputum atypia, history of smoking, and airflow obstruction, or a prior surgically cured nonsmall cell lung cancer (disease free, >3 years).
  • Subjects were randomly assigned to receive either 13-cis RA, 13-cis RA plus alpha tocopherol (13-cis RA/alpha toco) or observation for 12 months.
  • Seventy-five subjects were randomized (27/22/26 to observations/13-cis RA/13-cis RA/alpha toco); 59 completed the trial; 55 had both baseline and follow-up bronchoscopy.
  • The risk of treatment failure was 55.6% (15 of 27) and 50% (24 of 48) in the observation and combined (13 cis RA plus 13 cis RA/alpha toco) treatment arms, respectively (odds ratio adjusted for baseline histology, 0.97; 95% confidence interval, 0.36-2.66; P = 0.95).
  • Similar (nonsignificant) results were observed for treatment effects on endobronchial proliferation as assessed by Ki-67 immunolabeling.
  • Twelve-month treatment with 13-cis RA produced nonsignificant changes in bronchial histology, consistent with results in other trials.
  • The addition of alpha tocopherol did not affect toxicity.

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  • [Cites] Acta Cytol. 1982 Jan-Feb;26(1):78-85 [7039202.001]
  • [Cites] J Natl Cancer Inst. 1980 Dec;65(6):1307-16 [6776329.001]
  • [Cites] Stat Med. 1989 Apr;8(4):431-40 [2727467.001]
  • [Cites] N Engl J Med. 1993 Jan 7;328(1):15-20 [8416267.001]
  • [Cites] Invest New Drugs. 1992 Nov;10(4):239-53 [1487397.001]
  • [Cites] N Engl J Med. 1994 Apr 14;330(15):1029-35 [8127329.001]
  • [Cites] Am J Clin Nutr. 1995 Dec;62(6 Suppl):1431S-1438S [7495244.001]
  • [Cites] N Engl J Med. 1996 May 2;334(18):1150-5 [8602180.001]
  • [Cites] Cancer. 1996 Sep 1;78(5):1004-10 [8780538.001]
  • [Cites] Ann Oncol. 1997 Jan;8(1):85-9 [9093712.001]
  • [Cites] J Natl Cancer Inst. 1999 Apr 21;91(8):691-6 [10218506.001]
  • [Cites] J Natl Cancer Inst. 1999 Aug 4;91(15):1317-21 [10433621.001]
  • [Cites] Ann Intern Med. 2005 Feb 15;142(4):233-9 [15710956.001]
  • [Cites] J Natl Cancer Inst. 2005 Nov 16;97(22):1652-62 [16288118.001]
  • [Cites] Clin Cancer Res. 2006 Jan 1;12(1):314-20 [16397057.001]
  • [Cites] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2281-8 [16609045.001]
  • [Cites] Clin Cancer Res. 2006 Jun 15;12(12):3661-97 [16778094.001]
  • [Cites] JAMA. 2006 Jun 21;295(23):2727-41 [16754727.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1562-4 [16896051.001]
  • [Cites] Am J Respir Crit Care Med. 2007 May 15;175(10):1061-5 [17290039.001]
  • [Cites] J Natl Cancer Inst. 2007 Nov 7;99(21):1603-12 [17971525.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Nov;16(11):2425-31 [18006932.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] N Engl J Med. 2003 Jul 17;349(3):215-24 [12824459.001]
  • [Cites] J Natl Cancer Inst. 2000 Jun 21;92(12):977-86 [10861309.001]
  • [Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):2973-9 [10955773.001]
  • [Cites] Histopathology. 2001 Mar;38(3):202-8 [11260299.001]
  • [Cites] J Natl Cancer Inst. 2001 Apr 18;93(8):605-18 [11309437.001]
  • [Cites] J Natl Cancer Inst. 2001 Jul 18;93(14):1042-3 [11459858.001]
  • [Cites] J Natl Cancer Inst. 2001 Jul 18;93(14):1081-8 [11459869.001]
  • [Cites] J Natl Cancer Inst. 2001 Sep 19;93(18):1385-91 [11562389.001]
  • [Cites] Clin Cancer Res. 2002 Feb;8(2):314-46 [11839647.001]
  • [Cites] N Engl J Med. 2002 Apr 4;346(14):1054-9 [11932472.001]
  • [Cites] J Natl Cancer Inst. 2002 Jul 3;94(13):1001-9 [12096085.001]
  • [Cites] J Natl Cancer Inst. 2003 Feb 5;95(3):206-14 [12569142.001]
  • [Cites] Stat Med. 2004 May 30;23(10):1571-8 [15122737.001]
  • [Cites] Clin Cancer Res. 2004 Oct 1;10(19):6502-11 [15475437.001]
  • [Cites] Fed Proc. 1976 May 1;35(6):1332-8 [770206.001]
  • [Cites] N Engl J Med. 1986 Dec 11;315(24):1501-5 [3537787.001]
  • (PMID = 19401528.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058187; United States / NCI NIH HHS / CA / P50 CA058187-14; United States / NCI NIH HHS / CA / CA058187-14; United States / NCI NIH HHS / CA / P30 CA046934; United States / NCI NIH HHS / CA / P30 CA 46934; United States / NCI NIH HHS / CA / P50 CA 058187
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 1406-66-2 / Tocopherols; EH28UP18IF / Isotretinoin
  • [Other-IDs] NLM/ NIHMS268583; NLM/ PMC3103211
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49. Kretschmar C, Kleinberg L, Greenberg M, Burger P, Holmes E, Wharam M: Pre-radiation chemotherapy with response-based radiation therapy in children with central nervous system germ cell tumors: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2007 Mar;48(3):285-91
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  • [Title] Pre-radiation chemotherapy with response-based radiation therapy in children with central nervous system germ cell tumors: a report from the Children's Oncology Group.
  • BACKGROUND: This Phase II study was designed to determine response to chemotherapy and survival after response-based radiation (RT) in children with CNS germ cell tumors.
  • Children with nongerminomatous tumors or with abnormal markers received doubled doses of cisplatin and CPM.
  • For germinoma patients in complete response (CR), RT was decreased from 50.4 to 30.6 Gy.
  • High-risk patients received neuraxis RT: 50.4 Gy local + 30.6 Gy neuraxis in CR; 54 Gy local + 36 Gy if less than CR.
  • RESULTS: Of 12 germinoma patients, 4 had cerebrospinal fluid (CSF) human chorionic gonadotropin (HCG) 6.9-21 mIU/ml.
  • Of 14 nongerminomatous patients, HCG in serum or CSF was >50 mIU/ml in 9, alpha-fetoprotein (AFP) abnormal in 9.
  • Four germinoma patients attained CR, six PR, one SD, one not evaluable after resection.
  • Two nongerminomatous patients had CR, three PR, three SD, one PD, four not evaluable after resection; one inadequately treated patient had progressive disease (PD).
  • Eleven germinoma patients are PF at median 66 months; one patient in CR refused RT, had PD at 10 months, received RT, and was PF at 56 months.

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • [Cites] J Neurosurg. 1985 Aug;63(2):155-67 [2991485.001]
  • [Cites] Ann Oncol. 2000 Mar;11(3):263-71 [10811491.001]
  • [Cites] J Neurooncol. 1985;3(2):147-52 [3897472.001]
  • [Cites] J Neurosurg. 1986 Oct;65(4):470-5 [2428955.001]
  • [Cites] N Engl J Med. 1987 Jun 4;316(23):1435-40 [2437455.001]
  • [Cites] J Neurosurg. 1987 Jul;67(1):65-70 [2439668.001]
  • [Cites] Prog Exp Tumor Res. 1987;30:307-12 [2819945.001]
  • [Cites] J Neurosurg. 1989 May;70(5):676-81 [2540291.001]
  • [Cites] J Neurosurg. 1989 May;70(5):707-13 [2709111.001]
  • [Cites] Neuro Oncol. 2001 Jul;3(3):174-83 [11465398.001]
  • [Cites] J Neurooncol. 2001 Sep;54(3):311-6 [11767296.001]
  • [Cites] J Clin Oncol. 2002 Feb 1;20(3):857-65 [11821471.001]
  • [Cites] J Clin Oncol. 2004 Mar 1;22(5):846-53 [14990640.001]
  • [Cites] J Clin Oncol. 2004 May 15;22(10):1934-43 [15143087.001]
  • [Cites] J Clin Oncol. 2004 Jul 1;22(13):2691-700 [15226336.001]
  • [Cites] Pediatr Blood Cancer. 2004 Aug;43(2):126-33 [15236278.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Mar;18(3):541-5 [2318686.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Apr;18(4):773-81 [2323968.001]
  • [Cites] Med Pediatr Oncol. 1990;18(4):304-10 [2355890.001]
  • [Cites] Pediatr Hematol Oncol. 1990;7(2):183-8 [2206859.001]
  • [Cites] Neurosurgery. 1990 Sep;27(3):454-60 [1700327.001]
  • [Cites] J Neurosurg. 1991 Apr;74(4):545-51 [1848284.001]
  • [Cites] J Neurooncol. 1992 Jan;12(1):47-52 [1541978.001]
  • [Cites] Ann Neurol. 1992 Oct;32(4):551-4 [1456739.001]
  • [Cites] N Engl J Med. 1993 Jan 14;328(2):87-94 [8416438.001]
  • [Cites] Acta Neurochir (Wien). 1993;120(3-4):111-7 [7681619.001]
  • [Cites] Cancer. 1993 May 15;71(10):3182-4 [8490849.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Jan 1;28(1):229-45 [8270446.001]
  • [Cites] Neuropediatrics. 1994 Feb;25(1):26-32 [8208347.001]
  • [Cites] Cancer. 1994 Aug 1;74(3):940-4 [8039122.001]
  • [Cites] Med Pediatr Oncol. 1995 Jun;24(6):368-72 [7536294.001]
  • [Cites] Neurosurgery. 1995 Mar;36(3):459-64; discussion 464-6 [7538635.001]
  • [Cites] J Child Neurol. 1995 May;10(3):209-12 [7642890.001]
  • [Cites] J Clin Oncol. 1996 Nov;14(11):2908-15 [8918487.001]
  • [Cites] J Neurosurg. 1997 Mar;86(3):446-55 [9046301.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Feb 1;37(3):505-10 [9112445.001]
  • [Cites] Klin Padiatr. 1997 Jul-Aug;209(4):222-7 [9293454.001]
  • [Cites] J Neurosurg. 1998 Jan;88(1):66-72 [9420074.001]
  • [Cites] J Neurooncol. 1998 May;37(3):229-39 [9524081.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1723-8 [9586884.001]
  • [Cites] Eur J Cancer. 1998 Jan;34(1):104-10 [9624246.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):933-40 [10071287.001]
  • [Cites] Br J Cancer. 1999 Mar;79(7-8):1199-204 [10098759.001]
  • [Cites] J Neurooncol. 1997 Mar;32(1):71-80 [9049865.001]
  • [Cites] J Clin Oncol. 1999 Jul;17(7):2127-36 [10561268.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2585-92 [10561326.001]
  • [Cites] Neurosurgery. 1999 Dec;45(6):1292-7; discussion 1297-8 [10598695.001]
  • [Cites] Childs Nerv Syst. 1999 Nov;15(11-12):770-3 [10603021.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Mar 15;46(5):1171-6 [10725628.001]
  • [Cites] Cancer. 1985 Oct 1;56(7 Suppl):1841-6 [4027923.001]
  • (PMID = 16598761.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin; 0 / alpha-Fetoproteins; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS582771; NLM/ PMC4086720
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50. Han ZB, Ren H, Zhao H, Chi Y, Chen K, Zhou B, Liu YJ, Zhang L, Xu B, Liu B, Yang R, Han ZC: Hypoxia-inducible factor (HIF)-1 alpha directly enhances the transcriptional activity of stem cell factor (SCF) in response to hypoxia and epidermal growth factor (EGF). Carcinogenesis; 2008 Oct;29(10):1853-61
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  • [Title] Hypoxia-inducible factor (HIF)-1 alpha directly enhances the transcriptional activity of stem cell factor (SCF) in response to hypoxia and epidermal growth factor (EGF).
  • Stem cell factor (SCF) plays important roles in tumor growth and angiogenesis.
  • Here, we report that hypoxia upregulated the expression of SCF in MCF-7 breast cancer cells in both messenger RNA and protein levels.
  • When hypoxia-inducible factor (HIF)-1 alpha expression was knocked down by RNA interference, the MCF-7 cell expression of SCF was decreased significantly.
  • Furthermore, the SCF receptor, c-kit phosphorylation was significantly strengthened by the condition culture media from hypoxic MCF-7 and MCF-7-c cells.
  • The survival of A549 cells was more dependent on SCF under hypoxia.
  • Chromatin immunoprecipitation assay demonstrated that HIF-1 alpha directly bound to this region under normoxia, and this binding activity was significantly enhanced under hypoxia.
  • Overexpression of HIF-1 alpha significantly upregulated the expression of luciferase reporter gene under control of the SCF promoters in both MCF-7 cells and human embryonic kidney 293 cells, but mutation of the HRE site completely blocked this effect.
  • Epidermal growth factor was also able to enhance the SCF expression under normoxia in MCF-7 cells, which was dependent on HIF-1 alpha.
  • Taken together, our data demonstrated that HIF-1 alpha was a key regulator of SCF expression in breast cancer cells.
  • Hypoxia and epidermal growth factor receptor signal coexisted in the tumor microenvironment and might promote angiogenesis through HIF-1 alpha-mediated upregulation of SCF and other angiogenic factors.
  • [MeSH-major] Cell Hypoxia. Epidermal Growth Factor / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Stem Cell Factor / physiology. Transcription, Genetic
  • [MeSH-minor] Cell Line, Tumor. Humans. Neovascularization, Pathologic / etiology. Promoter Regions, Genetic. Proto-Oncogene Proteins c-kit / physiology. Signal Transduction

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  • (PMID = 18339685.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Stem Cell Factor; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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51. Stier S, Totzke G, Gruewald E, Neuhaus T, Fronhoffs S, Schoneborn S, Vetter H, Ko Y: Identification of p54(nrb) and the 14-3-3 Protein HS1 as TNF-alpha-inducible genes related to cell cycle control and apoptosis in human arterial endothelial cells. J Biochem Mol Biol; 2005 Jul 31;38(4):447-56
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  • [Title] Identification of p54(nrb) and the 14-3-3 Protein HS1 as TNF-alpha-inducible genes related to cell cycle control and apoptosis in human arterial endothelial cells.
  • TNF-alpha plays a pivotal role in inflammation processes which are mainly regulated by endothelial cells.
  • While TNF-alpha induces apoptosis of several cell types like tumor cells, endothelial cells are resistant to TNFa mediated cell death.
  • The cytotoxic effects of TNF-alpha on most cells are only evident if RNA or protein synthesis is inhibited, suggesting that de novo RNA or protein synthesis protect cells from TNF-alpha cytotoxicity, presumably by NF-kappaB mediated induction of protective genes.
  • However, the cytoprotective genes involved in NF-kappaB dependent endothelial cell survival have not been sufficiently identified.
  • In the present study, the suppression subtractive hybridization (SSH) method was employed to identify rarely transcribed TNF-alpha inducible genes in human arterial endothelial cells related to cell survival and cell cycle.
  • The TNF-alpha-induced expression of the RNA binding protein p54(nrb) and the 14-3-3 protein HS1 as shown here for the first time may contribute to the TNF-alpha mediated cell protection of endothelial cells.
  • These genes have been shown to play pivotal roles in cell survival and cell cycle control in different experimental settings.
  • The concerted expression of these genes together with other genes related to cell protection and cell cycle like DnaJ, p21(cip1) and the ubiquitin activating enzyme E1 demonstrates the identification of new genes in the context of TNF-alpha induced gene expression patterns mediating the prosurvival effect of TNF-alpha in endothelial cells.
  • [MeSH-major] Apoptosis / drug effects. Blood Proteins / metabolism. Cell Cycle / drug effects. Endothelium, Vascular / metabolism. Nuclear Matrix-Associated Proteins / metabolism. Octamer Transcription Factors / metabolism. RNA-Binding Proteins / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Cells, Cultured. Humans. NF-kappa B / metabolism. Nucleic Acid Hybridization. Subtraction Technique. Umbilical Cord

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  • (PMID = 16053712.001).
  • [ISSN] 1225-8687
  • [Journal-full-title] Journal of biochemistry and molecular biology
  • [ISO-abbreviation] J. Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / HCLS1 protein, human; 0 / NF-kappa B; 0 / NONO protein, human; 0 / Nuclear Matrix-Associated Proteins; 0 / Octamer Transcription Factors; 0 / RNA-Binding Proteins; 0 / Tumor Necrosis Factor-alpha
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52. Prasad S, Mathur A, Gupta N, Jaggi M, Singh AT, Rajendran P, Sanna VK, Datta K, Mukherjee R: Bombesin analogs containing alpha-amino-isobutyric acid with potent anticancer activity. J Pept Sci; 2007 Jan;13(1):54-62
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  • [Title] Bombesin analogs containing alpha-amino-isobutyric acid with potent anticancer activity.
  • Six octapeptide bombesin (BN) analogs were synthesized by substituting alpha-aminoisobutyric acid (Aib), in place of Ala9 or Gly11, or both, in the [D-Phe6, desMet14]-BN (6-14) sequence: D-Phe6-Gln7-Trp8-Ala9-Val10-Gly11-His12-Leu13-NH2 (P0).
  • The antiproliferative activity of the analogs was tested in vitro on human pancreatic (MiaPaCa-2) and colon cancer (SW620, HT29 and PTC) cell lines using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.
  • The analogs demonstrated anticancer activity in the above cell lines at concentrations ranging from 0.01 nM to 1 microM.
  • One of the analogs, P6, was evaluated for in vivo tumor regression in a xenograft model of human primary colon cancer in athymic nude mice and was found to cause significant reduction in tumor volume.
  • NMR and molecular dynamics (MD) simulation studies for this analog revealed the presence of a mixed 3(10)/alpha-helical structure.
  • [MeSH-major] Aminoisobutyric Acids / chemistry. Antineoplastic Agents / pharmacology. Bombesin / pharmacology. Cell Proliferation / drug effects
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. HT29 Cells. Humans. Magnetic Resonance Spectroscopy. Mice. Mice, Inbred BALB C. Mice, Nude. Models, Molecular. Molecular Structure. Structure-Activity Relationship. Thermodynamics. Xenograft Model Antitumor Assays / methods

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  • [Copyright] (c) 2006 European Peptide Society and John Wiley & Sons, Ltd.
  • (PMID = 17031871.001).
  • [ISSN] 1075-2617
  • [Journal-full-title] Journal of peptide science : an official publication of the European Peptide Society
  • [ISO-abbreviation] J. Pept. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoisobutyric Acids; 0 / Antineoplastic Agents; 1E7ZW41IQU / 2-aminoisobutyric acid; PX9AZU7QPK / Bombesin
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53. Ting HJ, Stice JP, Schaff UY, Hui DY, Rutledge JC, Knowlton AA, Passerini AG, Simon SI: Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha. Circ Res; 2007 Feb 16;100(3):381-90
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  • [Title] Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha.
  • TGRL isolated from human plasma during the postprandial state was examined for its capacity to bind to cultured human aortic endothelial cells (HAECs) and alter the acute inflammatory response to tumor necrosis factor-alpha.
  • This was reflected by increased mitogen-activated protein kinase activation, nuclear translocation of NF-kappaB, amplified expression of endothelial selectin and VCAM-1, and a subsequent increase in monocyte-specific recruitment under shear flow as quantified in a microfabricated vascular mimetic device.
  • [MeSH-major] Aortic Diseases / etiology. Arteriosclerosis / etiology. Arteritis / etiology. Dietary Fats / adverse effects. Endothelial Cells / drug effects. Hypertriglyceridemia / complications. LDL-Receptor Related Proteins / metabolism. Lipoproteins, HDL / toxicity. Lipoproteins, LDL / toxicity. Lipoproteins, VLDL / toxicity. Low Density Lipoprotein Receptor-Related Protein-1 / metabolism. Membrane Transport Proteins / metabolism. Receptors, LDL / metabolism. Triglycerides / toxicity. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Aorta. Apolipoprotein C-III / metabolism. Apolipoprotein C-III / pharmacology. Cell Adhesion / drug effects. Cell Adhesion Molecules / metabolism. Cells, Cultured / drug effects. Cells, Cultured / metabolism. Chylomicrons / blood. E-Selectin / biosynthesis. E-Selectin / genetics. Endocytosis. Endothelium, Vascular / cytology. Fat Emulsions, Intravenous / pharmacology. Gene Expression Regulation / drug effects. Humans. Hypoglycemia. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / genetics. LDL-Receptor Related Protein-Associated Protein / pharmacology. Leukocytes / cytology. Leukocytes / drug effects. Lipopolysaccharides / pharmacology. Models, Cardiovascular. Monocytes / cytology. Monocytes / drug effects. NF-kappa B / metabolism. Oxidative Stress. Rheology. Signal Transduction / drug effects. Vascular Cell Adhesion Molecule-1 / biosynthesis. Vascular Cell Adhesion Molecule-1 / genetics. p38 Mitogen-Activated Protein Kinases / metabolism

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  • [CommentIn] Circ Res. 2007 Apr 13;100(7):e81 [17431191.001]
  • [CommentIn] Circ Res. 2007 Feb 16;100(3):299-301 [17307968.001]
  • (PMID = 17234968.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG19327; United States / NIAID NIH HHS / AI / AI47294; United States / NHLBI NIH HHS / HL / HL077281; United States / NHLBI NIH HHS / HL / HL55667; United States / NHLBI NIH HHS / HL / HL61332
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apolipoprotein C-III; 0 / Cell Adhesion Molecules; 0 / Chylomicrons; 0 / Dietary Fats; 0 / E-Selectin; 0 / Fat Emulsions, Intravenous; 0 / HDL-triglyceride; 0 / LDL-Receptor Related Protein-Associated Protein; 0 / LDL-Receptor Related Proteins; 0 / Lipopolysaccharides; 0 / Lipoproteins, HDL; 0 / Lipoproteins, LDL; 0 / Lipoproteins, VLDL; 0 / Low Density Lipoprotein Receptor-Related Protein-1; 0 / Membrane Transport Proteins; 0 / NF-kappa B; 0 / Receptors, LDL; 0 / SORL1 protein, human; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 0 / VLDL receptor; 0 / Vascular Cell Adhesion Molecule-1; 0 / low density lipoprotein triglyceride; 0 / very low density lipoprotein triglyceride; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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54. Milner CM, Tongsoongnoen W, Rugg MS, Day AJ: The molecular basis of inter-alpha-inhibitor heavy chain transfer on to hyaluronan. Biochem Soc Trans; 2007 Aug;35(Pt 4):672-6
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  • [Title] The molecular basis of inter-alpha-inhibitor heavy chain transfer on to hyaluronan.
  • The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).
  • HC.HA, which is formed for example in the synovial fluids of arthritis patients, is more aggregated than unmodified HA and has altered mechanical and cell-binding properties.
  • It has been shown recently that TSG-6-mediated HC.HA formation is essential for the formation of HA-rich pericellular matrix and for cell migration in a model of wound healing.
  • In contrast, in this model, the formation of cell-associated HA cable-like structures, although requiring the transfer of HCs on to HA, might not involve TSG-6.
  • [MeSH-major] Alpha-Globulins / metabolism. Hyaluronic Acid / metabolism

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  • (PMID = 17635118.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U138274352
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alpha-Globulins; 39346-44-6 / inter-alpha-inhibitor; 9004-61-9 / Hyaluronic Acid
  • [Number-of-references] 18
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55. O'Connor JC, Julian J, Lim SD, Carson DD: MUC1 expression in human prostate cancer cell lines and primary tumors. Prostate Cancer Prostatic Dis; 2005;8(1):36-44
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  • [Title] MUC1 expression in human prostate cancer cell lines and primary tumors.
  • MUC1 expression was evaluated in normal prostate epithelial cells (PrEC), and prostate cancer cell lines in response to dihydrotestosterone (DHT), interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) treatment.
  • Expression of MUC1 core protein was stimulated in PrEC and PC-3 cells after cytokine treatment, but was highly and constitutively expressed by DU-145 cells.
  • MUC1 was not expressed by LNCaP, C4-2 or C4-2B cells under any condition.
  • DHT alone or in combination with cytokines had no effect on MUC1 expression in any cell line tested.
  • Using antibodies capable of detecting all isoforms of MUC1 core protein independent of their glycosylation state, immunohistochemical staining of tissue microarrays containing both nontumor and tumor tissue revealed that only 17% of tumor tissues and 41% of nontumor tissues stained positively for MUC1.
  • Staining patterns in tumor tissue varied from focal apical staining to diffuse cytoplasmic staining.
  • Furthermore, IFN-gamma and TNF-alpha strongly induce MUC1 expression in both normal prostate epithelia and certain prostate tumor cell lines and may exacerbate pathologies associated with MUC1-positive prostate cancers.
  • [MeSH-major] Gene Expression Profiling. Mucin-1 / biosynthesis. Prostatic Neoplasms / genetics. Prostatic Neoplasms / immunology
  • [MeSH-minor] Blotting, Western. Cytokines / pharmacology. Dihydrotestosterone / pharmacology. Humans. Immunohistochemistry. Male. Neoplasm Staging. Tumor Cells, Cultured

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  • (PMID = 15477874.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA098912
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Mucin-1; 08J2K08A3Y / Dihydrotestosterone
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56. Suriano AR, Sanford AN, Kim N, Oh M, Kennedy S, Henderson MJ, Dietzmann K, Sullivan KE: GCF2/LRRFIP1 represses tumor necrosis factor alpha expression. Mol Cell Biol; 2005 Oct;25(20):9073-81
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  • [Title] GCF2/LRRFIP1 represses tumor necrosis factor alpha expression.
  • Tumor necrosis factor alpha (TNF-alpha) is an important mediator of inflammation, apoptosis, and the development of secondary lymphoid structures.
  • The TNF-alpha -308 promoter polymorphism is a G-to-A transition which has been statistically associated with various autoimmune disorders.
  • Some studies have found that it may directly mediate the increased transcription of TNF-alpha in some circumstances.
  • GCF2/LRRFIP1 appears to act as a repressor and occupies the -308 site in cells that do not make TNF-alpha.
  • Cells competent to produce TNF-alpha have Ets-1 bound to the -308 promoter site.
  • Active transcription is accompanied by NF-kappaB and c-Jun binding to the proximal promoter.
  • Thus, dynamic changes on the TNF-alpha promoter, particularly at the -308 site, accompany the transition from repressed to active transcription.
  • GCF2/LRRFIP1 is the first TNF-alpha repressor identified.

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  • [Cites] J Biol Chem. 1998 Aug 21;273(34):21594-602 [9705290.001]
  • [Cites] Arthritis Rheum. 1997 Dec;40(12):2207-11 [9416858.001]
  • [Cites] Immunity. 1999 Mar;10(3):387-98 [10204494.001]
  • [Cites] Circ Res. 1999 Jun 11;84(11):1258-67 [10364563.001]
  • [Cites] Nat Genet. 1999 Jun;22(2):145-50 [10369255.001]
  • [Cites] Genomics. 1999 Jun 1;58(2):146-57 [10366446.001]
  • [Cites] J Leukoc Biol. 1999 Oct;66(4):562-6 [10534109.001]
  • [Cites] Cytokine. 2000 Feb;12(2):110-9 [10671295.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(6):2239-47 [10688670.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):3925-9 [10760264.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(16):6084-94 [10913190.001]
  • [Cites] EMBO J. 2000 Aug 1;19(15):4154-63 [10921895.001]
  • [Cites] J Invest Dermatol. 2000 Oct;115(4):726-30 [10998151.001]
  • [Cites] Ann Rheum Dis. 2001 Jan;60(1):36-42 [11114280.001]
  • [Cites] Exp Hematol. 2001 Mar;29(3):330-8 [11274761.001]
  • [Cites] EMBO J. 2001 Jul 2;20(13):3518-25 [11432838.001]
  • [Cites] J Immunol. 2001 Aug 15;167(4):2202-8 [11490006.001]
  • [Cites] J Immunol. 2001 Dec 15;167(12):6975-82 [11739517.001]
  • [Cites] Nat Genet. 2003 Apr;33(4):469-75 [12627232.001]
  • [Cites] J Leukoc Biol. 2003 Jun;73(6):862-71 [12773519.001]
  • [Cites] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Dec;87(24):9769-73 [2263628.001]
  • [Cites] J Exp Med. 1991 Jul 1;174(1):73-81 [2056282.001]
  • [Cites] J Biol Chem. 1992 Nov 5;267(31):22102-7 [1429562.001]
  • [Cites] Mol Cell Biol. 1992 Dec;12(12):5355-62 [1448070.001]
  • [Cites] Eur J Immunol. 1994 Jan;24(1):191-5 [8020556.001]
  • [Cites] Clin Exp Immunol. 1994 Jul;97(1):45-7 [8033419.001]
  • [Cites] Dermatology. 1994;189 Suppl 1:135-7 [7914110.001]
  • [Cites] Biochem Mol Biol Int. 1996 Sep;40(1):43-51 [8886268.001]
  • [Cites] Neurosci Lett. 1996 Sep 6;215(2):75-8 [8887999.001]
  • [Cites] J Clin Invest. 1994 Oct;94(4):1449-55 [7929820.001]
  • [Cites] Nature. 1994 Oct 6;371(6497):508-10 [7935762.001]
  • [Cites] Clin Exp Immunol. 1995 Feb;99(2):303-10 [7851026.001]
  • [Cites] Cell Immunol. 1995 Mar;161(1):125-31 [7867077.001]
  • [Cites] Hum Immunol. 1994 Dec;41(4):259-66 [7883593.001]
  • [Cites] J Biol Chem. 1995 Mar 24;270(12):6577-83 [7896795.001]
  • [Cites] J Immunol. 1995 Jul 15;155(2):902-8 [7608567.001]
  • [Cites] Dis Markers. 1995 Mar;12(2):127-33 [7614782.001]
  • [Cites] Ann Rheum Dis. 1995 Jul;54(7):601-3 [7668906.001]
  • [Cites] Hum Genet. 1995 Oct;96(4):433-6 [7557966.001]
  • [Cites] J Exp Med. 1995 Nov 1;182(5):1259-64 [7595196.001]
  • [Cites] Mol Cell Biol. 1996 Feb;16(2):459-67 [8552071.001]
  • [Cites] J Inflamm. 1995;45(3):183-92 [8597873.001]
  • [Cites] Hum Genet. 1996 Jun;97(6):813-8 [8641702.001]
  • [Cites] N Engl J Med. 1996 Jun 27;334(26):1717-25 [8637518.001]
  • [Cites] Scand J Immunol. 1996 Apr;43(4):456-63 [8668926.001]
  • [Cites] Ann Acad Med Singapore. 1996 Jan;25(1):90-3 [8779554.001]
  • [Cites] Mol Cell Biol. 1996 Oct;16(10):5232-44 [8816436.001]
  • [Cites] J Inflamm. 1995-1996;46(1):32-41 [8832970.001]
  • [Cites] J Inflamm. 1995-1996;46(1):42-50 [8832971.001]
  • [Cites] J Rheumatol. 1996 Mar;23(3):416-8 [8832975.001]
  • [Cites] J Rheumatol. 1996 Oct;23(10):1725-8 [8895148.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3195-9 [9096369.001]
  • [Cites] J Biol Chem. 1997 Jul 11;272(28):17795-801 [9211933.001]
  • [Cites] Mol Immunol. 1997 Apr;34(5):391-9 [9293772.001]
  • [Cites] Cytokine. 1997 Oct;9(10):787-90 [9344512.001]
  • [Cites] J Interferon Cytokine Res. 1997 Oct;17(10):631-5 [9355965.001]
  • [Cites] Tissue Antigens. 1998 Oct;52(4):359-67 [9820599.001]
  • (PMID = 16199883.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R21 AI090914; United States / NIAID NIH HHS / AI / R01 AI44127; United States / NIAID NIH HHS / AI / R01 AI051323; United States / NIAMS NIH HHS / AR / R29 AR/AI43172; United States / NIAID NIH HHS / AI / R01 AI044127
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS1 protein, human; 0 / LRRFIP1 protein, human; 0 / Proto-Oncogene Protein c-ets-1; 0 / RNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Necrosis Factor-alpha; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC1265793
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57. El-Obeid A, Al-Harbi S, Al-Jomah N, Hassib A: Herbal melanin modulates tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and vascular endothelial growth factor (VEGF) production. Phytomedicine; 2006 May;13(5):324-33
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  • [Title] Herbal melanin modulates tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and vascular endothelial growth factor (VEGF) production.
  • Recent studies have indicated that cytokines can enhance immunogenicity and promote tumor regression.
  • In this study we report the effects of a herbal melanin, extracted from Nigella sativa L., on the production of three cytokines [tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and vascular endothelial growth factor (VEGF)], by human monocytes, total peripheral blood mononuclear cells (PBMC) and THP-1 cell line.
  • Cells were treated with variable concentrations of melanin and the expression of TNF-alpha, IL-6 and VEGF mRNA in cell lysates and secretion of proteins in the supernatants were detected by RT-PCR and ELISA.
  • Melanin induced TNF-alpha, IL-6 and VEGF mRNA expression by the monocytes, PBMC and THP-1 cell line.
  • On the protein level, melanin significantly induced TNF-alpha and IL-6 protein production and inhibited VEGF production by monocytes and PBMC.
  • In the THP-1 cell line melanin induced production of all three cytokine proteins.
  • [MeSH-minor] Actins / analysis. Adult. Cell Line. DNA Primers / chemistry. Gene Expression / drug effects. Humans. Interleukin-6 / biosynthesis. Interleukin-6 / genetics. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. Middle Aged. RNA, Messenger / analysis. Seeds / chemistry. Toxicity Tests, Acute / methods. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / drug effects. Tumor Necrosis Factor-alpha / genetics. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / drug effects. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 16635740.001).
  • [ISSN] 0944-7113
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Actins; 0 / Cytokines; 0 / DNA Primers; 0 / Interleukin-6; 0 / Melanins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A
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58. Kato T, Madono K, Saito J, Kakuta Y, Tanigawa G, Yazawa K, Hosomi M, Ito K: [Successful preoperative interferon-alpha therapy of advanced renal cell carcinoma with tumor thrombus extending into the inferior vena cava: a case report]. Hinyokika Kiyo; 2008 Feb;54(2):119-22
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  • [Title] [Successful preoperative interferon-alpha therapy of advanced renal cell carcinoma with tumor thrombus extending into the inferior vena cava: a case report].
  • We report a case of renal cell carcinoma in which interferon-a therapy was effective in reducing the tumor thrombus extending into the inferior vena cava.
  • We made a diagnosis of a left renal cell carcinoma with tumor thrombus by imaging examination.
  • Twenty-two months after the start of interferon-a therapy, the tumor thrombus was markedly reduced in size, and the clinical response was evaluated as partial response by the response criteria for urological cancer treatrment.
  • Because of improvement of the performance status and downsizing of tumor thrombus, we performed radical nephrectomy.
  • Pathological examinations revealed that viable renal cell carcinomas were found in the primary lesion and the tumor thrombus.
  • In some cases, interferon-alpha therapy is useful and safe in the treatment of the tumor thrombus.
  • Furthermore, radical nephrectomy and complete resection of the tumor thrombus prolongs postoperative survival.
  • [MeSH-major] Carcinoma, Renal Cell / drug therapy. Interferon-alpha / therapeutic use. Kidney Neoplasms / drug therapy. Neoplastic Cells, Circulating / pathology. Thrombosis / pathology. Vena Cava, Inferior / pathology

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  • (PMID = 18323170.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Interferon-alpha
  • [Number-of-references] 9
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59. Cameron AJ, Procyk KJ, Leitges M, Parker PJ: PKC alpha protein but not kinase activity is critical for glioma cell proliferation and survival. Int J Cancer; 2008 Aug 15;123(4):769-79
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  • [Title] PKC alpha protein but not kinase activity is critical for glioma cell proliferation and survival.
  • Protein kinase C alpha (PKCalpha) has been implicated in tumor development with high levels of PKCalpha expression being associated with various malignancies including glioblastomas and tumors of the breast and prostate.
  • To account for its upregulation in these cancers, studies have suggested that PKCalpha plays a role in promoting cell survival.
  • Here we show by siRNA depletion in U87MG glioma cells that a critical threshold level of PKCalpha protein expression is essential for their growth in the presence of serum and for their survival following serum deprivation.
  • Derivation of PKCalpha wt and KO mouse embryo fibroblast cell lines confirms a role for PKCalpha in protecting cells from apoptosis induced by serum deprivation.
  • Notably, PKCalpha was found to mediate chemo-protection in these fibroblastic cell lines.
  • In U87MG cells PKCalpha does not confer chemoprotection though this likely reflects growth arrest associated with its depletion.
  • In contrast to loss of PKCalpha protein, inhibition of PKC kinase activity in glioma cell lines does not significantly inhibit growth or survival.
  • These results indicate an essential pro-proliferative and pro-survival role for PKCalpha in glioma but question the use of ATP competitive inhibitors as therapeutics, either alone, or in combination with chemotoxic agents.
  • [MeSH-major] Glioblastoma / enzymology. Protein Kinase C-alpha / metabolism
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Animals. Cell Cycle / physiology. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / physiology. Cells, Cultured. Culture Media, Serum-Free. Fibroblasts / cytology. Fibroblasts / enzymology. Humans. Indoles / pharmacology. Maleimides / pharmacology. Mice. Mice, Knockout. Naphthalenes / pharmacology. Protein Kinase Inhibitors / pharmacology. RNA, Small Interfering / genetics. Rats

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18508315.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl)-3-(1H-indol-3-yl)maleimide; 0 / Culture Media, Serum-Free; 0 / Indoles; 0 / Maleimides; 0 / Naphthalenes; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; 121263-19-2 / calphostin C; 133052-90-1 / bisindolylmaleimide I; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.11.13 / Protein Kinase C-alpha
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60. Yoshida T, Park JS, Yokosuka K, Jimbo K, Yamada K, Sato K, Nagata K: Effect of a nonprotein bioactive agent on the reduction of cyclooxygenase-2 and tumor necrosis factor-alpha in human intervertebral disc cells in vitro. J Neurosurg Spine; 2008 Nov;9(5):411-8
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  • [Title] Effect of a nonprotein bioactive agent on the reduction of cyclooxygenase-2 and tumor necrosis factor-alpha in human intervertebral disc cells in vitro.
  • In the present study the authors sought to clarify the focal antiinflammatory effects of Neurotropin in intervertebral disc cells, and these effects were compared with those induced by the selective cyclooxygenase (COX)-2 inhibitor 6-methoxy-2-naphthylacetic acid (nabumetone).
  • Cells were stimulated with 500 pg/ml of interleukin (IL)-1beta in the presence of various concentrations of Neurotropin (0, 10(-5), 10(-4), and 10(-3) Neurotropin Units/ml) or 50 microg/ml of nabumetone for 3 hours.
  • The mRNA was extracted for polymerase chain reaction (PCR), and real-time PCR was used to quantify the mRNA levels of COX- 2, tumor necrosis factor (TNF)-alpha, and phospholipase A2.
  • RESULTS: Neurotropin was found to significantly suppress the expression of COX-2 and TNFalpha at mRNA levels as well as the concentration of COX-2 at protein levels in a dose-dependent manner.
  • CONCLUSIONS: Results in this study suggest that Neurotropin has an analgesic effect through the suppression of COX-2 and TNFalpha in a focal area, and nabumetone shows this same effect through the suppression of PGE2 production.
  • [MeSH-major] Analgesics / pharmacology. Cyclooxygenase 2 / metabolism. Intervertebral Disc / drug effects. Lumbar Vertebrae. Polysaccharides / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adult. Butanones. Cell Culture Techniques. Dinoprostone / metabolism. Female. Humans. Interleukin-1beta. Intervertebral Disc Displacement / metabolism. Intervertebral Disc Displacement / pathology. Intervertebral Disc Displacement / surgery. Male. Phospholipases A2 / genetics. Phospholipases A2 / metabolism. RNA, Messenger / metabolism

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  • (PMID = 18976171.001).
  • [ISSN] 1547-5654
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics; 0 / Butanones; 0 / Interleukin-1beta; 0 / Polysaccharides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 42924-53-8 / nabumetone; 57657-35-9 / neurotropin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.1.1.4 / Phospholipases A2; K7Q1JQR04M / Dinoprostone
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61. Stigliano A, Cerquetti L, Borro M, Gentile G, Bucci B, Misiti S, Piergrossi P, Brunetti E, Simmaco M, Toscano V: Modulation of proteomic profile in H295R adrenocortical cell line induced by mitotane. Endocr Relat Cancer; 2008 Mar;15(1):1-10
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  • [Title] Modulation of proteomic profile in H295R adrenocortical cell line induced by mitotane.
  • In this type of cancer, the biological mechanism induced by this treatment remains still unknown.
  • In this study, we have already shown a greater impairment in the first steps of the steroidogenesis and recognized a little effect on cell cycle.
  • We also evaluated the variation of proteomic profile of the H295R ACC cell line, either in total cell extract or in mitochondria-enriched fraction after treatment with mitotane.
  • In total cell extracts, triose phosphate isomerase, alpha-enolase, D-3-phosphoglycerate dehydrogenase, peroxiredoxin II and VI, heat shock protein 27, prohibitin, histidine triad nucleotide-binding protein, and profilin-1 showed a different expression.
  • It permits to identify some protein classes affected by the drug involved in energetic metabolism, stress response, cytoskeleton structure, and tumorigenesis.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Carcinoma / metabolism. Antineoplastic Agents, Hormonal / pharmacology. Biomarkers, Tumor / metabolism. Mitotane / pharmacology. Neoplasm Proteins / metabolism. Proteomics
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Proliferation / drug effects. Electrophoresis, Gel, Two-Dimensional. Humans. Hydrocortisone / metabolism. Mitochondria / drug effects. Mitochondria / metabolism. Progesterone / metabolism. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Testosterone / metabolism. Tumor Cells, Cultured / drug effects

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  • (PMID = 18310271.001).
  • [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 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 3XMK78S47O / Testosterone; 4G7DS2Q64Y / Progesterone; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
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62. Kawaguchi K, Honda M, Yamashita T, Shirota Y, Kaneko S: Differential gene alteration among hepatoma cell lines demonstrated by cDNA microarray-based comparative genomic hybridization. Biochem Biophys Res Commun; 2005 Apr 1;329(1):370-80
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  • [Title] Differential gene alteration among hepatoma cell lines demonstrated by cDNA microarray-based comparative genomic hybridization.
  • We assayed chromosomal abnormalities in hepatoma cell lines using the microarray-based comparative genomic hybridization (array-CGH) method and investigated the relationship between genomic copy number alterations and expression profiles in these hepatoma cell lines.
  • We modified a cDNA array-CGH assay to compare genomic DNAs from seven hepatoma cell lines, as well as DNA from two non-hepatoma cell lines and from normal cells.
  • We predominantly found alterations of apoptosis-related genes in Hep3B and HepG2, cell adhesion and receptor molecules in HLE, and cytokine-related genes in PLC/PRF/5.
  • Hierarchical clustering analysis showed that the expression of these genes allows differentiation between alpha-fetoprotein (AFP)-producing and AFP-negative cell lines. cDNA array-CGH is a sensitive method that can be used to detect alterations in genomic copy number in tumor cells.
  • Differences in DNA copy alterations between AFP-producing and AFP-negative cells may lead to differential gene expression and may be related to the phenotype of these cells.
  • [MeSH-major] Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Liver Neoplasms / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Apoptosis. Blotting, Southern. Carcinoma, Hepatocellular / metabolism. Cell Adhesion. Cell Line, Tumor. Chromosome Mapping. Cluster Analysis. DNA, Complementary / metabolism. Gene Deletion. Humans. Phenotype. Protein Binding. RNA, Messenger / metabolism. alpha-Fetoproteins / metabolism

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  • (PMID = 15721316.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / RNA, Messenger; 0 / alpha-Fetoproteins
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63. Kreckler LM, Gizewski E, Wan TC, Auchampach JA: Adenosine suppresses lipopolysaccharide-induced tumor necrosis factor-alpha production by murine macrophages through a protein kinase A- and exchange protein activated by cAMP-independent signaling pathway. J Pharmacol Exp Ther; 2009 Dec;331(3):1051-61
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  • [Title] Adenosine suppresses lipopolysaccharide-induced tumor necrosis factor-alpha production by murine macrophages through a protein kinase A- and exchange protein activated by cAMP-independent signaling pathway.
  • Adenosine is generated during tissue hypoxia and stress, which reduces inflammation by suppressing the activity of most immune cells.
  • Among its various actions, adenosine suppresses the production of proinflammatory cytokines including tumor necrosis factor (TNF)-alpha, through the cAMP-elevating A(2A) adenosine receptor (AR) subtype.
  • In this study, we examined the signaling mechanisms by which A(2A)AR activation inhibits TNF-alpha production in thioglycollate-elicited mouse peritoneal macrophages.
  • Pretreating murine macrophages with the nonselective AR agonist adenosine-5'-N-ethylcarboxamide (NECA), the A(2A)AR agonist 2-[p-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21680), or the cAMP-elevating agent forskolin reduced TNF-alpha production in response to lipopolysaccharide (LPS) by greater than 60%.
  • However, we were surprised to find that treating macrophages with three different PKA inhibitors or small interfering RNA-mediated knockdown of the exchange protein activated by cAMP (Epac-1) failed to block the suppressive actions of NECA or forskolin on LPS-induced TNF-alpha release.
  • Subsequent studies showed that NECA and forskolin decreased LPS-induced steady-state TNF-alpha mRNA levels; this effect was due to a decreased rate of transcription based on assays examining the rate of generation of primary TNF-alpha transcripts.
  • Treatment with NECA or forskolin did not interfere with LPS-induced translocation or DNA binding of the RelA/p65 subunit of nuclear factor-kappaB or phosphorylation of inhibitor of nuclear factor-kappaB-alpha, extracellular signal-regulated kinase 1/2, c-Jun NH(2)-terminal kinase, or p38 kinase.
  • Our results suggest that AR activation inhibits LPS-induced TNF-alpha production by murine macrophages at the level of gene transcription through a unique cAMP-dependent, but PKA- and Epac-independent, signaling pathway involving protein phosphatase activity.

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  • [Cites] J Immunol. 2006 Jan 1;176(1):451-62 [16365438.001]
  • [Cites] J Leukoc Biol. 2005 Aug;78(2):515-23 [15894584.001]
  • [Cites] Nat Neurosci. 2006 Apr;9(4):501-10 [16531999.001]
  • [Cites] Trends Biochem Sci. 2006 Dec;31(12):680-6 [17084085.001]
  • [Cites] J Leukoc Biol. 2006 Dec;80(6):1542-52 [16940330.001]
  • [Cites] Exp Mol Med. 2007 Aug 31;39(4):421-38 [17934330.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 2008 Jun;377(4-6):345-57 [18176800.001]
  • [Cites] Nat Rev Drug Discov. 2008 Sep;7(9):759-70 [18758473.001]
  • [Cites] Am J Respir Cell Mol Biol. 2009 Mar;40(3):251-9 [18703794.001]
  • [Cites] Am J Physiol. 1999 Dec;277(6 Pt 1):C1021-8 [10600752.001]
  • [Cites] J Leukoc Biol. 2000 Apr;67(4):520-8 [10770285.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 2000 Nov;362(4-5):364-74 [11111830.001]
  • [Cites] Mol Pharmacol. 2001 Jan;59(1):76-82 [11125027.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(20):7065-77 [11564889.001]
  • [Cites] Cell. 2002 Apr;109 Suppl:S81-96 [11983155.001]
  • [Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]
  • [Cites] Nat Cell Biol. 2002 Nov;4(11):901-6 [12402047.001]
  • [Cites] J Leukoc Biol. 2002 Nov;72(5):1027-36 [12429726.001]
  • [Cites] Biochem Pharmacol. 2003 Feb 15;65(4):493-501 [12566076.001]
  • [Cites] Oncogene. 2003 Feb 27;22(8):1206-18 [12606947.001]
  • [Cites] J Pharmacol Exp Ther. 2003 Sep;306(3):1042-9 [12766259.001]
  • [Cites] Brain Res Mol Brain Res. 2003 Sep 10;117(1):1-7 [14499475.001]
  • [Cites] Trends Immunol. 2004 Jan;25(1):33-9 [14698282.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 May;5(5):392-401 [15122352.001]
  • [Cites] J Biol Chem. 2004 Jun 4;279(23):24873-80 [15140884.001]
  • [Cites] J Immunol. 2004 Jul 1;173(1):21-4 [15210754.001]
  • [Cites] Cell Signal. 2004 Oct;16(10):1113-21 [15240006.001]
  • [Cites] Eur J Pharmacol. 2004 Aug 16;497(1):87-95 [15321739.001]
  • [Cites] Virology. 2004 Oct 1;327(2):186-95 [15351206.001]
  • [Cites] Mol Pharmacol. 2004 Nov;66(5):1147-59 [15286208.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] EMBO J. 1995 May 1;14(9):1991-2004 [7744006.001]
  • [Cites] J Biol Chem. 1996 Jul 19;271(29):17114-8 [8663342.001]
  • [Cites] Nature. 1998 Dec 3;396(6710):474-7 [9853756.001]
  • [Cites] Am J Physiol. 1999 May;276(5 Pt 2):H1468-81 [10330229.001]
  • [Cites] Eur J Immunol. 2005 Jan;35(1):31-41 [15580656.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8686-91 [15937121.001]
  • [Cites] J Pharmacol Exp Ther. 2006 Apr;317(1):172-80 [16339914.001]
  • (PMID = 19749080.001).
  • [ISSN] 1521-0103
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL077707; United States / NHLBI NIH HHS / HL / R01-HL60051; United States / NHLBI NIH HHS / HL / HL077707-04; United States / NHLBI NIH HHS / HL / R01 HL060051; United States / NHLBI NIH HHS / HL / R01 HL077707-04; United States / NHLBI NIH HHS / HL / R01 HL077707-05; United States / NHLBI NIH HHS / HL / R01-HL077707
  • [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 / Adenosine A2 Receptor Agonists; 0 / Epac protein, mouse; 0 / Guanine Nucleotide Exchange Factors; 0 / Lipopolysaccharides; 0 / Receptor, Adenosine A2A; 0 / Tumor Necrosis Factor-alpha; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; K72T3FS567 / Adenosine
  • [Other-IDs] NLM/ PMC2784717
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64. Decker WK, Li S, Xing D, Robinson SN, Yang H, Steiner D, Komanduri KV, Bollard CM, Shpall EJ: Deficient T(H)-1 responses from TNF-alpha-matured and alpha-CD40-matured dendritic cells. J Immunother; 2008 Feb-Mar;31(2):157-65
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  • [Title] Deficient T(H)-1 responses from TNF-alpha-matured and alpha-CD40-matured dendritic cells.
  • The ultimate success of dendritic cell (DC) vaccination for the active immunotherapy of neoplasia is thought to be dependent on a very large number of variables, including DC generation protocol, loading methodology, dose, route of administration, and maturation method.
  • Although the use of a maturation cocktail comprising interleukin (IL)-1beta, tumor necrosis factor-alpha, IL-6, and prostaglandin E2 (ITIP) has recently appeared in the literature, much of the data in the basic and clinical literature have been generated using DCs matured with the single inflammatory cytokine TNF-alpha.
  • Here, we demonstrate that DCs matured with TNF-alpha alone or in combination with CD40 agonism are highly deficient, both physiologically and functionally, in comparison with DCs matured with IL-1beta, TNF-alpha, IL-6, and prostaglandin E2.
  • Empirically, the data suggest that DCs matured with these agents are deficient in the induction of type 1 T-helper responses.
  • [MeSH-major] Antigens, CD40 / agonists. Cell Differentiation / drug effects. Dendritic Cells / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Antigens, CD / metabolism. CD8-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / drug effects. CD8-Positive T-Lymphocytes / immunology. Cell Proliferation / drug effects. Dinoprostone / pharmacology. Humans. Interferon-gamma / metabolism. Interleukin-10 / metabolism. Interleukin-12 / metabolism. Interleukin-1beta / pharmacology. Interleukin-6 / pharmacology. Lymphocyte Activation / drug effects. Lymphocyte Activation / immunology. T-Lymphocytes / immunology. T-Lymphocytes / metabolism

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  • (PMID = 18481385.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 R01 CA061508-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD40; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma; K7Q1JQR04M / Dinoprostone
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65. He J, King Y, Jiang J, Safavi KE, Spångberg LS, Zhu Q: Enamel matrix derivative inhibits TNF-alpha-induced apoptosis in osteoblastic MC3T3-E1 cells. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2005 Jun;99(6):761-7
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  • [Title] Enamel matrix derivative inhibits TNF-alpha-induced apoptosis in osteoblastic MC3T3-E1 cells.
  • OBJECTIVE: The purpose of this study was to examine the effect of enamel matrix derivative (EMD) on TNF-alpha-induced apoptosis in osteoblastic MC3T3-E1 cells.
  • STUDY DESIGN: MC3T3-E1 cells were cultured at an initial density of 5000/cm 2 in Dulbecco's modified eagle medium (DMEM) with 10% fetal bovine serum (FBS) and allowed to adhere for 24 hours.
  • After 16 hours, cells were treated with EMD (100 microg/mL) alone, tumor necrosis factor alpha (TNF-alpha) (20 ng/mL) alone, transforming growth factor beta 1 (TGF-beta1) (10 ng/mL) alone, TNF-alpha plus TGF-beta1, or TNF-alpha plus EMD.
  • Cells cultured with DMEM and 0.5% FBS served as control.
  • Following 24-hour incubation, apoptosis was assessed by terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay, and quantified by cell death enzyme-linked immunosorbent assay (ELISA).
  • RESULTS: Both TUNEL assay and cell death ELISA show that TNF-alpha induces apoptosis in MC3T3-E1 cells.
  • TNF-alpha increases cell death by approximately 2-fold, which is attenuated by both EMD and TGF-beta1.
  • [MeSH-minor] 3T3 Cells. Animals. Enzyme-Linked Immunosorbent Assay / methods. In Situ Nick-End Labeling. Mice. Transforming Growth Factor beta / pharmacology. Transforming Growth Factor beta1. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 15897865.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / DE14126
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dental Enamel Proteins; 0 / Tgfb1 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 0 / enamel matrix proteins
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66. Yu H, Jiang X, Shen C, Karunakaran KP, Jiang J, Rosin NL, Brunham RC: Chlamydia muridarum T-cell antigens formulated with the adjuvant DDA/TDB induce immunity against infection that correlates with a high frequency of gamma interferon (IFN-gamma)/tumor necrosis factor alpha and IFN-gamma/interleukin-17 double-positive CD4+ T cells. Infect Immun; 2010 May;78(5):2272-82
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  • [Title] Chlamydia muridarum T-cell antigens formulated with the adjuvant DDA/TDB induce immunity against infection that correlates with a high frequency of gamma interferon (IFN-gamma)/tumor necrosis factor alpha and IFN-gamma/interleukin-17 double-positive CD4+ T cells.
  • Major impediments to developing a Chlamydia vaccine lie in identifying immunologically relevant T-cell antigens and delivery in a manner to stimulate protective immunity.
  • Using an immunoproteomic approach, we previously identified three immunodominant Chlamydia T-cell antigens (PmpG-1, PmpE/F-2, and RplF).
  • Therefore, in this study, we evaluated protection against Chlamydia infection in the genital tract in C57BL/6 mice immunized with Chlamydia-specific membrane proteins PmpG-1, PmpE/F-2, and major outer membrane protein (MOMP; as a reference) or a combination of them formulated with one of three adjuvants, CpG oligodeoxynucleotide (CpG-ODN), AbISCO-100 (AbISCO), or DDA/TDB (dimethyldioctadecylammonium bromide/D-(+)-trehalose 6,6'-dibehenate).
  • The results show that immunization with the CpG-ODN formulation failed to provide protection against Chlamydia infection; the AbISCO formulation conferred moderate protection, and the DDA/TDB formulation showed the highest degree of protective efficacy.
  • We measured cell-mediated immune cytokine responses in mice immunized with PmpG-1 mixed with each of the three adjuvants.
  • The results demonstrate that mice immunized with the DDA/TDB formulation induced the strongest gamma interferon (IFN-gamma) and interleukin-17 (IL-17) responses, characterized by the highest frequency of IFN-gamma/tumor necrosis factor alpha (TNF-alpha) and IFN-gamma/IL-17 double-positive CD4(+) T cells.
  • In conclusion, a Chlamydia vaccine based on the recombinant proteins PmpG-1, PmpE/F-2, and MOMP delivered in a DDA/TDB adjuvant conferred protection against infection that correlated with IFN-gamma/TNF-alpha and IFN-gamma/IL-17 double-positive CD4(+) T cells.

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  • [Cites] Eur J Immunol. 1999 Nov;29(11):3782-92 [10556835.001]
  • [Cites] Int J Cancer. 1979 Dec 15;24(6):780-5 [544531.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Sep;298(3):1185-92 [11504819.001]
  • [Cites] Infect Immun. 2001 Oct;69(10):6240-7 [11553566.001]
  • [Cites] J Virol. 2002 Sep;76(18):9002-10 [12186884.001]
  • [Cites] J Immunol. 2003 May 15;170(10):5228-34 [12734371.001]
  • [Cites] Vaccine. 2003 Jun 2;21(19-20):2433-40 [12744876.001]
  • [Cites] Expert Rev Vaccines. 2003 Feb;2(1):129-46 [12901604.001]
  • [Cites] Infect Immun. 2004 Mar;72(3):1608-17 [14977968.001]
  • [Cites] J Virol. 2004 Apr;78(7):3333-42 [15016855.001]
  • [Cites] Immunol Rev. 2004 Jun;199:201-16 [15233736.001]
  • [Cites] Am J Ophthalmol. 1967 May;63(5):Suppl:1615-30 [4960884.001]
  • [Cites] J Infect Dis. 1980 Apr;141(4):473-8 [7373082.001]
  • [Cites] Infect Immun. 1981 Mar;31(3):1161-76 [7228399.001]
  • [Cites] J Immunol. 1990 Dec 15;145(12):4306-10 [2175327.001]
  • [Cites] Infect Immun. 1995 Sep;63(9):3302-8 [7642259.001]
  • [Cites] J Immunol. 1996 Jun 1;156(11):4338-44 [8666805.001]
  • [Cites] J Exp Med. 1997 Nov 17;186(10):1623-31 [9362523.001]
  • [Cites] J Immunol. 1999 Mar 15;162(6):3541-8 [10092812.001]
  • [Cites] Sex Transm Dis. 1978 Apr-Jun;5(2):73-7 [10328037.001]
  • [Cites] Nat Rev Immunol. 2005 Feb;5(2):149-61 [15688042.001]
  • [Cites] Infect Dis Clin North Am. 2005 Jun;19(2):477-90, xi [15963884.001]
  • [Cites] J Immunol. 2005 Sep 1;175(5):3197-206 [16116210.001]
  • [Cites] J Infect Dis. 2005 Nov 15;192(10):1836-44 [16235186.001]
  • [Cites] Infect Immun. 2005 Dec;73(12):8153-60 [16299310.001]
  • [Cites] Biochim Biophys Acta. 2005 Dec 10;1718(1-2):22-31 [16321607.001]
  • [Cites] Vaccine. 2006 Feb 6;24(6):766-75 [16199110.001]
  • [Cites] J Exp Med. 2006 May 15;203(5):1249-58 [16636134.001]
  • [Cites] Vaccine. 2006 Jun 29;24(26):5452-60 [16675077.001]
  • [Cites] Immunity. 2006 Jun;24(6):677-88 [16782025.001]
  • [Cites] Nat Immunol. 2007 Apr;8(4):369-77 [17351619.001]
  • [Cites] Annu Rev Immunol. 2007;25:821-52 [17201677.001]
  • [Cites] Science. 2007 Jun 15;316(5831):1628-32 [17569868.001]
  • [Cites] Nat Med. 2007 Jul;13(7):843-50 [17558415.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1849-61 [17635957.001]
  • [Cites] J Exp Med. 2007 Oct 29;204(11):2733-46 [17954572.001]
  • [Cites] Curr Opin Immunol. 2007 Dec;19(6):652-7 [17766098.001]
  • [Cites] J Immunol. 2008 Feb 15;180(4):2459-65 [18250455.001]
  • [Cites] Nat Rev Immunol. 2008 Apr;8(4):313-7 [18309315.001]
  • [Cites] J Infect Dis. 2008 Sep 1;198(5):758-67 [18652549.001]
  • [Cites] Int Immunol. 2008 Sep;20(9):1129-38 [18599501.001]
  • [Cites] J Exp Med. 2009 Jan 16;206(1):89-97 [19139169.001]
  • [Cites] J Immunol. 2009 Feb 1;182(3):1602-8 [19155509.001]
  • [Cites] FEMS Immunol Med Microbiol. 2009 Mar;55(2):215-25 [19281567.001]
  • [Cites] J Immunol. 2009 Jun 15;182(12):8063-70 [19494332.001]
  • [Cites] J Exp Med. 2009 Jul 6;206(7):1549-64 [19546248.001]
  • [Cites] J Immunol. 2009 Jul 15;183(2):1291-300 [19542374.001]
  • [Cites] Infect Immun. 2009 Nov;77(11):5059-70 [19737908.001]
  • [Cites] J Immunol. 2009 Nov 1;183(9):5886-95 [19812198.001]
  • [Cites] J Exp Med. 2009 Dec 21;206(13):2879-88 [20008526.001]
  • [Cites] Infect Immun. 2000 Dec;68(12):6979-87 [11083822.001]
  • (PMID = 20231405.001).
  • [ISSN] 1098-5522
  • [Journal-full-title] Infection and immunity
  • [ISO-abbreviation] Infect. Immun.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI076483; United States / NIAID NIH HHS / AI / R01AI076483
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens, Bacterial; 0 / Bacterial Vaccines; 0 / Interleukin-17; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2863536
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67. Poli UR, Swarnalata G, Maturi R, Rao ST: Recurrent alpha-fetoprotein secreting Sertoli-Leydig cell tumor of ovary with an unusual presentation. Indian J Cancer; 2009 Jan-Mar;46(1):64-6
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  • [Title] Recurrent alpha-fetoprotein secreting Sertoli-Leydig cell tumor of ovary with an unusual presentation.
  • Alpha-fetoprotein secreting (AFP) Sertoli-Leydig cell tumors of ovary (SLCT) are now identified as a distinct entity among the uncommon group of sex cord tumors of ovary.
  • We report an unusual case of recurrent AFP secreting ovarian tumors and as ileocecal mesenteric cyst in a 25-year-old patient resulting in difficulty in initial diagnosis of AFP producing SLCT.
  • Although six recurrent cases were described out of the 25 reported cases of AFP secreting SLCTs, this patient with an unusual presentation of recurrence is the second case in the literature to the best of our knowledge.
  • [MeSH-major] Cecal Neoplasms / pathology. Ileal Neoplasms / pathology. Leydig Cell Tumor / metabolism. Mesenteric Cyst / pathology. Neoplasm Recurrence, Local / pathology. Ovarian Neoplasms / metabolism. Sertoli Cell Tumor / metabolism. alpha-Fetoproteins / metabolism

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  • (PMID = 19282570.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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68. Oehadian A, Koide N, Mu MM, Hassan F, Islam S, Yoshida T, Yokochi T: Interferon (IFN)-beta induces apoptotic cell death in DHL-4 diffuse large B cell lymphoma cells through tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Cancer Lett; 2005 Jul 8;225(1):85-92
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  • [Title] Interferon (IFN)-beta induces apoptotic cell death in DHL-4 diffuse large B cell lymphoma cells through tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
  • The effect of interferon (IFN)-alpha, beta and gamma on the growth of DHL-4 diffuse large B cell lymphoma cells was studied.
  • IFN-beta significantly inhibited the cell growth, and the effect was stronger than that of IFN-alpha.
  • IFN-gamma did not inhibit the cell growth because of lack of IFN-gamma receptors.
  • IFN-beta caused apoptotic cell death which was accompanied by DNA fragmentation, caspase 3 activation and annexin V binding.
  • IFN-beta lead to the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mRNA.
  • It was suggested that IFN-beta might cause apoptosis in DHL-4 cells through TRAIL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Interferon-beta / pharmacology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Membrane Glycoproteins / biosynthesis. Membrane Glycoproteins / physiology. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Apoptosis Regulatory Proteins. Cell Proliferation. DNA Damage. Gene Expression Profiling. Humans. Interferon-alpha / pharmacology. Interferon-gamma / pharmacology. TNF-Related Apoptosis-Inducing Ligand. Tumor Cells, Cultured

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  • (PMID = 15922860.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Interferon-alpha; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 77238-31-4 / Interferon-beta; 82115-62-6 / Interferon-gamma
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69. Huang TT, Chen JY, Tseng CE, Su YC, Ho HC, Lee MS, Chang CT, Wong YK, Chen HR: Decreased GRP78 protein expression is a potential prognostic marker of oral squamous cell carcinoma in Taiwan. J Formos Med Assoc; 2010 May;109(5):326-37
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  • [Title] Decreased GRP78 protein expression is a potential prognostic marker of oral squamous cell carcinoma in Taiwan.
  • BACKGROUND/PURPOSE: Oral squamous cell carcinoma (OSCC) is an aggressive tumor and its occurrence in Taiwan is closely related to chronic smoking, alcohol consumption, and especially to betel quid chewing.
  • It became the fourth most common malignant tumor of Taiwanese men in 2006.
  • Unfortunately, there are few biomarkers for diagnosis and treatment of this disease.
  • METHODS: To find potential markers, two domestic cell lines (OC2 and OCSL) derived from different grades of OSCC were established and their proteins were compared by global proteomic analysis.
  • The expression differences of GRP78 protein in these two cell lines and clinical samples from OSCC patients were verified.
  • RESULTS: Of the 11 candidate proteins expressed differentially in both cell lines, six [heat shock protein 90 kDa beta member 1 (94 kDa glucose-regulated protein; GRP94), protein disulfide-isomerase precursor, vimentin, tubulin beta-2C chain, 78 kDa glucose-regulated protein precursor (GRP78), and annexin A2] were increased in OC2 cells (low-grade OSCC), and five (heat shock protein 90-beta, annexin A1, stress-induced phosphoprotein 1, elongation factor-2, and integrin alpha-3 precursor) were increased in OCSL cells (high-grade OSCC).
  • Some of these proteins have been previously associated with malignant tumors, but no previous association of GRP78 with OSCC has been reported.
  • GRP78 protein expression in these two OSCC cell lines was confirmed by Western blotting.
  • Immunohistochemical staining of clinical samples from OSCC patients revealed that decreased GRP78 protein expression was significantly correlated with advance tumor stage (p < 0.001) and neck lymph node metastasis (p = 0.001).

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  • [Copyright] Copyright 2010 Formosan Medical Association & Elsevier. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20497865.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Heat-Shock Proteins; 0 / molecular chaperone GRP78
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70. Russell MR, Liu Q, Lei H, Kazlauskas A, Fatatis A: The alpha-receptor for platelet-derived growth factor confers bone-metastatic potential to prostate cancer cells by ligand- and dimerization-independent mechanisms. Cancer Res; 2010 May 15;70(10):4195-203
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  • [Title] The alpha-receptor for platelet-derived growth factor confers bone-metastatic potential to prostate cancer cells by ligand- and dimerization-independent mechanisms.
  • Metastatic dissemination requires a complex series of coordinated events that result in cells that escape from the primary tumor into the circulation and eventually colonize a distant organ.
  • The ability of these cells to evolve into macroscopic metastases depends strongly on their compatibility with, and ability to utilize, this new microenvironment.
  • We previously showed that bone-metastatic prostate cancer cells exposed to human bone marrow respond by activation of cell survival pathways, such as phosphoinositide 3-kinase/Akt, and that these events are mediated by the alpha-receptor for platelet-derived growth factor (PDGFRalpha).
  • Our studies show that this truncated PDGFRalpha is able to restore bone-metastatic potential of prostate cancer cells as effectively as the full-length form of the receptor.

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  • [Copyright] (c)2010 AACR.
  • [Cites] Neoplasia. 2004 Sep-Oct;6(5):503-12 [15548358.001]
  • [Cites] Cancer Res. 2004 Jul 15;64(14):4693-8 [15256432.001]
  • [Cites] Breast Cancer Res. 2005;7(5):R788-95 [16168125.001]
  • [Cites] Oncogene. 2005 Oct 13;24(45):6848-54 [16007172.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11318-22 [16844778.001]
  • [Cites] Invest Urol. 1979 Jul;17(1):16-23 [447482.001]
  • [Cites] Cell. 1989 Sep 22;58(6):1121-33 [2550144.001]
  • [Cites] Differentiation. 1991 Nov;48(2):115-25 [1773917.001]
  • [Cites] EMBO J. 1992 Dec;11(12):4251-9 [1425569.001]
  • [Cites] Mod Pathol. 1994 Jun;7(5):549-54 [7524068.001]
  • [Cites] Cytokine Growth Factor Rev. 1996 Jun;7(1):3-10 [8864349.001]
  • [Cites] Biochim Biophys Acta. 1998 Aug 19;1378(1):F79-113 [9739761.001]
  • [Cites] J Biol Chem. 1999 Oct 1;274(40):28335-43 [10497192.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2009 Jul;50(7):3394-403 [19324843.001]
  • [Cites] Am J Ophthalmol. 2010 Jan;149(1):32-6 [19875090.001]
  • [Cites] Anticancer Agents Med Chem. 2009 Dec;9(10):1079-88 [19719455.001]
  • [Cites] Physiol Rev. 1999 Oct;79(4):1283-316 [10508235.001]
  • [Cites] Am J Pathol. 1999 Oct;155(4):1271-9 [10514409.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):555-62 [17234763.001]
  • [Cites] Cancer Metastasis Rev. 2008 Mar;27(1):41-55 [18071636.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2358-62 [18258742.001]
  • [Cites] Nature. 2008 Sep 18;455(7211):391-5 [18701889.001]
  • [Cites] APMIS. 2008 Jul-Aug;116(7-8):586-601 [18834404.001]
  • [Cites] APMIS. 2008 Jul-Aug;116(7-8):742-53 [18834416.001]
  • [Cites] Cancer Lett. 2009 Jan 18;273(2):177-93 [18632203.001]
  • [Cites] Oncogene. 2009 Jan 22;28(3):412-21 [18850002.001]
  • [Cites] J Biol Chem. 2009 Mar 6;284(10):6329-36 [19126548.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6387-94 [11533228.001]
  • [Cites] Semin Cancer Biol. 2002 Apr;12(2):89-96 [12027580.001]
  • [Cites] Nat Rev Cancer. 2002 May;2(5):389-96 [12044015.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):584-93 [12154351.001]
  • [Cites] Urology. 2002 Sep;60(3 Suppl 1):115-21; discussion 122 [12231066.001]
  • [Cites] Nat Rev Cancer. 2003 Jun;3(6):453-8 [12778135.001]
  • [Cites] J Biol Chem. 2003 Nov 7;278(45):44075-82 [12941962.001]
  • [Cites] Mol Cancer Ther. 2005 Mar;4(3):369-79 [15767546.001]
  • (PMID = 20442296.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY012509; United States / NEI NIH HHS / EY / R01 EY012509; United States / NCI NIH HHS / PC / PC080987; United States / NEI NIH HHS / EY / EY012509-10A1; United States / NEI NIH HHS / EY / R01 EY012509-10A1
  • [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 / Ligands; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ NIHMS190973; NLM/ PMC2875778
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71. Elgqvist J, Andersson H, Bäck T, Claesson I, Hultborn R, Jensen H, Johansson BR, Lindegren S, Olsson M, Palm S, Warnhammar E, Jacobsson L: Alpha-radioimmunotherapy of intraperitoneally growing OVCAR-3 tumors of variable dimensions: Outcome related to measured tumor size and mean absorbed dose. J Nucl Med; 2006 Aug;47(8):1342-50
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  • [Title] Alpha-radioimmunotherapy of intraperitoneally growing OVCAR-3 tumors of variable dimensions: Outcome related to measured tumor size and mean absorbed dose.
  • (b) image the tumor growth on the peritoneum; and (c) calculate the specific energy and mean absorbed dose to tumors and critical organs.
  • METHODS: Two experiments with 5-wk-old nude mice (n = 100 + 93), intraperitoneally inoculated with approximately 1 x 10(7) NIH:OVCAR-3 cells, were done.
  • At the time of treatment 29 animals were sacrificed and biopsies were taken for determination of tumor sizes using scanning electron microscopy (SEM).
  • Eight weeks after each treatment the animals were sacrificed and the presence of macro- and microscopic tumors and ascites was determined.
  • The specific energy and mean absorbed dose to tumors were calculated.
  • RESULTS: When given treatment 1, 3, 4, 5, or 7 wk after cell inoculation the tumor-free fraction (TFF) was 95%, 68%, 58%, 47%, 26%, and 100%, 80%, 20%, 20%, and 0% when treated with 211At-MX35 F(ab')2 or 211At-Rituximab F(ab')2, respectively.
  • The SEM images revealed maximum tumor radius of approximately 30 mum 1 wk after cell inoculation, increasing to approximately 340 mum at 7 wk.
  • Specific energy to cell nuclei varied between 0 and approximately 540 Gy, depending on assumptions regarding activity distribution and tumor size.
  • CONCLUSION: Treatment with 211At-MX35 F(ab')2 or 211At-Rituximab F(ab')2 resulted in a TFF of 95%-100% when the tumor radius was < or =30 microm.
  • The TFF was decreased (TFF < or = 20%) for 211At-Rituximab F(ab')2 when the tumor radius exceeded the range of the alpha-particles.
  • The specific antibody gave for these tumor sizes a significantly better TFF, explained by a high mean absorbed dose (>22 Gy) from the activity bound to the tumor surface and probably some contribution from penetrating activity.
  • [MeSH-major] Ovarian Neoplasms / radionuclide imaging. Ovarian Neoplasms / therapy. Radioimmunotherapy / methods
  • [MeSH-minor] Alpha Particles. Animals. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Microscopy, Electron. Neoplasm Transplantation. Rituximab. Treatment Outcome

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  • [CommentIn] J Nucl Med. 2006 Aug;47(8):1238-40 [16882999.001]
  • (PMID = 16883015.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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72. Shahid M, Francis J, Majid DS: Tumor necrosis factor-alpha induces renal vasoconstriction as well as natriuresis in mice. Am J Physiol Renal Physiol; 2008 Dec;295(6):F1836-44
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  • [Title] Tumor necrosis factor-alpha induces renal vasoconstriction as well as natriuresis in mice.
  • Tumor necrosis factor-alpha (TNF-alpha) has been implicated in the pathogenesis of hypertension and renal injury.
  • However, the direct effects of TNF-alpha on renal hemodynamic and excretory function are not yet clearly defined.
  • We examined the renal responses to infusion of TNF-alpha (0.33 ng.g(-1).min(-1)) in anesthetized mice.
  • Following the 60-min control clearance period, TNF-alpha infusion was initiated and 15 min were given for stabilization followed by another 60-min clearance period.
  • TNF-alpha alone (n = 7) caused decreases in RBF (7.9 +/- 0.3 to 6.4 +/- 0.3 ml.min(-1).g(-1)) and GFR (1.04 +/- 0.06 to 0.62 +/- 0.08 ml.min(-1).g(-1)) as well as increases in absolute (0.8 +/- 0.3 to 1.4 +/- 0.3 micromol.min(-1).g(-1)) and fractional excretion of sodium (0.5 +/- 0.2 to 1.5 +/- 0.4%) without affecting arterial pressure.
  • TNF-alpha also increased 8-isoprostane excretion (8.10 +/- 1.09 to 11.13 +/- 1.34 pg.min(-1).g(-1)).
  • Pretreatment with TNF-alpha blocker etanercept (5 mg/kg sc; 24 and 3 h before TNF-alpha infusion; n = 6) abolished these responses.
  • However, TNF-alpha induced an increase in RBF and caused attenuation of the GFR reduction in mice pretreated with superoxide (O(2)(-)) scavenger tempol (2 microg.g(-1).min(-1); n = 6).
  • Pretreatment with nitric oxide (NO) synthase inhibitor nitro-l-arginine methyl ester (0.1 microg.g(-1).min(-1); n = 6) resulted in further enhancement in vasoconstriction while natriuresis remained unaffected in response to TNF-alpha.
  • These data suggest that TNF-alpha induces renal vasoconstriction and hypofiltration via enhancing the activity of O(2)(-) and thus reducing the activity of NO.
  • The natriuretic response to TNF-alpha is related to its direct effects on tubular sodium reabsorption.

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  • [Cites] Free Radic Res. 1999 Dec;31(6):651-69 [10630688.001]
  • [Cites] Brain Res. 2008 Aug 21;1226:89-98 [18620339.001]
  • [Cites] Hypertension. 2000 Oct;36(4):561-8 [11040236.001]
  • [Cites] Physiol Rev. 2001 Jan;81(1):345-418 [11152761.001]
  • [Cites] Ann N Y Acad Sci. 2000;917:38-67 [11268364.001]
  • [Cites] Neurobiol Aging. 2001 Jul-Aug;22(4):671-6 [11445267.001]
  • [Cites] Trends Endocrinol Metab. 2001 Aug;12(6):243-7 [11445440.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Dec;281(6):R1808-16 [11705765.001]
  • [Cites] Hypertension. 2002 Feb;39(2):293-7 [11847200.001]
  • [Cites] J Pharmacol Exp Ther. 2002 May;301(2):418-26 [11961039.001]
  • [Cites] Circulation. 2002 May 7;105(18):2198-205 [11994255.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2003 Apr;284(4):R916-27 [12626358.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2003 Jul;285(1):R117-24 [12609817.001]
  • [Cites] Hypertension. 2004 Feb;43(2):335-40 [14718366.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2004 Jun;286(6):H2264-71 [15148057.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2004 Jul;287(1):R27-32 [15044181.001]
  • [Cites] Circulation. 2004 Oct 5;110(14):2003-9 [15451797.001]
  • [Cites] Kidney Int. 1989 May;35(5):1111-8 [2549293.001]
  • [Cites] Hypertension. 1992 May;19(5):464-74 [1568765.001]
  • [Cites] Annu Rev Immunol. 1992;10:411-52 [1590993.001]
  • [Cites] Kidney Int. 1992 Aug;42(2):383-9 [1405321.001]
  • [Cites] J Am Soc Nephrol. 1993 Dec;4(6):1257-74 [8130353.001]
  • [Cites] FEBS Lett. 1994 Jun 27;347(2-3):178-80 [7518396.001]
  • [Cites] Physiol Rev. 1996 Apr;76(2):425-536 [8618962.001]
  • [Cites] Pflugers Arch. 1997 Apr;433(6):691-8 [9049158.001]
  • [Cites] J Hypertens. 1997 Dec;15(12 Pt 1):1481-4 [9431855.001]
  • [Cites] Am J Physiol. 1998 Jan;274(1 Pt 2):F148-55 [9458834.001]
  • [Cites] Circulation. 1998 Apr 14;97(14):1382-91 [9577950.001]
  • [Cites] Mol Cell Biochem. 1998 Oct;187(1-2):1-10 [9788737.001]
  • [Cites] Br J Pharmacol. 1998 Dec;125(7):1543-50 [9884083.001]
  • [Cites] Hypertension. 1999 Oct;34(4 Pt 2):943-9 [10523389.001]
  • [Cites] J Hypertens. 2005 Jan;23(1):165-74 [15643139.001]
  • [Cites] J Hypertens. 2005 Jul;23(7):1375-82 [15942460.001]
  • [Cites] Hypertension. 2005 Oct;46(4):1026-31 [16103275.001]
  • [Cites] Clin Vaccine Immunol. 2006 Feb;13(2):281-8 [16467339.001]
  • [Cites] Curr Opin Nephrol Hypertens. 2006 Mar;15(2):159-66 [16481883.001]
  • [Cites] Hypertension. 2006 Mar;47(3):568-72 [16401762.001]
  • [Cites] Hypertension. 2006 Mar;47(3):557-62 [16415373.001]
  • [Cites] Cytokine. 2006 Feb 7;33(3):138-44 [16488623.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2006 Dec;291(6):R1817-24 [16840655.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2007 Feb;292(2):H954-62 [17028163.001]
  • [Cites] Kidney Int. 2007 Apr;71(7):619-28 [17311071.001]
  • [Cites] Shock. 2007 May;27(5):542-51 [17438460.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1847-52 [17616742.001]
  • [Cites] Shock. 2007 Sep;28(3):309-16 [17545946.001]
  • [Cites] Apoptosis. 2007 Oct;12(10):1795-802 [17701456.001]
  • [Cites] J Exp Med. 2007 Oct 1;204(10):2449-60 [17875676.001]
  • [Cites] Am J Physiol Renal Physiol. 2007 Oct;293(4):F1178-86 [17634398.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2007 Nov;293(5):H2726-37 [17675574.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2008 Jan;294(1):R76-83 [17989143.001]
  • [Cites] Hypertension. 2008 May;51(5):1345-51 [18391105.001]
  • [Cites] Annu Rev Physiol. 2000;62:515-34 [10845101.001]
  • (PMID = 18922887.001).
  • [ISSN] 1931-857X
  • [Journal-full-title] American journal of physiology. Renal physiology
  • [ISO-abbreviation] Am. J. Physiol. Renal Physiol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL-66432
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 27415-26-5 / 8-epi-prostaglandin F2alpha; 9NEZ333N27 / Sodium; B7IN85G1HY / Dinoprost; RWP5GA015D / Potassium
  • [Other-IDs] NLM/ PMC2604828
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73. Sondarva G, Kundu CN, Mehrotra S, Mishra R, Rangasamy V, Sathyanarayana P, Ray RS, Rana B, Rana A: TRAF2-MLK3 interaction is essential for TNF-alpha-induced MLK3 activation. Cell Res; 2010 Jan;20(1):89-98
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  • [Title] TRAF2-MLK3 interaction is essential for TNF-alpha-induced MLK3 activation.
  • Mixed lineage kinase 3 (MLK3) is a mitogen-activated protein kinase kinase kinase that is activated by tumor necrosis factor-alpha (TNF-alpha) and specifically activates c-Jun N-terminal kinase (JNK) on TNF-alpha stimulation.
  • The mechanism by which TNF-alpha activates MLK3 is still not known.
  • TNF receptor-associated factors (TRAFs) are adapter molecules that are recruited to cytoplasmic end of TNF receptor and mediate the downstream signaling, including activation of JNK.
  • Endogenous TRAF2 and MLK3 associate with each other in response to TNF-alpha treatment in a time-dependent manner.
  • The association between MLK3 and TRAF2 mediates MLK3 activation and competition with the TRAF2 deletion mutant that binds to MLK3 attenuates MLK3 kinase activity in a dose-dependent manner, on TNF-alpha treatment.
  • Furthermore the downstream target of MLK3, JNK was activated by TNF-alpha in a TRAF2-dependent manner.
  • Hence, our data show that the direct interaction between TRAF2 and MLK3 is required for TNF-alpha-induced activation of MLK3 and its downstream target, JNK.

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  • [Cites] Mol Cell Biol. 2000 Apr;20(7):2556-68 [10713178.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7272-7 [10852963.001]
  • [Cites] Science. 2000 Jun 30;288(5475):2351-4 [10875917.001]
  • [Cites] Mol Cell. 2000 Apr;5(4):649-58 [10882101.001]
  • [Cites] Chem Phys Lipids. 1999 Nov;102(1-2):157-66 [11001570.001]
  • [Cites] Genes Dev. 2001 Jan 15;15(2):241-53 [11157779.001]
  • [Cites] EMBO Rep. 2001 Mar;2(3):222-8 [11266364.001]
  • [Cites] Trends Cell Biol. 2001 Sep;11(9):372-7 [11514191.001]
  • [Cites] J Cell Sci. 2002 Feb 15;115(Pt 4):679-88 [11865024.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Sep;3(9):663-72 [12209126.001]
  • [Cites] Mol Cell. 2002 Dec;10(6):1527-33 [12504027.001]
  • [Cites] J Biol Chem. 2003 Feb 7;278(6):3897-902 [12458207.001]
  • [Cites] Cell Death Differ. 2003 Jan;10(1):45-65 [12655295.001]
  • [Cites] Cell. 1993 May 7;73(3):431-45 [8387891.001]
  • [Cites] J Biol Chem. 1995 Jul 14;270(28):16514-7 [7622454.001]
  • [Cites] Cell. 1995 Dec 29;83(7):1243-52 [8548810.001]
  • [Cites] Science. 1996 Feb 23;271(5252):1128-31 [8599092.001]
  • [Cites] J Biol Chem. 1996 Aug 9;271(32):19025-8 [8702571.001]
  • [Cites] J Biol Chem. 1996 Oct 4;271(40):24788-93 [8798750.001]
  • [Cites] Nature. 1996 Oct 3;383(6599):443-6 [8837778.001]
  • [Cites] Nature. 1997 Feb 6;385(6616):540-4 [9020361.001]
  • [Cites] J Biol Chem. 1997 Jun 13;272(24):15167-73 [9182538.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9792-6 [9275204.001]
  • [Cites] Immunity. 1997 Nov;7(5):715-25 [9390694.001]
  • [Cites] Trends Biochem Sci. 1998 Feb;23(2):74-9 [9538693.001]
  • [Cites] J Biol Chem. 1998 Aug 28;273(35):22681-92 [9712898.001]
  • [Cites] Genes Dev. 1998 Sep 15;12(18):2821-30 [9744859.001]
  • [Cites] Mol Cell. 1998 Sep;2(3):389-95 [9774977.001]
  • [Cites] Genes Dev. 1999 May 15;13(10):1297-308 [10346818.001]
  • [Cites] Oncogene. 1999 Oct 14;18(42):5814-20 [10523862.001]
  • [Cites] Mol Cell Biol. 2005 May;25(9):3670-81 [15831472.001]
  • [Cites] J Biol Chem. 2007 Oct 19;282(42):30393-405 [17711861.001]
  • [Cites] Cell Signal. 2009 Nov;21(11):1620-5 [19586614.001]
  • (PMID = 19918265.001).
  • [ISSN] 1748-7838
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM055835-07A3; United States / NCI NIH HHS / CA / R21 CA121221; United States / NIGMS NIH HHS / GM / GM55835; United States / NCI NIH HHS / CA / CA121221; United States / NIGMS NIH HHS / GM / R01 GM055835-07A3; United States / NIGMS NIH HHS / GM / R01 GM055835
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TNF Receptor-Associated Factor 2; 0 / TNF Receptor-Associated Factor 5; 0 / TNF Receptor-Associated Factor 6; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / mitogen-activated protein kinase kinase kinase 11
  • [Other-IDs] NLM/ NIHMS149286; NLM/ PMC2801772
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74. Koschmieder S, D'Alò F, Radomska H, Schöneich C, Chang JS, Konopleva M, Kobayashi S, Levantini E, Suh N, Di Ruscio A, Voso MT, Watt JC, Santhanam R, Sargin B, Kantarjian H, Andreeff M, Sporn MB, Perrotti D, Berdel WE, Müller-Tidow C, Serve H, Tenen DG: CDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer binding protein alpha. Blood; 2007 Nov 15;110(10):3695-705
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  • [Title] CDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer binding protein alpha.
  • 2-Cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) induces differentiation and apoptosis of tumor cells in vitro and in vivo.
  • Here we assessed the effects of CDDO on CCAAT enhancer-binding protein alpha (CEBPA), a transcription factor critical for granulocytic differentiation.
  • In HL60 acute myeloid leukemia (AML) cells, CDDO (0.01 to 2 muM) induces apoptosis in a dose-dependent manner.
  • Conversely, subapoptotic doses of CDDO promote phagocytic activity and granulocytic-monocytic differentiation of HL60 cells through increased de novo synthesis of p42 CEBPA protein.
  • In concordance with these results, CDDO induces a CEBPA ratio change and differentiation of primary blasts from patients with acute myeloid leukemia (AML).

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  • [Cites] Acta Haematol. 1999;102(4):163-71 [10725757.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):36273-82 [16118208.001]
  • [Cites] Genes Dev. 2000 Aug 1;14(15):1920-32 [10921906.001]
  • [Cites] Mol Endocrinol. 2000 Oct;14(10):1550-6 [11043571.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] Mol Pharmacol. 2001 May;59(5):1094-9 [11306692.001]
  • [Cites] Int J Hematol. 2001 Jan;73(1):71-7 [11372758.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):48-58 [11753385.001]
  • [Cites] Blood. 2002 Jan 1;99(1):326-35 [11756188.001]
  • [Cites] Cell. 2002 Feb 22;108(4):545-56 [11909525.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3377-90 [12032776.001]
  • [Cites] Mol Cell Biol. 2002 Oct;22(20):7242-57 [12242300.001]
  • [Cites] Mol Cancer Ther. 2002 Jan;1(3):177-84 [12467212.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Feb;36(2):167-74 [12508245.001]
  • [Cites] Nat Rev Cancer. 2003 Feb;3(2):89-101 [12563308.001]
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1371-6 [12649201.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2798-806 [12855660.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5551-8 [14500394.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5926-39 [14522919.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3163-71 [12869508.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2122-9 [12931220.001]
  • [Cites] Mol Pharmacol. 2004 Feb;65(2):309-18 [14742672.001]
  • [Cites] Mol Cancer Ther. 2004 Jan;3(1):39-45 [14749474.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1635-40 [14604977.001]
  • [Cites] Mol Pharmacol. 2004 Mar;65(3):744-52 [14978253.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):119-26 [15236178.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13312-7 [15326310.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74 [9012825.001]
  • [Cites] Mol Cancer Ther. 2006 Feb;5(2):317-28 [16505105.001]
  • [Cites] Clin Cancer Res. 2006 Mar 15;12(6):1828-38 [16551868.001]
  • [Cites] Mol Pharmacol. 2006 Apr;69(4):1182-93 [16410408.001]
  • [Cites] Mol Cancer Ther. 2006 Jun;5(6):1452-8 [16818503.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1223-9 [16645168.001]
  • [Cites] Mol Cancer. 2006;5:22 [16759389.001]
  • [Cites] Blood. 2007 Aug 1;110(3):994-1003 [17475908.001]
  • [Cites] Mol Cell Biol. 2001 Jun;21(11):3789-806 [11340171.001]
  • [Cites] J Biol Chem. 1998 Jan 23;273(4):2008-14 [9442037.001]
  • [Cites] Mol Cell Biol. 1998 Jul;18(7):4301-14 [9632814.001]
  • [Cites] J Cancer Res Clin Oncol. 1998;124(2):113-6 [9654194.001]
  • [Cites] Cancer Res. 1999 Jan 15;59(2):336-41 [9927043.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7927-35 [15520199.001]
  • [Cites] Blood. 2005 Jan 1;105(1):324-34 [15331442.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4799-808 [15930300.001]
  • [Cites] Cell Death Differ. 2005 May;12(5):523-31 [15746941.001]
  • [Cites] Mol Pharmacol. 2005 Jul;68(1):119-28 [15798084.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1350-4 [15931262.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1369-75 [15855281.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1519-24 [15914558.001]
  • [Cites] Int J Hematol. 2005 Jun;81(5):368-77 [16158816.001]
  • [Cites] Cell Growth Differ. 2000 May;11(5):261-7 [10845427.001]
  • (PMID = 17671235.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P30-CA 16672; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / R01 CA089346; United States / NCI NIH HHS / CA / 1 P50 CA100632; United States / NCI NIH HHS / CA / R01 CA89346; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / P01 CA55164; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Eukaryotic Initiation Factor-2; 0 / Eukaryotic Initiation Factor-4E; 6SMK8R7TGJ / Oleanolic Acid
  • [Other-IDs] NLM/ PMC2077317
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75. Bellezza G, Colella R, Sidoni A, Del Sordo R, Ferri I, Cioccoloni C, Cavaliere A: Immunohistochemical expression of Galectin-3 and HBME-1 in granular cell tumors: a new finding. Histol Histopathol; 2008 09;23(9):1127-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical expression of Galectin-3 and HBME-1 in granular cell tumors: a new finding.
  • Granular cell tumor (GCT) is a relatively rare neoplasm, usually located in the upper aerodigestive tract, skin and soft tissue.
  • Because of its uncertain histogenesis, GCT has been the object of many immunohistochemical and ultrastructural studies that have suggested a Schwann cell origin.
  • Our recent observation of a case of GCT immunoreactive for Galectin-3 and HBME-1 led us to further investigate the immunohistochemical profile of these neoplasms.
  • We evaluated the immunohistochemical expression of the traditional markers for GCT (S-100, CD68) along with new markers (Galectin-3, HBME-1, Calretinina and Inhibin-alpha) in 22 granular cell tumors.
  • Our results showed, in all cases, a constant diffuse positivity for S-100 protein, CD68 and Galectin-3.
  • The present study gives a new immunophenotypic profile for GCT, which could help pathologists in distinguishing morphologically ambiguous granular lesions in unusual sites.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Galectin 3 / metabolism. Granular Cell Tumor / metabolism. Head and Neck Neoplasms / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 18581283.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3; 0 / HBME-1 antigen
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76. Charerntantanakul W, Platt R, Roth JA: Effects of porcine reproductive and respiratory syndrome virus-infected antigen-presenting cells on T cell activation and antiviral cytokine production. Viral Immunol; 2006;19(4):646-61
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  • [Title] Effects of porcine reproductive and respiratory syndrome virus-infected antigen-presenting cells on T cell activation and antiviral cytokine production.
  • The ability of porcine reproductive and respiratory syndrome virus (PRRSV) to suppress T cell expression of CD25 (alpha chain of interleukin [IL]-2 receptor), interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha) was determined by flow cytometry in naive porcine T cells in response to mitogen (concanavalin A) and cytokine inducers (phorbol 12-myristate 13-acetate plus ionomycin [PMA/I]).
  • Four PRRSV isolates of varying clinical virulence and three different types of porcine myeloid antigen-presenting cells (APCs) were used.
  • T cells cultured with monocytes infected with virulent PRRSV (VR-2385, SDSU-73, and VR-2332), but not with a vaccine strain (Ingelvac PRRS MLV; Boehringer Ingelheim Vetmedica, St. Joseph, MO), demonstrated significantly reduced CD25 expression (%CD25(+)) and IFN-gamma expression (%IFN-gamma (+)) compared with T cells incubated with uninoculated monocyte cultures.
  • T cells cultured with monocytes infected with all four PRRSV isolates demonstrated significantly reduced %TNF-alpha (+).
  • The significant reduction of %CD25(+), %IFN-gamma (+), and %TNF-alpha (+) was not detected in T cells cultured with monocyte-derived macrophages (MDMs) and immature monocyte-derived dendritic cells (MDCs) infected with any PRRSV isolates.
  • Heat-inactivated PRRSV did not induce significantly reduced T cell responses in any APC cultures.
  • The reduction of T cell response in monocyte cultures was not due to PRRSV-induced T cell death.
  • Increased IL-10 gene expression contributed to significantly reduced %IFN-gamma (+) and %TNF-alpha (+), but not %CD25(+), as determined by IL-10 neutralization assay.
  • This study reports that PRRSV has the ability to suppress T cell responses.
  • [MeSH-major] Porcine Reproductive and Respiratory Syndrome / immunology. Porcine respiratory and reproductive syndrome virus / physiology. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Antigen-Presenting Cells / immunology. Cells, Cultured. Coculture Techniques. Dendritic Cells / virology. Down-Regulation. Gene Expression. Interferon-gamma / biosynthesis. Interferon-gamma / metabolism. Interleukin-10 / genetics. Interleukin-2 Receptor alpha Subunit / metabolism. Macrophages / virology. Monocytes / physiology. Monocytes / virology. Swine. Tumor Necrosis Factor-alpha / biosynthesis. Virulence

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  • (PMID = 17201660.001).
  • [ISSN] 0882-8245
  • [Journal-full-title] Viral immunology
  • [ISO-abbreviation] Viral Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-2 Receptor alpha Subunit; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 82115-62-6 / Interferon-gamma
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77. Roomi MW, Monterrey JC, Kalinovsky T, Niedzwiecki A, Rath M: Modulation of MMP-2 and MMP-9 by cytokines, mitogens and inhibitors in lung cancer and malignant mesothelioma cell lines. Oncol Rep; 2009 Dec;22(6):1283-91
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  • [Title] Modulation of MMP-2 and MMP-9 by cytokines, mitogens and inhibitors in lung cancer and malignant mesothelioma cell lines.
  • Matrix metalloproteinases (MMPs) secreted by lung cancer (LC) and malignant mesothelioma (MM), especially MMP-2 and MMP-9, play crucial roles in tumor invasion and metastasis.
  • We examined the effect of cytokines, mitogens and inhibitors on MMP-2 and MMP-9 expression in LC and MM cell lines.
  • Human LC (A-549) and MM (MSTO-211H) cell lines were cultured in appropriate media.
  • At near confluence, the cells were washed with PBS and incubated in serum-free medium with various concentrations of several cytokines, mitogens and inhibitors.
  • TNF-alpha, IL-1beta, LPS and PMA, stimulated MMP-2 in LC and inhibited MMP-2 in MM, but had no effect on MMP-9.
  • Doxycycline, EGCG and NM inhibited MMP-2 and MMP-9 expression, in both cell lines.
  • Actinomycin-D, cyclohexamide, retinoic acid and dexamethasone inhibited MMP-2 in both cancer cell lines and inhibited MMP-9 in MM.
  • Our results show that cytokines and inhibitors have an up- or down-regulatory effect on MMP-2 and MMP-9 expression in LC and MM, suggesting the clinical value of targeting these proteases for management of LC and MM and their pathogenesis.
  • [MeSH-major] Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Lung Neoplasms / metabolism. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Mesothelioma / metabolism
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Line, Tumor. Culture Media / pharmacology. Cytokines / metabolism. Humans. Lipopolysaccharides / pharmacology. Neoplasm Metastasis. Tetradecanoylphorbol Acetate / pharmacology. Time Factors

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  • (PMID = 19885578.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Culture Media; 0 / Cytokines; 0 / Lipopolysaccharides; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; NI40JAQ945 / Tetradecanoylphorbol Acetate
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78. Xu G, Tan X, Wang H, Sun W, Shi Y, Burlingame S, Gu X, Cao G, Zhang T, Qin J, Yang J: Ubiquitin-specific peptidase 21 inhibits tumor necrosis factor alpha-induced nuclear factor kappaB activation via binding to and deubiquitinating receptor-interacting protein 1. J Biol Chem; 2010 Jan 8;285(2):969-78
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  • [Title] Ubiquitin-specific peptidase 21 inhibits tumor necrosis factor alpha-induced nuclear factor kappaB activation via binding to and deubiquitinating receptor-interacting protein 1.
  • Ubiquitination and deubiquitination of receptor-interacting protein 1 (RIP1) play an important role in the positive and negative regulation of the tumor necrosis factor alpha (TNFalpha)-induced nuclear factor kappaB (NF-kappaB) activation.
  • Using a combination of functional genomic and proteomic approaches, we have identified ubiquitin-specific peptidase 21 (USP21) as a deubiquitinase for RIP1.
  • Notably, knockdown of USP21 in HeLa cells enhances TNFalpha-induced RIP1 ubiquitination, IkappaB kinase beta (IKKbeta), and NF-kappaB phosphorylation, inhibitor of NF-kappaB alpha (IkappaB alpha) phosphorylation and ubiquitination, as well as NF-kappaB-dependent gene expression.
  • Therefore, our results demonstrate that USP21 plays an important role in the down-regulation of TNFalpha-induced NF-kappaB activation through deubiquitinating RIP1.

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  • [Cites] Nat Cell Biol. 2005 Aug;7(8):758-65 [16056267.001]
  • [Cites] Science. 1999 Apr 9;284(5412):309-13 [10195894.001]
  • [Cites] Cell. 2005 Dec 2;123(5):773-86 [16325574.001]
  • [Cites] Nat Cell Biol. 2006 Apr;8(4):398-406 [16547522.001]
  • [Cites] Mol Cell. 2006 Apr 21;22(2):245-57 [16603398.001]
  • [Cites] EMBO J. 2007 Mar 21;26(6):1532-41 [17318178.001]
  • [Cites] J Biol Chem. 2007 Jun 15;282(24):17330-4 [17478428.001]
  • [Cites] Genes Dev. 2008 Jan 1;22(1):37-49 [18172164.001]
  • [Cites] Nat Immunol. 2008 Mar;9(3):254-62 [18246070.001]
  • [Cites] J Biol Chem. 2008 Mar 14;283(11):7036-45 [18178551.001]
  • [Cites] Nat Rev Immunol. 2008 Jul;8(7):501-11 [18535581.001]
  • [Cites] EMBO J. 2009 Mar 4;28(5):513-22 [19131965.001]
  • [Cites] EMBO J. 2009 Mar 4;28(5):455-6 [19262463.001]
  • [Cites] J Biol Chem. 2009 Mar 27;284(13):8209 [19008216.001]
  • [Cites] J Biol Chem. 2009 Mar 27;284(13):8217-21 [19008218.001]
  • [Cites] J Biol Chem. 2000 May 12;275(19):14212-6 [10799498.001]
  • [Cites] Science. 2000 Sep 29;289(5488):2350-4 [11009421.001]
  • [Cites] Trends Cell Biol. 2001 Sep;11(9):372-7 [11514191.001]
  • [Cites] Cell. 2002 Apr;109 Suppl:S81-96 [11983155.001]
  • [Cites] Science. 2002 May 31;296(5573):1634-5 [12040173.001]
  • [Cites] Nature. 2003 Aug 14;424(6950):797-801 [12917690.001]
  • [Cites] Nature. 2004 Aug 5;430(7000):694-9 [15258597.001]
  • [Cites] Mol Cell Biol. 1990 Feb;10(2):561-8 [2405250.001]
  • [Cites] Mol Cell Biol. 1990 May;10(5):2327-34 [2183031.001]
  • [Cites] Mol Cell Biol. 1990 Jul;10(7):3818-23 [2192263.001]
  • [Cites] Genes Dev. 1993 Nov;7(11):2064-70 [8224838.001]
  • [Cites] Cell. 1994 Aug 26;78(4):681-92 [8069916.001]
  • [Cites] Genes Dev. 1995 Nov 15;9(22):2723-35 [7590248.001]
  • [Cites] Immunity. 1996 Apr;4(4):387-96 [8612133.001]
  • [Cites] Annu Rev Immunol. 1996;14:649-83 [8717528.001]
  • [Cites] Cell. 1997 Jul 25;90(2):373-83 [9244310.001]
  • [Cites] Nature. 1997 Aug 7;388(6642):548-54 [9252186.001]
  • [Cites] Cell. 1997 Oct 17;91(2):243-52 [9346241.001]
  • [Cites] Science. 1997 Oct 31;278(5339):860-6 [9346484.001]
  • [Cites] Science. 1997 Oct 31;278(5339):866-9 [9346485.001]
  • [Cites] Cell. 1998 Jun 26;93(7):1231-40 [9657155.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1305-8 [9721089.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1360-3 [9721103.001]
  • [Cites] Nature. 1998 Sep 17;395(6699):297-300 [9751060.001]
  • [Cites] Annu Rev Biochem. 1998;67:425-79 [9759494.001]
  • [Cites] Cell Signal. 2006 Jan;18(1):83-92 [16214042.001]
  • (PMID = 19910467.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK079638; United States / NCI NIH HHS / CA / R21 CA106513; United States / NCI NIH HHS / CA / 1R21CA106513-01A2; United States / NIDDK NIH HHS / DK / DK079638
  • [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 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.1 / RIPK1 protein, human; EC 2.7.11.1 / Receptor-Interacting Protein Serine-Threonine Kinases; EC 2.7.11.1 / Ripk1 protein, mouse; EC 2.7.11.10 / I-kappa B Kinase; EC 3.1.2.15 / USP21 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase
  • [Other-IDs] NLM/ PMC2801298
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79. Frick LR, Arcos ML, Rapanelli M, Zappia MP, Brocco M, Mongini C, Genaro AM, Cremaschi GA: Chronic restraint stress impairs T-cell immunity and promotes tumor progression in mice. Stress; 2009 Mar;12(2):134-43
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  • [Title] Chronic restraint stress impairs T-cell immunity and promotes tumor progression in mice.
  • The T-cell response is an important component of anti-tumoral immunity.
  • Hence, impairment of the immune function induced by a chronic stressor has been postulated to alter the immunosurveillance of tumors, thus leading to a worse neoplastic prognosis.
  • Here, we show that chronic restraint stress affects T-cell mediated immunity in mice.
  • This was evidenced by a decrease of mitogen-induced T-cell proliferation, a reduction in CD4(+)T lymphocyte number and a decrease of tumor necrosis factor-alpha (TNF-alpha) and Interferon-gamma (IFN-gamma) production in stressed mice.
  • Additionally, mice subjected to chronic restraint stress displayed an enhancement of tumor growth in a syngeneic lymphoma model, i.e. an increase of tumor proliferation and a reduction of animal survival.
  • Finally, stressed mice had a reduced specific cytotoxic response against these tumor cells.
  • These results suggest that chronic exposure to stress promotes cancer establishment and subsequent progression, probably by depressing T-cell mediated immunity.
  • The T-cell immunity impairment as well as the tumor progression enhancement emphasize the importance of the therapeutic management of stress to improve the prognosis of cancer patients.
  • [MeSH-major] Lymphoma, T-Cell / immunology. Stress, Psychological / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Behavior, Animal. CD4-Positive T-Lymphocytes / immunology. Cell Proliferation. Female. Interferon-gamma / biosynthesis. Killer Cells, Natural / immunology. Mice. Mice, Inbred BALB C. Restraint, Physical. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 18609297.001).
  • [ISSN] 1607-8888
  • [Journal-full-title] Stress (Amsterdam, Netherlands)
  • [ISO-abbreviation] Stress
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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80. Castillo-Avila W, Piulats JM, Garcia Del Muro X, Vidal A, Condom E, Casanovas O, Mora J, Germà JR, Capellà G, Villanueva A, Viñals F: Sunitinib inhibits tumor growth and synergizes with cisplatin in orthotopic models of cisplatin-sensitive and cisplatin-resistant human testicular germ cell tumors. Clin Cancer Res; 2009 May 15;15(10):3384-95
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  • [Title] Sunitinib inhibits tumor growth and synergizes with cisplatin in orthotopic models of cisplatin-sensitive and cisplatin-resistant human testicular germ cell tumors.
  • PURPOSE: Germ cell tumors (GCT) of the testis are highly curable, but those patients who are refractory to cisplatin (CDDP)-based combination chemotherapy have a poor prognosis.
  • Therefore, identifying new alternatives for treatment remains a priority.
  • EXPERIMENTAL DESIGN: Mice were implanted with four different testicular tumors: a yolk sac, two choriocarcinomas, and a CDDP-resistant choriocarcinoma variant induced in mice by continuous exposure to CDDP.
  • Mice were treated with vehicle, CDDP, sunitinib, or the combination of both drugs and their effects on tumors were analyzed.
  • RESULTS: We observed a significant inhibition in tumor growth accompanied by longer survival after sunitinib treatment.
  • Sunitinib induced apoptosis, reduced tumor cell proliferation and tumor vasculature, and inhibited vascular endothelial growth factor receptor 1, 2, and 3 and platelet-derived growth factor receptor alpha phosphorylation without affecting phosphorylation of other tyrosine kinase receptors.
  • More importantly, tumor growth inhibition induced by sunitinib was also observed in the induced CDDP-resistant choriocarcinoma model.
  • CONCLUSIONS: Taken together, these results suggest that sunitinib might be a new alternative for treatment of CDDP-refractory patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Indoles / therapeutic use. Neoplasms, Germ Cell and Embryonal / drug therapy. Pyrroles / therapeutic use. Testicular Neoplasms / drug therapy. Xenograft Model Antitumor Assays
  • [MeSH-minor] Angiogenesis Inhibitors / administration & dosage. Angiogenesis Inhibitors / pharmacology. Angiogenesis Inhibitors / therapeutic use. Animals. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Cisplatin / administration & dosage. Cisplatin / pharmacology. Drug Resistance, Neoplasm. Drug Synergism. Humans. Male. Mice. Mice, Nude. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / prevention & control. Receptors, Platelet-Derived Growth Factor / genetics. Receptors, Platelet-Derived Growth Factor / metabolism. Receptors, Vascular Endothelial Growth Factor / genetics. Receptors, Vascular Endothelial Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Tumor Burden / drug effects

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  • (PMID = 19417025.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; Q20Q21Q62J / Cisplatin
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81. Xiang J, Munegowda MA, Deng Y: Transgene expression of alpha tumor necrosis factor with mutations D142N and A144R under control of human telomerase reverse transcriptase promoter eradicates well-established tumors and induces long-term antitumor immunity. Cancer Gene Ther; 2009 May;16(5):430-8
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  • [Title] Transgene expression of alpha tumor necrosis factor with mutations D142N and A144R under control of human telomerase reverse transcriptase promoter eradicates well-established tumors and induces long-term antitumor immunity.
  • Recombinant adenoviral vectors (AdVTNF-alpha) expressing alpha tumor necrosis factor (TNF-alpha) under control of cytomegalovirus (CMV) promoter have been used in cancer gene therapy.
  • To reduce its cytotoxicity, we constructed a recombinant AdV(TERT)mTNF-alpha expressing a mutant TNF-alpha (mTNF-alpha) with mutations at D142N and A144R under control of human telomerase reverse transcriptase (hTERT) promoter for treatment of well-established ovalbumin (OVA)-expressing murine B16 melanoma (BL6-10(OVA)) (6 mm in diameter).
  • We demonstrated that the mTNF-alpha with mutations at D142N and A144R has less in vitro cytotoxicity, but maintains its functional effect in the stimulation of T-cell proliferation.
  • The in vitro and in vivo transgene expressions under control of hTERT promoter are highly restricted in tumor cells compared with those under the control of the CMV promoter.
  • AdV(TERT)mTNF-alpha gene therapy by intratumoral injection of AdV(TERT)mTNF-alpha vector (2 x 10(9) PFU) expressing the mutant mTNF-alpha under control of hTERT promoter reduces its in vivo toxicity, eradicates well-established BL6-10(OVA) tumors in 4/10 tumor-bearing mice, and induces OVA-specific CD8(+) T-cell-mediated long-term antitumor immunity.
  • Therefore, AdV(TERT)mTNF-alpha gene therapy may be very useful in the immunotherapy of cancer.
  • [MeSH-major] Gene Expression Regulation. Genetic Therapy. Mutation / genetics. Promoter Regions, Genetic. Telomerase / genetics. Transgenes / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Animals. Antineoplastic Agents / immunology. Antineoplastic Agents / pharmacology. CD8-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / immunology. Cell Proliferation. Disease Models, Animal. Female. Humans. Immunotherapy. Mice. Mice, Inbred C57BL. Tumor Cells, Cultured / drug effects

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  • (PMID = 19096444.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Necrosis Factor-alpha; EC 2.7.7.49 / Telomerase
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82. Liu YP, Lin HI, Tzeng SF: Tumor necrosis factor-alpha and interleukin-18 modulate neuronal cell fate in embryonic neural progenitor culture. Brain Res; 2005 Aug 30;1054(2):152-8
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  • [Title] Tumor necrosis factor-alpha and interleukin-18 modulate neuronal cell fate in embryonic neural progenitor culture.
  • Neural progenitor cells (NPCs) in developing and adult CNS are capable of giving rise to various neuronal and glial cell populations.
  • Yet, little is known about the effect of microglia-derived factors on the cell fate of embryonic NPCs.
  • Treatment with pentoxifylline (PTX), an inhibitor for tumor necrosis factor-alpha (TNF-alpha) secretion from LPS-activated microglia, blocked the reduction of betaIII-tubulin+ cells in NPC culture.
  • Furthermore, treatment of NPCs with interleukin-18 (IL-18), a recently discovered proinflammatory cytokine, also decreased the number of betaIII-tubulin+ cells in a dose- and time-dependent manner.
  • Surprisingly, we also observed that the remaining betaIII-tubulin+ cells in the LPS/M-CM-treated culture exhibited more branching neurites.
  • Thus, the activated microglia-derived cytokines, TNF-alpha and IL-18, may either inhibit the neuronal differentiation or induce neuronal cell death in the NPC culture, whereas these cells may also produce factors to improve the neurite branching in the NPC culture.
  • [MeSH-major] Interleukin-18 / metabolism. Neurons / physiology. Stem Cells / physiology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Animals, Newborn. Blotting, Western / methods. Cell Count / methods. Cell Death / drug effects. Cell Death / physiology. Cell Differentiation / drug effects. Cell Differentiation / physiology. Cells, Cultured. Dose-Response Relationship, Drug. Embryo, Mammalian. Immunohistochemistry / methods. Lipopolysaccharides / pharmacology. Microglia / drug effects. Microglia / physiology. Pertussis Toxin / pharmacology. Rats. Rats, Sprague-Dawley. Tubulin / metabolism

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  • (PMID = 16054598.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-18; 0 / Lipopolysaccharides; 0 / Tubb3 protein, rat; 0 / Tubulin; 0 / Tumor Necrosis Factor-alpha; EC 2.4.2.31 / Pertussis Toxin
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83. Amigó M, Payá M, De Rosa S, Terencio MC: Antipsoriatic effects of avarol-3'-thiosalicylate are mediated by inhibition of TNF-alpha generation and NF-kappaB activation in mouse skin. Br J Pharmacol; 2007 Oct;152(3):353-65
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  • [Title] Antipsoriatic effects of avarol-3'-thiosalicylate are mediated by inhibition of TNF-alpha generation and NF-kappaB activation in mouse skin.
  • EXPERIMENTAL APPROACH: Human neutrophils and monocytes as well as the human keratinocyte cell line HaCaT were used to study the effect of TA on oxidative stress, the arachidonic acid pathway, tumour necrosis factor-alpha (TNF-alpha) release and nuclear factor-kappaB (NF-kappaB) activation.
  • All these parameters were also determined in vivo using the zymosan induced mouse air pouch model and the 12-O-tetradecanoylphorbol-13-acetate (TPA) induced mouse epidermal hyperplasia model.
  • KEY RESULTS: TA showed antioxidant properties in human neutrophils and in the hypoxanthine/xanthine oxidase assay.
  • This compound reduced, in a concentration-dependent manner, leukotriene B(4), prostaglandin E(2) and TNF-alpha production in activated leukocytes.
  • Oral and intrapouch administration of TA in the mouse air pouch model produced a dose-dependent reduction of all these inflammatory mediators.
  • In TPA-induced mouse epidermal hyperplasia, topical administration of TA reduced oedema, leukocyte infiltration, eicosanoid levels and TNF-alpha in skin.
  • [MeSH-major] Antioxidants / pharmacology. NF-kappa B / drug effects. Psoriasis / drug therapy. Salicylates / pharmacology. Sesquiterpenes / pharmacology. Tumor Necrosis Factor-alpha / drug effects
  • [MeSH-minor] Animals. Arachidonic Acid / metabolism. Cell Line. Disease Models, Animal. Dose-Response Relationship, Drug. Female. Humans. Hyperplasia / drug therapy. Hyperplasia / physiopathology. Inflammation Mediators / metabolism. Keratinocytes / drug effects. Keratinocytes / metabolism. Mice. Monocytes / drug effects. Monocytes / metabolism. Neutrophils / drug effects. Neutrophils / metabolism. Oxidative Stress / drug effects. Protein Transport / drug effects

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  • [Cites] J Invest Dermatol. 2006 Aug;126(8):1689-91 [16845406.001]
  • [Cites] Cytokine Growth Factor Rev. 2006 Oct;17(5):349-66 [16911870.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 2000 Jan;361(1):98-106 [10651154.001]
  • [Cites] J Biol Chem. 2000 Mar 3;275(9):6259-66 [10692422.001]
  • [Cites] Am J Physiol Cell Physiol. 2000 Apr;278(4):C822-33 [10751330.001]
  • [Cites] Cytokine. 2000 Aug;12(8):1189-94 [10930295.001]
  • [Cites] J Clin Invest. 2001 Jan;107(1):7-11 [11134171.001]
  • [Cites] Cancer Lett. 2001 Mar 26;164(2):119-26 [11179825.001]
  • [Cites] J Clin Invest. 2001 Jan;107(2):135-42 [11160126.001]
  • [Cites] Vet Dermatol. 2001 Jun;12(3):129-37 [11420928.001]
  • [Cites] J Biol Chem. 2001 Aug 10;276(32):30527-36 [11390371.001]
  • [Cites] J Clin Invest. 2001 Aug;108(4):527-36 [11518726.001]
  • [Cites] J Am Acad Dermatol. 2002 Jan;46(1):1-23; quiz 23-6 [11756941.001]
  • [Cites] Eur J Pharmacol. 2002 Jan 11;434(3):177-85 [11779581.001]
  • [Cites] Trends Immunol. 2002 Jan;23(1):47-53 [11801454.001]
  • [Cites] J Med Chem. 2002 Feb 14;45(4):930-6 [11831905.001]
  • [Cites] Cell Signal. 2003 Jan;15(1):1-7 [12401514.001]
  • [Cites] Mol Cells. 2002 Oct 31;14(2):163-7 [12442886.001]
  • [Cites] J Invest Dermatol. 2002 Dec;119(6):1244-53 [12485424.001]
  • [Cites] J Invest Dermatol. 2003 Jan;120(1):86-95 [12535202.001]
  • [Cites] Biochem Pharmacol. 2006 Nov 30;72(11):1493-505 [16723122.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2003 Jan;17(1):34-6 [12602965.001]
  • [Cites] J Surg Res. 2003 Aug;113(2):189-94 [12957128.001]
  • [Cites] Clin Dermatol. 2003 Sep-Oct;21(5):392-7 [14678719.001]
  • [Cites] J Eur Acad Dermatol Venereol. 2003 Nov;17(6):663-9 [14761133.001]
  • [Cites] J Med Chem. 2004 Apr 8;47(8):1930-8 [15055993.001]
  • [Cites] Exp Dermatol. 2004 Apr;13(4):193-222 [15086336.001]
  • [Cites] Br J Dermatol. 2004 May;150(5):917-28 [15149504.001]
  • [Cites] Inflammation. 1994 Feb;18(1):1-12 [8206642.001]
  • [Cites] Eur J Pharmacol. 1994 Feb 21;253(1-2):75-82 [8013550.001]
  • [Cites] J Dermatol. 2004 Mar;31(3):200-17 [15187340.001]
  • [Cites] J Clin Invest. 2004 Jun;113(12):1664-75 [15199399.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):32633-42 [15145954.001]
  • [Cites] Biol Pharm Bull. 2004 Aug;27(8):1158-64 [15305013.001]
  • [Cites] Biochem Pharmacol. 2004 Sep 15;68(6):1221-9 [15313420.001]
  • [Cites] J Nat Prod. 2004 Sep;67(9):1459-63 [15387642.001]
  • [Cites] J Lipid Res. 1974 Jul;15(4):380-8 [4212237.001]
  • [Cites] J Cell Biol. 1988 Mar;106(3):761-71 [2450098.001]
  • [Cites] Br J Pharmacol. 1988 Jun;94(2):528-39 [2840160.001]
  • [Cites] J Pharm Pharmacol. 1988 Nov;40(11):787-92 [2907559.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7708-12 [2217203.001]
  • [Cites] Biochem Pharmacol. 1992 Jul 22;44(2):205-14 [1322662.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 1995 Mar;351(3):298-304 [7609784.001]
  • [Cites] Int J Immunopharmacol. 1995 Jun;17(6):475-80 [7499023.001]
  • [Cites] Arch Dermatol Res. 1997 Aug;289(9):540-6 [9341975.001]
  • [Cites] Mol Carcinog. 1998 May;22(1):16-25 [9609097.001]
  • [Cites] J Immunol. 1998 Oct 1;161(7):3421-30 [9759860.001]
  • [Cites] J Dermatol Sci. 1999 Nov;21(3):135-46 [10527374.001]
  • [Cites] Int J Cancer. 2005 Jan 20;113(3):423-33 [15455341.001]
  • [Cites] Nat Med. 2005 Jan;11(1):17-8 [15635435.001]
  • [Cites] Trends Mol Med. 2005 Jan;11(1):43-8 [15649822.001]
  • [Cites] J Invest Dermatol. 2005 Jan;124(1):204-11 [15654975.001]
  • [Cites] Biotechnol Bioeng. 2005 Apr 20;90(2):201-22 [15739169.001]
  • [Cites] J Biol Chem. 2005 May 13;280(19):18973-80 [15722350.001]
  • [Cites] Br J Dermatol. 2005 Jun;152(6):1098-107 [15948970.001]
  • [Cites] J Invest Dermatol. 2005 Jun;124(6):1275-83 [15955104.001]
  • [Cites] J Invest Dermatol. 2005 Jun;124(6):1284-92 [15955105.001]
  • [Cites] J Am Acad Dermatol. 2005 Jul;53(1 Suppl 1):S17-25 [15968260.001]
  • [Cites] J Am Acad Dermatol. 2005 Jul;53(1 Suppl 1):S3-16 [15968262.001]
  • [Cites] Cell Mol Life Sci. 2005 Aug;62(15):1682-91 [15924263.001]
  • [Cites] J Invest Dermatol. 2005 Sep;125(3):473-81 [16117788.001]
  • [Cites] Curr Drug Targets Inflamm Allergy. 2005 Aug;4(4):517-9 [16127829.001]
  • [Cites] Br J Dermatol. 2005 Oct;153(4):725-32 [16181452.001]
  • [Cites] J Am Acad Dermatol. 2006 Mar;54(3 Suppl 2):S67-80 [16488332.001]
  • [Cites] Biochem Pharmacol. 2006 Apr 28;71(9):1331-6 [16487490.001]
  • (PMID = 17641670.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Inflammation Mediators; 0 / NF-kappa B; 0 / Salicylates; 0 / Sesquiterpenes; 0 / Tumor Necrosis Factor-alpha; 0 / avarol-3'-thiosalicylate; 27YG812J1I / Arachidonic Acid
  • [Other-IDs] NLM/ PMC2042954
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84. Tawfik OW, Kramer B, Shideler B, Danley M, Kimler BF, Holzbeierlein J: Prognostic significance of CD44, platelet-derived growth factor receptor alpha, and cyclooxygenase 2 expression in renal cell carcinoma. Arch Pathol Lab Med; 2007 Feb;131(2):261-7
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  • [Title] Prognostic significance of CD44, platelet-derived growth factor receptor alpha, and cyclooxygenase 2 expression in renal cell carcinoma.
  • CONTEXT: Pathologic stage is the main prognostic factor for predicting outcome in renal cell carcinoma (RCC).
  • Because of its unreliability in predicting tumor progression, other factors are needed to provide additional prognostic information.
  • OBJECTIVE: The expression of CD44, cyclooxygenase 2, and platelet-derived growth factor receptor alpha (PDGFR-alpha) was evaluated as a potential prognostic factor for survival in patients with RCC.
  • DESIGN: Sixty-two patients (42 men and 20 women; median age, 61 years), undergoing partial (10 cases) or radical (55 cases) nephrectomy for RCC were retrospectively analyzed by immunohistochemical analysis for CD44, cyclooxygenase 2, and PDGFR-alpha expression.
  • Impact of various factors on disease-specific and overall survival was calculated using Cox proportional hazards models.
  • RESULTS: There was a gradual increase in CD44 and cyclooxygenase 2 expression with increasing RCC nuclear grade.
  • In contrast, PDGFR-alpha expression showed no consistent relationship with nuclear grade.
  • On univariate analysis, metastasis at time of surgery (P < .001), tumor size (P = .004), pathologic stage group (P = .001), and nuclear grade (P = .004) were correlated with disease-specific survival.
  • For overall survival, metastasis (P < .001), tumor size (P = .02), pathologic stage group (P = .01), nuclear grade (P = .003), and PDGFR-alpha (P = .03) were significant on univariate analysis.
  • Only metastasis (P = .001) and PDGFR-alpha (P = .03) were significant on multivariate analysis.
  • CONCLUSIONS: When combined with other variables, PDGFR-alpha expression in RCC may provide additional predictive value related to the patient's overall survival.
  • [MeSH-major] Antigens, CD44 / biosynthesis. Carcinoma, Renal Cell / metabolism. Cyclooxygenase 2 / biosynthesis. Kidney Neoplasms / metabolism. Platelet-Derived Growth Factor / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 17284111.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Biomarkers, Tumor; 0 / Platelet-Derived Growth Factor; 0 / platelet-derived growth factor A; EC 1.14.99.1 / Cyclooxygenase 2
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85. Geng LY, Shi ZZ, Dong Q, Cai XH, Zhang YM, Cao W, Peng JP, Fang YM, Zheng L, Zheng S: Expression of SNC73, a transcript of the immunoglobulin alpha-1 gene, in human epithelial carcinomas. World J Gastroenterol; 2007 Apr 28;13(16):2305-11
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  • [Title] Expression of SNC73, a transcript of the immunoglobulin alpha-1 gene, in human epithelial carcinomas.
  • AIM: To investigate the expression of SNC73, a trans-cript of the immunoglobulin alpha-1 gene (IgA1-H chain), in human epithelia-derived tumor cells.
  • METHODS: Total RNAs and cell lysates were prepared from five different human epithelial cell lines derived from lung, stomach, liver, skin, and breast, respectively.
  • RT-PCR and immunoblot analysis of these five cell lines were done.
  • Both RT-PCR and immunochemistry were used to detect the expression of SNC73 in these cell lines.
  • We also examined the expression of SNC73 in normal epithelial cells of colon mucosa by in situ hybridization.
  • The expression of three immunoglobulin transcription factors, EBF, E2A and Pax5, and the heavy chain of IgA1 and two types of light chains of immunoglobulin (kappa and lambda) in the aforementioned cell lines were analyzed by RT-PCR and immunochemistry, respectively.
  • RESULTS: The results of RT-PCR and immunochemistry showed that both mRNA and protein of SNC73 were expressed in five human epithelia-derived cancer cell lines.
  • These data were further confirmed in the normal epithelial cells of colon mucosa by in situ hybridization.
  • Also, the heavy chain of IgA1 and kappa light chain were detected in these cells, but no lambda light chain was obse-rved.
  • Both RAG1 and RAG2 were expressed in these human epithelia-derived cancer cell lines and the sequence was identical to that expressed in pre-B and pre-T cells.
  • In addition to RAG1 and RAG2, the mRNA in one of the immunoglobulin transcription factors, EBF, was also detected in these cell lines, and Pax5 was only expressed in SW480 cells, but no expression of E2A was observed in all the five cell lines.
  • CONCLUSION: Immunoglobulin A1 is originally expressed and V(D)J recombination machine is also present in non-lymphoid cells, suggesting that V(D)J recombination machine mediates the assembly of immunoglobulin A1 in non-lymphoid cells as in pre-lymphocytes.
  • [MeSH-major] Breast Neoplasms / metabolism. Colorectal Neoplasms / metabolism. Immunoglobulins / metabolism. Liver Neoplasms / metabolism. Uterine Cervical Neoplasms / metabolism
  • [MeSH-minor] B-Cell-Specific Activator Protein / genetics. B-Cell-Specific Activator Protein / metabolism. Cell Line, Tumor. Colon / metabolism. Colon / pathology. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Epithelial Cells / metabolism. Female. Gene Expression Regulation, Neoplastic. HeLa Cells. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Trans-Activators / genetics. Trans-Activators / metabolism. VDJ Exons / genetics

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  • [Cites] Mol Cell. 2000 Feb;5(2):343-53 [10882075.001]
  • [Cites] Zhonghua Yi Xue Za Zhi. 2001 Apr 25;81(8):485-8 [11798924.001]
  • [Cites] Genes Chromosomes Cancer. 1998 May;22(1):83-6 [9591639.001]
  • [Cites] Cell. 1991 Jan 11;64(1):189-200 [1986864.001]
  • [Cites] J Cancer Res Clin Oncol. 1997;123(8):447-51 [9292708.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6488-95 [14559841.001]
  • (PMID = 17511028.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / DNA-Binding Proteins; 0 / EBF1 protein, human; 0 / Homeodomain Proteins; 0 / Immunoglobulins; 0 / Nuclear Proteins; 0 / PAX5 protein, human; 0 / RAG2 protein, human; 0 / SNC73 protein, human; 0 / Trans-Activators; 128559-51-3 / RAG-1 protein
  • [Other-IDs] NLM/ PMC4147138
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86. Wei LH, Baumann H, Tracy E, Wang Y, Hutson A, Rose-John S, Henderson BW: Interleukin-6 trans signalling enhances photodynamic therapy by modulating cell cycling. Br J Cancer; 2007 Dec 3;97(11):1513-22
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  • [Title] Interleukin-6 trans signalling enhances photodynamic therapy by modulating cell cycling.
  • Photodynamic therapy (PDT) of solid tumours causes tissue damage that elicits local and systemic inflammation with major involvement of interleukin-6 (IL-6).
  • We have previously reported that PDT-treated cells lose responsiveness to IL-6 cytokines.
  • Therefore, it is unclear whether PDT surviving tumour cells are subject to regulation by IL-6 and whether this regulation could contribute to tumour control by PDT.
  • We demonstrate in epithelial tumour cells that while the action of IL-6 cytokines through their membrane receptors is attenuated, regulation by IL-6 via trans-signalling is established.
  • Soluble interleukin-6 receptor-alpha (IL-6Ralpha) (sIL-6Ralpha) and IL-6 were released by leucocytes in the presence of conditioned medium from PDT-treated tumour cells.
  • Cells that had lost their membrane receptor IL-6Ralpha due to PDT responded to treatment with the IL-6R-IL-6 complex (Hyper-IL-6) with activation of signal transducers and activator of transcription (STAT3) and ERK.
  • Photodynamic therapy-treated cells, which were maintained during post-PDT recovery in presence of IL-6 or Hyper-IL-6, showed an enhanced suppression of proliferation.
  • The IL-6 trans-signalling-mediated attenuation of cell proliferation was also effective in vivo detectable by an improved Colon26 tumour cure by PDT combined with Hyper-IL-6 treatment.
  • The data suggest that the post-PDT tumour milieu contains the necessary components to establish effective IL-6 trans-signalling, thus providing a means for more effective tumour control.
  • [MeSH-major] Cell Cycle / physiology. Interleukin-6 / physiology. Signal Transduction / physiology
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Chlorophyll / analogs & derivatives. Chlorophyll / pharmacology. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Culture Media, Conditioned / pharmacology. Cyclin E / metabolism. Cyclin-Dependent Kinase 2 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Dose-Response Relationship, Drug. HeLa Cells. Humans. Macrophages / drug effects. Macrophages / metabolism. Mice. Mice, Inbred BALB C. Photochemotherapy. Receptors, Interleukin-6 / metabolism. STAT3 Transcription Factor / metabolism. cdc25 Phosphatases / metabolism

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  • [Cites] Biochem Biophys Res Commun. 2006 Jan 13;339(2):569-76 [16300726.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):2908-11 [8674038.001]
  • [Cites] Lasers Surg Med. 2006 Jun;38(5):509-15 [16788921.001]
  • [Cites] J Biol Chem. 2007 Feb 2;282(5):3014-26 [17148439.001]
  • [Cites] Nat Immunol. 2007 Apr;8(4):345-50 [17375096.001]
  • [Cites] Clin Cancer Res. 2007 Jun 1;13(11):3156-63 [17545518.001]
  • [Cites] Blood. 2007 Sep 15;110(6):1748-55 [17567983.001]
  • [Cites] Oncogene. 2003 Mar 13;22(10):1517-27 [12629515.001]
  • [Cites] Br J Cancer. 2003 Jun 2;88(11):1772-9 [12771994.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3812-8 [12839978.001]
  • [Cites] Oncogene. 2003 Jul 10;22(28):4413-24 [12853978.001]
  • [Cites] Photochem Photobiol. 2003 Jul;78(1):75-81 [12929752.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):2120-6 [15026352.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6579-87 [15374971.001]
  • [Cites] Cell. 1989 Aug 11;58(3):573-81 [2788034.001]
  • [Cites] Cytokine. 1992 Jan;4(1):6-11 [1617157.001]
  • [Cites] Cancer Res. 1994 Mar 1;54(5):1374-80 [8118827.001]
  • [Cites] Biochem J. 1994 Jun 1;300 ( Pt 2):281-90 [8002928.001]
  • [Cites] Oncogene. 2000 May 11;19(20):2447-54 [10828887.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2548-56 [10851053.001]
  • [Cites] Oncogene. 2000 Jul 27;19(32):3675-83 [10951574.001]
  • [Cites] Oncogene. 2001 Jan 11;20(2):198-208 [11313947.001]
  • [Cites] Int J Cancer. 2001 Aug 15;93(4):475-80 [11477550.001]
  • [Cites] J Photochem Photobiol B. 2001 Oct;63(1-3):103-13 [11684457.001]
  • [Cites] Growth Factors. 2001;19(3):153-62 [11811789.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1604-8 [11912128.001]
  • [Cites] Br J Cancer. 1996 Jul;74(1):30-6 [8679454.001]
  • [Cites] J Mol Med (Berl). 1996 Jan;74(1):1-12 [8834766.001]
  • [Cites] Cancer Res. 1996 Dec 15;56(24):5647-52 [8971170.001]
  • [Cites] Nat Biotechnol. 1997 Feb;15(2):142-5 [9035138.001]
  • [Cites] Cancer Res. 1997 Sep 15;57(18):3904-9 [9307269.001]
  • [Cites] J Clin Laser Med Surg. 1996 Oct;14(5):329-34 [9612200.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):6977-82 [9618524.001]
  • [Cites] J Biol Chem. 1999 Jan 15;274(3):1257-66 [9880494.001]
  • [Cites] Oncogene. 1999 Mar 11;18(10):1891-6 [10086343.001]
  • [Cites] J Biol Chem. 2005 Apr 22;280(16):15673-81 [15677471.001]
  • [Cites] J Immunol. 2005 Sep 15;175(6):3463-8 [16148087.001]
  • [Cites] BMC Cancer. 2005;5:145 [16271139.001]
  • [Cites] Cancer Res. 1995 Jun 1;55(11):2262-5 [7757973.001]
  • [Cites] Cancer Res. 1995 Jun 1;55(11):2373-9 [7757989.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1243-54 [7632928.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):3963-6 [8632998.001]
  • [Cites] Scand J Immunol. 2006 May;63(5):321-9 [16640655.001]
  • (PMID = 17987036.001).
  • [ISSN] 0007-0920
  • [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 / Culture Media, Conditioned; 0 / Cyclin E; 0 / Interleukin-6; 0 / Receptors, Interleukin-6; 0 / STAT3 Transcription Factor; 0 / interleukin-6 receptor alpha; 1406-65-1 / Chlorophyll; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149402-51-7 / 2-(1-hexyloxyethyl)-2-devinyl pyropheophorbide-a; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 3.1.3.48 / cdc25 Phosphatases
  • [Other-IDs] NLM/ PMC2360250
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87. Branchini G, Schneider L, Cericatto R, Capp E, Brum IS: Progesterone receptors A and B and estrogen receptor alpha expression in normal breast tissue and fibroadenomas. Endocrine; 2009 Jun;35(3):459-66
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  • [Title] Progesterone receptors A and B and estrogen receptor alpha expression in normal breast tissue and fibroadenomas.
  • Fibroadenomas are the most common benign breast tumors, occurring mainly in young women.
  • Their responses to the hormonal environment are similar to those of normal breast tissue, which suggests that steroid receptors may play a role in tumor development.
  • We evaluated the gene and protein expression of progesterone receptors A and B (PRA and PRB) and the protein expression of estrogen receptor alpha (ER-alpha) in fibroadenoma samples, comparing with adjacent normal breast tissue, from 11 premenopausal women.
  • No alterations in the PRs gene and protein expression and the ER-alpha protein expression were observed between the follicular and luteal phases, in normal breast versus fibroadenomas.
  • Protein levels of PRA and PRB were higher in fibroadenomas compared to normal breast tissue (P = 0.038 and P = 0.031), while the PRs mRNA levels were similar in both tissues (P = 0.721 and P = 0.139).
  • There were no differences in ER-alpha protein expression between normal breast tissue and fibroadenomas (P = 0.508).
  • Our data suggest a role of PRs in the growth and development of fibroadenomas, although without alterations of the PRA:PRB ratio in these tumors.
  • The absence of alterations in ER-alpha protein levels could be a characteristic behavior of fibroadenomas, unlike breast cancer.
  • [MeSH-major] Breast Neoplasms / genetics. Estrogen Receptor alpha / genetics. Fibroadenoma / genetics. Mammary Glands, Human / metabolism. Receptors, Progesterone / genetics
  • [MeSH-minor] Adult. Female. Gene Expression. Gene Expression Regulation, Neoplastic. Humans

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  • [Cites] J Steroid Biochem Mol Biol. 2006 Mar;98(4-5):218-27 [16466914.001]
  • [Cites] Breast J. 1999 Jul;5(4):256-261 [11348297.001]
  • [Cites] Steroids. 2000 Oct-Nov;65(10-11):571-7 [11108861.001]
  • [Cites] Breast Cancer Res Treat. 2003 Jun;79(3):287-99 [12846413.001]
  • [Cites] Endocr Relat Cancer. 2003 Jun;10(2):193-202 [12790782.001]
  • [Cites] Breast. 2003 Oct;12 (5):302-7 [14659144.001]
  • [Cites] Cancer Res. 1993 Sep 1;53(17):4071-4 [8395336.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5209-18 [11717311.001]
  • [Cites] Steroids. 2003 Nov;68(10-13):771-8 [14667967.001]
  • [Cites] J Clin Pathol. 2001 Jan;54(1):37-41 [11271786.001]
  • [Cites] Endocr Rev. 1997 Aug;18(4):502-19 [9267762.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2000 Jul;5(3):325-38 [14973394.001]
  • [Cites] Mol Endocrinol. 1999 Oct;13(10):1657-71 [10517668.001]
  • [Cites] Cell. 1997 Feb 7;88(3):323-31 [9039259.001]
  • [Cites] Maturitas. 2004 Sep 24;49(1):16-24 [15351092.001]
  • [Cites] Endocrine. 2009 Feb;35(1):118-22 [19002614.001]
  • [Cites] Steroids. 2005 Mar;70(3):153-60 [15763593.001]
  • [Cites] Breast Cancer Res. 2002;4(5):187-90 [12223122.001]
  • [Cites] Br J Cancer. 1992 Apr;65(4):601-7 [1562470.001]
  • [Cites] Cell Mol Life Sci. 2008 Nov;65(23 ):3839-50 [18850315.001]
  • [Cites] Mol Endocrinol. 2005 Nov;19(11):2713-35 [15976005.001]
  • [Cites] Epidemiol Rev. 1997;19(2):310-27 [9494790.001]
  • [Cites] Gynecol Oncol. 2004 May;93(2):394-9 [15099952.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 2006 Nov;129(1):77-83 [16460873.001]
  • [Cites] J Clin Pathol. 2002 May;55(5):371-4 [11986344.001]
  • [Cites] Breast Cancer Res Treat. 2002 Mar;72(2):163-72 [12038707.001]
  • [Cites] Am J Obstet Gynecol. 1997 Jan;176(1 Pt 1):123-8 [9024102.001]
  • [Cites] EMBO J. 1990 May;9(5):1603-14 [2328727.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2005 Oct;10(4):325-35 [16900392.001]
  • [Cites] Curr Probl Diagn Radiol. 2007 Mar-Apr;36(2):66-82 [17331838.001]
  • [Cites] Anal Biochem. 1987 Apr;162(1):156-9 [2440339.001]
  • [Cites] Braz J Med Biol Res. 1996 Dec;29(12):1593-7 [9222417.001]
  • [Cites] J Mol Endocrinol. 2000 Feb;24(1):33-41 [10656995.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):4849-53 [12208729.001]
  • [Cites] Mol Endocrinol. 2005 Mar;19(3):574-87 [15563544.001]
  • [Cites] Jpn J Cancer Res. 2001 Mar;92(3):302-8 [11267940.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Aug;84(8):2963-71 [10443705.001]
  • [Cites] Endocr Relat Cancer. 2002 Mar;9(1):1-13 [11914179.001]
  • (PMID = 19367380.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Receptors, Progesterone; 0 / progesterone receptor A; 0 / progesterone receptor B
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88. Xiao H, Song Y, Li Y, Liao YH, Chen J: Qiliqiangxin regulates the balance between tumor necrosis factor-alpha and interleukin-10 and improves cardiac function in rats with myocardial infarction. Cell Immunol; 2009;260(1):51-5
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  • [Title] Qiliqiangxin regulates the balance between tumor necrosis factor-alpha and interleukin-10 and improves cardiac function in rats with myocardial infarction.
  • The study investigated the effects of traditional Chinese drug Qiliqiangxin on cardiac function and the expression of pro/anti-inflammatory cytokines TNF-alpha/IL-10 in rats with myocardial infarction (MI).
  • Rats in the MI-Q group were treated with crude drug of oral Qiliqiangxin 24h after operation at the dosage of 4g/kg/day for 4weeks, while in MI-C group and S group were treated with normal saline at the same time.
  • Echocardiography and hemodynamic parameters, histopathologic changes and the expression of myocardial cytokines including TNF-alpha and IL-10 were assessed 4weeks after the drug therapy.
  • The results indicated that rats of the MI-C group exhibited decreased cardiac function and increased ratio of TNF-alpha/IL-10 which principally secreted by myocardium compared with those of the S group and Qiliqiangxin treatment significantly improved cardiac function and histopathologic changes with down-regulated ratio of TNF-alpha/IL-10.
  • These data suggests that Qiliqiangxin may improve cardiac function of rats with MI through regulation the balance between TNF-alpha and IL-10.
  • [MeSH-major] Drugs, Chinese Herbal / therapeutic use. Heart / drug effects. Interleukin-10 / metabolism. Myocardial Infarction / drug therapy. Tumor Necrosis Factor-alpha / drug effects

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  • (PMID = 19833326.001).
  • [ISSN] 1090-2163
  • [Journal-full-title] Cellular immunology
  • [ISO-abbreviation] Cell. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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89. McCluggage WG, Aydin NE, Wong NA, Cooper K: Low-grade epithelial-myoepithelial carcinoma of bartholin gland: report of 2 cases of a distinctive neoplasm arising in the vulvovaginal region. Int J Gynecol Pathol; 2009 May;28(3):286-91
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  • [Title] Low-grade epithelial-myoepithelial carcinoma of bartholin gland: report of 2 cases of a distinctive neoplasm arising in the vulvovaginal region.
  • We report 2 cases of a distinctive neoplasm arising from Bartholin gland and presenting as a vulval or vaginal mass.
  • The tumors occurred in patients aged 44 and 51 years and were 2 and 3 cm in maximum dimension.
  • The neoplasms were unencapsulated and largely well circumscribed but with a focally infiltrative edge.
  • They were composed of tubular, trabecular, or insular arrangements with a double layer of inner cuboidal cells with round nuclei and outer cells with ovoid nuclei and clear cytoplasm, corresponding to epithelial and myoepithelial cells, respectively.
  • In both cases, a minor proportion of the neoplasm consisted of cribriform arrangements, creating an appearance reminiscent of adenoid cystic carcinoma, although the overall morphology was not typical of that lesion.
  • Immunohistochemically, the inner cells were positive with epithelial markers, including broad-spectrum cytokeratins and epithelial membrane antigen, and the outer cell layer was positive with myoepithelial markers p63, calponin, and alpha-smooth muscle actin.
  • Both neoplasms exhibited diffuse strong immunoreactivity of the epithelial cells with c-kit.
  • Activating mutations in KIT exons 9, 11, 13, and 17 and in platelet-derived growth factor receptor alpha exons 12, 14, and 18 were searched for by polymerase chain reaction and direct sequencing but were not identified.
  • We believe this represents a low-grade carcinoma arising from Bartholin gland composed of a dual population of epithelial and myoepithelial cells and closely resembling the salivary gland neoplasm termed epithelial-myoepithelial carcinoma.
  • [MeSH-major] Bartholin's Glands / pathology. Carcinoma / pathology. Vulvar Neoplasms / pathology


90. Edwards S, Lalor PF, Tuncer C, Adams DH: Vitronectin in human hepatic tumours contributes to the recruitment of lymphocytes in an alpha v beta3-independent manner. Br J Cancer; 2006 Dec 4;95(11):1545-54
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  • [Title] Vitronectin in human hepatic tumours contributes to the recruitment of lymphocytes in an alpha v beta3-independent manner.
  • The degree of lymphocyte infiltration is a prognostic factor in liver cancer, but to date the mechanisms by which lymphocytes infiltrate into and are retained in hepatic tumours are poorly understood.
  • We hypothesised that the extracellular matrix glycoprotein vitronectin, a major component of the stroma of hepatic tumours, might play a role in the recruitment and retention of tumour-infiltrating lymphocytes (TIL).
  • Soluble vitronectin-induced dose-dependent migration of TIL in in vitro chemotaxis and haptotaxis assays and vitronectin in tissue sections was able to support TIL adhesion to tumour stroma.
  • Neither adhesion nor migration was inhibited by a function blocking mAb against the major vitronectin receptor alpha v beta3 and we were unable to detect alpha v beta3 on TIL in vitro or in vivo on tumour tissue.
  • However, TIL did express high levels of urokinase-type plasminogen activator receptor (uPAR) and inhibitory antibodies and amiloride both significantly inhibited TIL adhesion to vitronectin and reduced transendothelial migration of lymphocytes across liver endothelium in vitro.
  • Thus, we provide evidence that vitronectin in liver tumours can support the recruitment and retention of effector lymphocytes by an uPAR-dependent mechanism.

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  • [Cites] Nat Immunol. 2004 Nov;5(11):1124-33 [15475957.001]
  • [Cites] J Immunol. 2004 Sep 15;173(6):3889-900 [15356137.001]
  • [Cites] FASEB J. 1991 Jun;5(9):2292-9 [1860621.001]
  • [Cites] Hepatology. 1992 Apr;15(4):629-36 [1372581.001]
  • [Cites] Annu Rev Cell Biol. 1991;7:275-310 [1725600.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jun 1;90(11):5021-5 [8389464.001]
  • [Cites] J Biol Chem. 1993 Oct 25;268(30):22874-82 [7693680.001]
  • [Cites] Curr Opin Cell Biol. 1993 Oct;5(5):864-8 [7694604.001]
  • [Cites] J Immunol. 1994 Jan 15;152(2):505-16 [8283034.001]
  • [Cites] Anticancer Res. 1993 Nov-Dec;13(6A):2229-37 [8297138.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jul 19;91(15):7144-8 [8041760.001]
  • [Cites] Hepatology. 1994 Dec;20(6):1412-7 [7527001.001]
  • [Cites] J Biol Chem. 1994 Dec 23;269(51):32380-8 [7528215.001]
  • [Cites] Crit Rev Oral Biol Med. 1996;7(1):59-86 [8727107.001]
  • [Cites] J Clin Invest. 1996 Sep 1;98(5):1133-41 [8787676.001]
  • [Cites] Crit Rev Immunol. 1995;15(3-4):285-316 [8834453.001]
  • [Cites] Br J Cancer. 1997;75(10):1421-31 [9166933.001]
  • [Cites] J Clin Invest. 1997 Jul 1;100(1):58-67 [9202057.001]
  • [Cites] Immunol Today. 1997 Sep;18(9):415-7 [9293155.001]
  • [Cites] Scand J Immunol. 1997 Nov;46(5):437-44 [9393625.001]
  • [Cites] Eur J Immunol. 1997 Dec;27(12):3242-52 [9464812.001]
  • [Cites] J Immunol. 1998 Apr 15;160(8):3978-88 [9558106.001]
  • [Cites] Br J Cancer. 1998 Apr;77(7):1072-81 [9569042.001]
  • [Cites] Hepatology. 2005 Jan;41(1):40-7 [15690480.001]
  • [Cites] Am J Pathol. 2005 Sep;167(3):887-99 [16127166.001]
  • [Cites] Hepatology. 1999 Jul;30(1):100-11 [10385645.001]
  • [Cites] J Biol Chem. 1999 Dec 31;274(53):37611-9 [10608816.001]
  • [Cites] FEBS Lett. 2000 Mar 17;470(1):40-6 [10722842.001]
  • [Cites] Dis Colon Rectum. 2000 Jul;43(7):980-6 [10910247.001]
  • [Cites] Curr Opin Cell Biol. 2000 Oct;12(5):621-8 [10978899.001]
  • [Cites] Dev Immunol. 2000;7(2-4):227-38 [11097214.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4091-5 [11110678.001]
  • [Cites] Histopathology. 2000 Dec;37(6):523-9 [11122434.001]
  • [Cites] J Cell Sci. 2001 Apr;114(Pt 8):1545-53 [11282030.001]
  • [Cites] Hum Pathol. 2001 Dec;32(12):1356-62 [11774169.001]
  • [Cites] J Immunol. 2002 Jul 15;169(2):983-92 [12097405.001]
  • [Cites] Hepatology. 2002 Aug;36(2):418-26 [12143051.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] J Surg Oncol. 2003 Jan;82(1):28-33 [12501166.001]
  • [Cites] J Exp Med. 1976 Sep 1;144(3):828-33 [956727.001]
  • (PMID = 17088900.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrin alphaVbeta3; 0 / PLAUR protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; 0 / Vitronectin
  • [Other-IDs] NLM/ PMC2360745
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91. Shmarina G, Pukhalsky A, Alioshkin V, Sabelnikov A: Melphalan reduces the severity of experimental colitis in mice by blocking tumor necrosis factor-alpha signaling pathway. Ann N Y Acad Sci; 2007 Jan;1096:97-105
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  • [Title] Melphalan reduces the severity of experimental colitis in mice by blocking tumor necrosis factor-alpha signaling pathway.
  • Its cytostatic effect can be realized in humans in the dose range of 0.6-1.4 mg/kg body weight.
  • However, previously it was shown that in the case of gradual dose decrease, the number of targets for alkylation was also reduced and the drug lost its cytostatic properties switching to cell growth modifier.
  • Daily administration of melphalan (25 microg/kg body weight) markedly reduced the severity of DSS-colitis as determined by clinical and quantitative histological criteria.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Colitis / drug therapy. Melphalan / pharmacology. Signal Transduction. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Anti-Inflammatory Agents / pharmacology. Cell Survival. Dextran Sulfate / pharmacology. Disease Models, Animal. Dose-Response Relationship, Drug. Male. Mice. Mice, Inbred BALB C

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  • (PMID = 17405921.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Necrosis Factor-alpha; 9042-14-2 / Dextran Sulfate; Q41OR9510P / Melphalan
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92. Fukushima S, Hirata S, Motomura Y, Fukuma D, Matsunaga Y, Ikuta Y, Ikeda T, Kageshita T, Ihn H, Nishimura Y, Senju S: Multiple antigen-targeted immunotherapy with alpha-galactosylceramide-loaded and genetically engineered dendritic cells derived from embryonic stem cells. J Immunother; 2009 Apr;32(3):219-31
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  • [Title] Multiple antigen-targeted immunotherapy with alpha-galactosylceramide-loaded and genetically engineered dendritic cells derived from embryonic stem cells.
  • Numerous tumor-associated antigens (TAA) have been identified and their use in immunotherapy is considered to be promising.
  • In the present study, we demonstrated the efficacy of multiple TAA-targeted dendritic cell (DC) vaccines and also the additive effects of loading alpha-galactosylceramide to DC using mouse melanoma models.
  • On the basis of previously established methods to generate DC from mouse embryonic stem cells (ES-DC), 4 kinds of genetically modified ES-DC, which expressed the melanoma-associated antigens, glypican-3, secreted protein acidic and rich in cysteine, tyrosinase-related protein-2, or gp100 were generated.
  • Anticancer effects elicited by immunization with the ES-DC were assessed in preventive and also therapeutic settings in the models of peritoneal dissemination and spontaneous metastasis to lymph node and lung.
  • The in vivo transfer of a mixture of 3 kinds of TAA-expressing ES-DC protected the recipient mice from melanoma cells more effectively than the transfer of ES-DC expressing single TAA, thus demonstrating the advantage of multiple as compared with single TAA-targeted immunotherapy.
  • Loading ES-DC with alpha-galactosylceramide further enhanced the anticancer effects, suggesting that excellent synergic effects of TAA-specific cytotoxic T lymphocytes and natural killer T cells against metastatic melanoma can be achieved by using genetically modified ES-DC.
  • With the aid of advancing technologies related to pluripotent stem cells, induced pluripotent stem cells, and ES cells, clinical application of DC highly potent in eliciting anticancer immunity will be realized in the near future.
  • [MeSH-major] Antigens, Neoplasm / immunology. Cancer Vaccines / immunology. Dendritic Cells / immunology. Immunotherapy, Active. Melanoma / therapy. Skin Neoplasms / therapy. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Animals. Embryonic Stem Cells / immunology. Galactosylceramides / immunology. Genetic Engineering. Glypicans / immunology. Glypicans / metabolism. Humans. Intramolecular Oxidoreductases / immunology. Intramolecular Oxidoreductases / metabolism. Membrane Glycoproteins / immunology. Membrane Glycoproteins / metabolism. Mice. Natural Killer T-Cells / immunology. Natural Killer T-Cells / metabolism. Osteonectin / immunology. Osteonectin / metabolism. Transfection. gp100 Melanoma Antigen

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  • (PMID = 19242378.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Galactosylceramides; 0 / Glypicans; 0 / Membrane Glycoproteins; 0 / Osteonectin; 0 / PMEL protein, human; 0 / Si protein, mouse; 0 / alpha-galactosylceramide; 0 / gp100 Melanoma Antigen; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase
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93. DiLillo DJ, Yanaba K, Tedder TF: B cells are required for optimal CD4+ and CD8+ T cell tumor immunity: therapeutic B cell depletion enhances B16 melanoma growth in mice. J Immunol; 2010 Apr 1;184(7):4006-16
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  • [Title] B cells are required for optimal CD4+ and CD8+ T cell tumor immunity: therapeutic B cell depletion enhances B16 melanoma growth in mice.
  • Previous studies have demonstrated augmented T cell-mediated tumor immunity in genetically B cell-deficient mice, suggesting that therapeutic B cell depletion would enhance tumor immunity.
  • To test this hypothesis and quantify B cell contributions to T cell-mediated anti-tumor immune responses, mature B cells were depleted from wild-type adult mice using CD20 mAb prior to syngeneic B16 melanoma tumor transfers.
  • Remarkably, s.c. tumor volume and lung metastasis were increased 2-fold in B cell-depleted mice.
  • Effector-memory and IFN-gamma-or TNF-alpha-secreting CD4(+) and CD8(+) T cell induction was significantly impaired in B cell-depleted mice with tumors.
  • Tumor Ag-specific CD8(+) T cell proliferation was also impaired in tumor-bearing mice that lacked B cells.
  • Thus, B cells were required for optimal T cell activation and cellular immunity in this in vivo nonlymphoid tumor model.
  • Although B cells may not have direct effector roles in tumor immunity, impaired T cell activation, and enhanced tumor growth in the absence of B cells argue against previous proposals to augment tumor immunity through B cell depletion.
  • Rather, targeting tumor Ags to B cells in addition to dendritic cells is likely to optimize tumor-directed vaccines and immunotherapies.

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  • [Cites] J Exp Med. 2000 Aug 21;192(4):475-82 [10952717.001]
  • [Cites] Semin Cancer Biol. 2000 Oct;10(5):351-7 [11100883.001]
  • [Cites] Immunology. 2001 Apr;102(4):486-97 [11328383.001]
  • [Cites] Int Immunol. 2001 Dec;13(12):1583-93 [11717199.001]
  • [Cites] Life Sci. 2002 Jan 4;70(7):791-8 [11833741.001]
  • [Cites] J Exp Med. 2003 Apr 7;197(7):875-83 [12668647.001]
  • [Cites] J Exp Med. 2003 Aug 18;198(4):569-80 [12925674.001]
  • [Cites] Am J Transplant. 2003 Nov;3(11):1355-62 [14525595.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2046-54 [14630810.001]
  • [Cites] J Immunol. 2004 Apr 15;172(8):4709-16 [15067046.001]
  • [Cites] J Exp Med. 2004 Jun 21;199(12):1659-69 [15210744.001]
  • [Cites] J Immunother. 2004 Jul-Aug;27(4):273-81 [15235388.001]
  • [Cites] Nat New Biol. 1973 Apr 4;242(118):148-9 [4512654.001]
  • [Cites] J Immunol. 1978 Jul;121(1):359-62 [307580.001]
  • [Cites] Int J Cancer. 1982 Mar 15;29(3):351-7 [6978293.001]
  • [Cites] Science. 1990 Aug 24;249(4971):921-3 [2118273.001]
  • [Cites] Transplantation. 1993 Jun;55(6):1356-61 [8100090.001]
  • [Cites] Cell. 1994 Jan 14;76(1):17-27 [8287475.001]
  • [Cites] Mol Cell Biol. 1994 Jun;14(6):3884-94 [7515149.001]
  • [Cites] Clin Immunol Immunopathol. 1994 Jul;72(1):1-8 [8020182.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2165-74 [8642326.001]
  • [Cites] J Immunol. 1997 Jul 15;159(2):952-63 [9218616.001]
  • [Cites] Immunol Cell Biol. 1998 Feb;76(1):34-40 [9553774.001]
  • [Cites] Nat Med. 1998 May;4(5):627-30 [9585241.001]
  • [Cites] J Virol. 1998 Nov;72(11):9208-16 [9765468.001]
  • [Cites] Int J Cancer. 1999 Sep 24;83(1):107-12 [10449616.001]
  • [Cites] J Immunol. 1999 Nov 1;163(9):4894-900 [10528191.001]
  • [Cites] Trends Immunol. 2004 Dec;25(12):659-64 [15530836.001]
  • [Cites] Scand J Immunol. 2004 Dec;60(6):543-51 [15584965.001]
  • [Cites] J Immunol. 2005 Apr 1;174(7):4389-99 [15778404.001]
  • [Cites] Cancer Cell. 2005 May;7(5):403-5 [15894259.001]
  • [Cites] Cancer Cell. 2005 May;7(5):411-23 [15894262.001]
  • [Cites] Nat Med. 2005 Sep;11(9):986-91 [16116429.001]
  • [Cites] Int J Cancer. 2005 Nov 20;117(4):574-86 [15912532.001]
  • [Cites] J Immunol. 2006 Mar 15;176(6):3498-506 [16517718.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7741-7 [16885377.001]
  • [Cites] Am J Pathol. 2006 Sep;169(3):954-66 [16936269.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):5009-16 [17510433.001]
  • [Cites] J Immunol. 2007 Jul 15;179(2):1369-80 [17617630.001]
  • [Cites] J Immunol. 2007 Sep 1;179(5):3351-61 [17709552.001]
  • [Cites] J Immunol. 2008 Jan 1;180(1):361-71 [18097037.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 26;104(52):20878-83 [18093919.001]
  • [Cites] J Immunol. 2008 Mar 1;180(5):2863-75 [18292508.001]
  • [Cites] J Immunol. 2008 Apr 1;180(7):4994-5003 [18354225.001]
  • [Cites] Immunity. 2008 May;28(5):639-50 [18482568.001]
  • [Cites] J Immunother. 2008 Jun;31(5):446-57 [18463540.001]
  • [Cites] Immunol Rev. 2008 Jun;223:284-99 [18613843.001]
  • [Cites] Cancer Immunol Immunother. 2008 Nov;57(11):1665-73 [18311487.001]
  • [Cites] Immunol Rev. 2008 Aug;224:201-14 [18759928.001]
  • [Cites] J Clin Invest. 2008 Oct;118(10):3420-30 [18802481.001]
  • [Cites] J Immunol. 2008 Oct 15;181(8):5257-63 [18832680.001]
  • [Cites] Ann N Y Acad Sci. 2010 Jan;1183:38-57 [20146707.001]
  • [Cites] J Immunol. 2000 Jan 15;164(2):916-25 [10623840.001]
  • [Cites] Cancer Immunol Immunother. 2000 Jan;48(10):541-9 [10630306.001]
  • [Cites] J Immunol. 2000 Nov 15;165(10):5558-65 [11067910.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):1095-9 [11221838.001]
  • (PMID = 20194720.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI56363; United States / NIAID NIH HHS / AI / U19 AI056363; United States / NCI NIH HHS / CA / R01 CA096547; United States / NCI NIH HHS / CA / R01 CA105001; United States / NCI NIH HHS / CA / CA96547; United States / NCI NIH HHS / CA / CA105001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS495260; NLM/ PMC3733120
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94. Razonable RR, Henault M, Watson HL, Paya CV: Nystatin induces secretion of interleukin (IL)-1beta, IL-8, and tumor necrosis factor alpha by a toll-like receptor-dependent mechanism. Antimicrob Agents Chemother; 2005 Aug;49(8):3546-9
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  • [Title] Nystatin induces secretion of interleukin (IL)-1beta, IL-8, and tumor necrosis factor alpha by a toll-like receptor-dependent mechanism.
  • Herein, we demonstrate that nystatin induces interleukin (IL)-1beta, IL-8, and tumor necrosis factor alpha secretion through its activation of toll-like receptor 1 (TLR1) and TLR2.
  • [MeSH-major] Anti-Bacterial Agents / pharmacology. Cytokines / secretion. Inflammation / chemically induced. Membrane Glycoproteins / metabolism. Nystatin / pharmacology. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Antibodies, Monoclonal / immunology. Cell Line. Humans. Interleukin-1 / secretion. Interleukin-8 / secretion. Toll-Like Receptor 1. Toll-Like Receptor 2. Toll-Like Receptors. Tumor Necrosis Factor-alpha / secretion

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  • [Cites] Homeopathy. 2004 Apr;93(2):84-7 [15139092.001]
  • [Cites] Scand J Infect Dis. 2003;35(9):555-62 [14620134.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Nov;48(11):4120-9 [15504830.001]
  • [Cites] Infection. 1980;8 Suppl 3:S 284-7 [6997205.001]
  • [Cites] Antimicrob Agents Chemother. 1987 Dec;31(12):1901-3 [3439799.001]
  • [Cites] Antimicrob Agents Chemother. 1997 Oct;41(10):2238-43 [9333054.001]
  • [Cites] J Antimicrob Chemother. 1999 Jan;43(1):95-103 [10381106.001]
  • [Cites] Antimicrob Agents Chemother. 1999 Oct;43(10):2463-7 [10508025.001]
  • [Cites] Science. 1950 Oct 13;112(2911):423 [14781786.001]
  • [Cites] Antimicrob Agents Chemother. 2005 Apr;49(4):1617-21 [15793154.001]
  • [Cites] Chest. 2000 Aug;118(2):503-8 [10936147.001]
  • [Cites] Int J Hematol. 2000 Dec;72(4):391-8 [11197203.001]
  • [Cites] Support Care Cancer. 2001 May;9(3):209-10 [11401107.001]
  • [Cites] Curr Opin Investig Drugs. 2001 Apr;2(4):488-95 [11566004.001]
  • [Cites] J Antimicrob Chemother. 2001 Dec;48(6):751-5 [11733457.001]
  • [Cites] J Immunol. 2002 Jul 1;169(1):10-4 [12077222.001]
  • [Cites] J Endotoxin Res. 2002;8(6):459-63 [12697090.001]
  • [Cites] J Pharm Pharm Sci. 2003 Jan-Apr;6(1):67-83 [12753730.001]
  • [Cites] J Biol Chem. 2003 Sep 26;278(39):37561-8 [12860979.001]
  • [Cites] EMBO Rep. 2004 Oct;5(10):1000-6 [15359270.001]
  • (PMID = 16048981.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antibodies, Monoclonal; 0 / Cytokines; 0 / Interleukin-1; 0 / Interleukin-8; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / TLR2 protein, human; 0 / Toll-Like Receptor 1; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha; 1400-61-9 / Nystatin
  • [Other-IDs] NLM/ PMC1196261
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95. Lankveld DP, Bull S, Van Dijk P, Fink-Gremmels J, Hellebrekers LJ: Ketamine inhibits LPS-induced tumour necrosis factor-alpha and interleukin-6 in an equine macrophage cell line. Vet Res; 2005 Mar-Apr;36(2):257-62
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  • [Title] Ketamine inhibits LPS-induced tumour necrosis factor-alpha and interleukin-6 in an equine macrophage cell line.
  • In horses, cytokines such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) play a pivotal role in the pathogenesis of equine endotoxaemia following gastrointestinal disorders.
  • Hence, the objective of this study was to assess the influence of ketamine on LPS-induced TNF-alpha and IL-6 formation in an equine macrophage cell line (eCAS cells).
  • The results demonstrate a cytokine-modulating activity of ketamine in an equine cell line, suggesting a beneficial role for ketamine in the treatment of equine endotoxaemia.
  • [MeSH-major] Anesthetics, Dissociative / pharmacology. Horses / immunology. Interleukin-6 / metabolism. Ketamine / pharmacology. Lipopolysaccharides / antagonists & inhibitors. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Humans. Macrophages / drug effects. Macrophages / immunology

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  • (PMID = 15720977.001).
  • [ISSN] 0928-4249
  • [Journal-full-title] Veterinary research
  • [ISO-abbreviation] Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anesthetics, Dissociative; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 690G0D6V8H / Ketamine
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96. Laskov R, Berger N, Scharff MD, Horwitz MS: Tumor necrosis factor-alpha and CD40L modulate cell surface morphology and induce aggregation in Ramos Burkitt's lymphoma cells. Leuk Lymphoma; 2006 Mar;47(3):507-19
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  • [Title] Tumor necrosis factor-alpha and CD40L modulate cell surface morphology and induce aggregation in Ramos Burkitt's lymphoma cells.
  • Interaction of CD40L and its cognate receptor is an essential component of B-lymphocyte signaling, affecting various aspects of B-cell differentiation pathways and immunoglobulin gene expression.
  • However, much less is known about the biological consequences of B-cell signaling through tumor necrosis factor (TNF)-alpha and its cognate receptors TNF-R1 and 2.
  • We used Ramos Burkitt's lymphoma cell line as a model system to study the direct effects of these cytokines on B cells.
  • Treatment of Ramos cells with either TNF-alpha or CD40L, but not with interleukin (IL)- 4, interferon (IFN)-gamma and transforming growth factor (TGF)-beta, resulted in enhanced cell aggregation and enhancement of adherence to glass cover-slips.
  • Scanning electron microscopy showed that Ramos cells have a polarized cell surface morphology and exhibit at least 3 cell surface morphological domains: microvilli, filopodia and ruffled membranes.
  • The cells adhered to the glass matrix through multiple filopodia/podopodia-like cell processes and demonstrated distinct ruffled-like membrane projections on their opposite pole.
  • Induction by TNF-alpha or CD40L, but not with IL-4, IFN-gamma and TGF-beta, resulted in increased number and complexity of both types of membrane projections.
  • TNF-alpha and CD40L upregulated the expression of the adhesion molecule intercellular adhesion molecule-1 and the Fas receptor on Ramos cells, without affecting the expression levels of membrane immunoglobulin M or its secretion rate.
  • Reverse transcriptase-polymerase chain reaction, and flow cytometry demonstrated that Ramos cells expressed TNF-R1 but very little if any TNF-R2, indicating that TNF-alpha exerted its effects on Ramos cells through the former receptor.
  • [MeSH-major] Burkitt Lymphoma / immunology. Burkitt Lymphoma / pathology. CD40 Ligand / pharmacology. Cell Aggregation / drug effects. Cell Membrane / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Antigens, CD95. Cell Adhesion / drug effects. Cell Line, Tumor. Humans. Intercellular Adhesion Molecule-1 / drug effects. Intercellular Adhesion Molecule-1 / immunology. Receptors, Tumor Necrosis Factor / drug effects. Receptors, Tumor Necrosis Factor / immunology. Receptors, Tumor Necrosis Factor, Type I / biosynthesis. Receptors, Tumor Necrosis Factor, Type II / biosynthesis. Signal Transduction / drug effects

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  • (PMID = 16523591.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1PO1 DK52956; United States / NIAID NIH HHS / AI / AI43937; United States / NCI NIH HHS / CA / CA72649
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / FAS protein, human; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 147205-72-9 / CD40 Ligand
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97. Choi B, Hwang Y, Kwon HJ, Lee ES, Park KS, Bang D, Lee S, Sohn S: Tumor necrosis factor alpha small interfering RNA decreases herpes simplex virus-induced inflammation in a mouse model. J Dermatol Sci; 2008 Nov;52(2):87-97
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  • [Title] Tumor necrosis factor alpha small interfering RNA decreases herpes simplex virus-induced inflammation in a mouse model.
  • OBJECTIVES: To inhibit the expression of TNFalpha, we used small interfering RNAs (siRNAs) to reduce over expression of TNFalpha in vitro in cell cultures and in an in vivo Behcet's disease-like (BD) mouse model for amelioration of chronic inflammation.
  • RESULTS: Intraperitoneal delivery of TNFalpha siRNA effectively decreased BD symptoms in 18 of 32 cases (56.3%).
  • CONCLUSION: We show that siRNAs can be employed to inhibit cytokine gene expression in an in vivo disease mouse model.
  • [MeSH-major] Behcet Syndrome / drug therapy. Behcet Syndrome / virology. RNA, Small Interfering / therapeutic use. Simplexvirus / pathogenicity. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Animals. Anti-Inflammatory Agents / pharmacology. Anti-Inflammatory Agents / therapeutic use. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Cells, Cultured. Cytokines / metabolism. Disease Models, Animal. Etanercept. Immunoglobulin G / pharmacology. Immunoglobulin G / therapeutic use. Infliximab. Lipopolysaccharides / metabolism. Macrophages / drug effects. Macrophages / metabolism. Male. Mice. Mice, Inbred ICR. Receptors, Tumor Necrosis Factor / therapeutic use. Treatment Outcome

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  • (PMID = 18585901.001).
  • [ISSN] 0923-1811
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Cytokines; 0 / Immunoglobulin G; 0 / Lipopolysaccharides; 0 / RNA, Small Interfering; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; OP401G7OJC / Etanercept
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98. Chaung HC, Huang TC, Yu JH, Wu ML, Chung WB: Immunomodulatory effects of beta-glucans on porcine alveolar macrophages and bone marrow haematopoietic cell-derived dendritic cells. Vet Immunol Immunopathol; 2009 Oct 15;131(3-4):147-57
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  • [Title] Immunomodulatory effects of beta-glucans on porcine alveolar macrophages and bone marrow haematopoietic cell-derived dendritic cells.
  • The immunopharmacological activities of beta-glucans with a backbone of beta-1,3/beta-1,6-linkages associated with anti-tumor, anti-viral, bacterial and fungal infections have been well documented.
  • Dectin-1, a specific pattern recognition receptor for beta-1,3/beta-1,6-glucans, is expressed mainly on phagocytes, especially macrophages and dendritic cells (DCs).
  • In this study, the encoding nucleotide for the carbohydrate-recognition domain (CRD) of porcine dectin-1 was sequenced for the first time, and the immunomodulatory functions of a synthetic particulate beta-glucan (p-beta-glucan) were examined.
  • Results showed that p-beta-glucan significantly enhanced cell activity and phagocytosis in porcine alveolar macrophages (AMs), immature DCs (imDCs) and mature DCs (mDCs), in a similar way to zymosan.
  • Zymosan enhanced dectin-1/TLR2/TLR4 expression and TNF-alpha/IL-10 production in all of three types of cell, whereas p-beta-glucan increased dectin-1/TLR4 and TNF-alpha/IL-12 production in AMs but inhibited IL-10 in mDCs.
  • These results indicate that the complex collaborating interactions between dectin-1 and TLRs in the recognition of beta-1,3/beta-1,6-glucans with different structural features may direct different cellular responses.
  • [MeSH-major] Dendritic Cells / drug effects. Dendritic Cells / immunology. Immunologic Factors / pharmacology. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / immunology. Sus scrofa / immunology. beta-Glucans / pharmacology
  • [MeSH-minor] Animals. Base Sequence. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Bone Marrow Cells / immunology. Cell Differentiation. Cloning, Molecular. DNA Primers / genetics. Host-Pathogen Interactions / immunology. Humans. In Vitro Techniques. Interleukin-10 / biosynthesis. Interleukin-12 / biosynthesis. Lectins, C-Type. Macromolecular Substances / chemistry. Macromolecular Substances / immunology. Macromolecular Substances / pharmacology. Male. Membrane Proteins / chemistry. Membrane Proteins / genetics. Membrane Proteins / immunology. Membrane Proteins / metabolism. Mice. Microscopy, Electron, Transmission. Molecular Sequence Data. Nerve Tissue Proteins / chemistry. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / immunology. Nerve Tissue Proteins / metabolism. Phagocytosis. Protein Structure, Tertiary. Sequence Homology, Nucleic Acid. Species Specificity. Toll-Like Receptor 2 / metabolism. Toll-Like Receptor 4 / metabolism. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 19410299.001).
  • [ISSN] 1873-2534
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Immunologic Factors; 0 / Lectins, C-Type; 0 / Macromolecular Substances; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha; 0 / beta-Glucans; 0 / dectin 1; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12
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99. McCluggage WG, Young RH: Ovarian sertoli-leydig cell tumors with pseudoendometrioid tubules (pseudoendometrioid sertoli-leydig cell tumors). Am J Surg Pathol; 2007 Apr;31(4):592-7
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  • [Title] Ovarian sertoli-leydig cell tumors with pseudoendometrioid tubules (pseudoendometrioid sertoli-leydig cell tumors).
  • The propensity for ovarian endometrioid adenocarcinomas to morphologically mimic Sertoli, Sertoli-Leydig, and granulosa cell tumors, is well known.
  • The converse situation, mimicry of an endometrioid neoplasm by a sex cord-stromal tumor, has not been emphasized.
  • In this report, we describe 9 ovarian Sertoli-Leydig cell tumors (5 well differentiated, 4 of intermediate differentiation) with areas containing hollow, sometimes dilated, tubules which resemble endometrioid glands; we refer to these as pseudoendometrioid tubules.
  • The tumors, all of which were unilateral except for one, ranged from 3.5 to 19 cm and were variously described as tan, pale, yellow, or gold.
  • The proportion of the tumor made up of pseudoendometrioid tubules ranged from 10% to >90%.
  • When widespread, their presence sometimes resulted in consideration of a borderline endometrioid adenofibroma or a well-differentiated endometrioid adenocarcinoma.
  • However, all the neoplasms contained typical Sertoli tubules and one or more of the characteristic patterns of Sertoli-Leydig cell tumors as well as Leydig cells, although the latter cells were inconspicuous in some cases.
  • Immunohistochemistry, performed in 4 cases, showed that the pseudoendometrioid tubules, as well as the more typical Sertoli cell elements, were either positive for alpha inhibin (3 of 4 cases) or calretinin (3 of 4 cases) or both, although sometimes focally so.
  • This report illustrates the potential for ovarian Sertoli-Leydig cell tumors to contain tubules with a pseudoendometrioid appearance which mimic a borderline or malignant endometrioid neoplasm.
  • The presence of more typical Sertoli cell elements and Leydig cells, an absence of squamous elements, endometriosis or associated adenofibroma, and the characteristic immunophenotype assist in diagnosis.
  • [MeSH-major] Ovarian Neoplasms / pathology. Sertoli-Leydig Cell Tumor / pathology
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor / analysis. Carcinoma, Endometrioid / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Middle Aged

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  • (PMID = 17414107.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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100. Tsao SM, Yin MC, Liu WH: Oxidant stress and B vitamins status in patients with non-small cell lung cancer. Nutr Cancer; 2007;59(1):8-13
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  • [Title] Oxidant stress and B vitamins status in patients with non-small cell lung cancer.
  • In this study, we examined oxidative stress and B vitamins status in non-small cell lung cancer (NSCLC) patients at different stages.
  • Plasma levels of alpha-tocopherol, beta-carotene, vitamin C, Se, Cu, Zn, reduced glutathione (GSH), oxidized glutathione (GSSG), lipid oxidation and the activities of glutathione peroxidase (GPX), superoxide dismutase (SOD), catalase, and xanthine oxidase (XO) were determined for evaluating oxidative status in these subjects.
  • Results showed that plasma level of ghrelin and lipid oxidation in NSCLC patients were significantly greater than control groups (P < 0.05).
  • Vitamins B(2) and B(6) levels in red blood cells (RBC) from NSCLC patients were significantly lower (P < 0.05), and both were negatively correlated with plasma ghrelin.
  • RBC levels of vitamins B2 and B6 were reduced in NSCLC patients; thus, the importance of vitamins B(2) and B(6) for NSCLC patients could not be ignored.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / blood. Glutathione Reductase / blood. Lung Neoplasms / blood. Oxidative Stress. Vitamin B Complex / blood
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Ascorbic Acid / blood. Biomarkers, Tumor / blood. Case-Control Studies. Catalase / blood. Erythrocytes / chemistry. Erythrocytes / enzymology. Female. Ghrelin / blood. Glutathione / blood. Glutathione Peroxidase / blood. Health Status. Humans. Lipid Peroxidation. Male. Middle Aged. Neoplasm Staging. Nutritional Status. Oxidation-Reduction. Superoxide Dismutase / blood. Xanthine Oxidase / blood. alpha-Tocopherol / blood. beta Carotene / blood

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  • (PMID = 17927496.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ghrelin; 01YAE03M7J / beta Carotene; 12001-76-2 / Vitamin B Complex; EC 1.11.1.6 / Catalase; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.17.3.2 / Xanthine Oxidase; EC 1.8.1.7 / Glutathione Reductase; GAN16C9B8O / Glutathione; H4N855PNZ1 / alpha-Tocopherol; PQ6CK8PD0R / Ascorbic Acid
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