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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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  • (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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6. Mirzoeva S, Kim ND, Chiu K, Franzen CA, Bergan RC, Pelling JC: Inhibition of HIF-1 alpha and VEGF expression by the chemopreventive bioflavonoid apigenin is accompanied by Akt inhibition in human prostate carcinoma PC3-M cells. Mol Carcinog; 2008 Sep;47(9):686-700
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  • [Title] Inhibition of HIF-1 alpha and VEGF expression by the chemopreventive bioflavonoid apigenin is accompanied by Akt inhibition in human prostate carcinoma PC3-M cells.
  • Progression of cancer leads to hypoxic solid tumors that mount specific cell signaling responses to low oxygen conditions.
  • An important objective of anti-cancer therapy is the development of new drugs that suppress hypoxic responses in solid tumors.
  • Apigenin is a natural flavone that has been shown to have chemopreventive and/or anti-cancer properties against a number of tumor types.
  • In this study, we have investigated the effects of apigenin on expression of hypoxia-inducible factor-1 (HIF-1) in human metastatic prostate PC3-M cancer cells.
  • We found that hypoxia induced a time-dependent increase in the level of HIF-1alpha subunit protein in PC3-M cells, and treatment with apigenin markedly decreased HIF-1alpha expression under both normoxic and hypoxic conditions.
  • Further, apigenin prevented the activation of the HIF-1 downstream target gene vascular endothelial growth factor (VEGF).
  • We also found that apigenin inhibited Akt and GSK-3beta phosphorylation in PC3-M cells.
  • Taken together, our results identify apigenin as a bioflavonoid that inhibits hypoxia-activated pathways linked to cancer progression in human prostate cancer, in particular the PI3K/Akt/GSK-3 pathway.
  • Further studies on the mechanism of action of apigenin will likely provide new insight into its applicability for pharmacologic targeting of HIF-1alpha for cancer therapeutic or chemopreventive purposes.
  • [MeSH-major] Apigenin / pharmacology. Flavonoids / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Prostatic Neoplasms / pathology. Vascular Endothelial Growth Factor A / genetics
  • [MeSH-minor] Cell Hypoxia. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Neoplasm Metastasis

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  • (PMID = 18240292.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA90386; United States / PHS HHS / / T32-0700085
  • [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 / Flavonoids; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 7V515PI7F6 / Apigenin
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7. Carlson CB, Mowery P, Owen RM, Dykhuizen EC, Kiessling LL: Selective tumor cell targeting using low-affinity, multivalent interactions. ACS Chem Biol; 2007 Feb 20;2(2):119-27
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  • [Title] Selective tumor cell targeting using low-affinity, multivalent interactions.
  • This report highlights the advantages of low-affinity, multivalent interactions to recognize one cell type over another.
  • Our goal was to devise a strategy to mediate selective killing of tumor cells, which are often distinguished from normal cells by their higher levels of particular cell surface receptors.
  • To test whether multivalent interactions could lead to highly specific cell targeting, we used a chemically synthesized small-molecule ligand composed of two distinct motifs:.
  • (1) an Arg-Gly-Asp (RGD) peptidomimetic that binds tightly (Kd approximately 10(-9)M) to alphavbeta3 integrins and (2) the galactosyl-alpha(1-3)galactose (alpha-Gal epitope), which is recognized by human anti-alpha-galactosyl antibodies (anti-Gal).
  • Importantly, anti-Gal binding requires a multivalent presentation of carbohydrate residues; anti-Gal antibodies interact weakly with the monovalent oligosaccharide (Kd approximately 10(-5)M) but bind tightly (Kd approximately 10(-11) M) to multivalent displays of alpha-Gal epitopes.
  • Such a display is generated when the bifunctional conjugate decorates a cell possessing a high level of alphavbeta3 integrin; the resulting cell surface, which presents many alpha-Gal epitopes, can recruit anti-Gal, thereby triggering complement-mediated lysis.
  • Only those cells with high levels of the integrin receptor are killed.
  • In contrast, doxorubicin tethered to the RGD-based ligand affords indiscriminate cell death.
  • These results highlight the advantages of exploiting the type of the multivalent recognition processes used by physiological systems to discriminate between cells.
  • Our results have implications for the treatment of cancer and other diseases characterized by the presence of deleterious cells.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Disaccharides / metabolism. Neoplasms / drug therapy. Oligopeptides / metabolism
  • [MeSH-minor] Cell Line, Tumor. Complement System Proteins / physiology. Doxorubicin / pharmacology. Drug Design. Humans. Integrin alphaVbeta3 / analysis. Integrin alphaVbeta3 / metabolism. Molecular Weight

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  • (PMID = 17291050.001).
  • [ISSN] 1554-8937
  • [Journal-full-title] ACS chemical biology
  • [ISO-abbreviation] ACS Chem. Biol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI55258; United States / NCI NIH HHS / CA / CA14520; United States / NIGMS NIH HHS / GM / GM07215
  • [Publication-type] 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 / Antineoplastic Agents; 0 / Disaccharides; 0 / Integrin alphaVbeta3; 0 / Oligopeptides; 13168-24-6 / galactosyl-(1-3)galactose; 80168379AG / Doxorubicin; 9007-36-7 / Complement System Proteins; 99896-85-2 / arginyl-glycyl-aspartic acid
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8. Tchinda VH, Tadem AD, Tako EA, Tene G, Fogako J, Nyonglema P, Sama G, Zhou A, Leke RG: Severe malaria in Cameroonian children: correlation between plasma levels of three soluble inducible adhesion molecules and TNF-alpha. Acta Trop; 2007 Apr;102(1):20-8
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  • [Title] Severe malaria in Cameroonian children: correlation between plasma levels of three soluble inducible adhesion molecules and TNF-alpha.
  • Plasma levels of three soluble inducible adhesion molecules, namely: intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1) and endothelial leucocyte adhesion molecule-1 (sELAM-1) or sE-selectin and the pro-inflammatory cytokine, tumour necrosis factor-alpha (TNF-alpha) were measured in well-defined clinical groups of children with severe and uncomplicated malaria.
  • Results showed significantly increased plasma concentrations of sICAM-1, sVCAM-1 and sE-selectin in children with severe malaria compared to those with uncomplicated malaria and healthy children (P<0.001).
  • TNF-alpha levels increased significantly in children with severe malaria, approximately 2-folds compared to those with uncomplicated malaria and about 3-folds compared to healthy children (P<0.001).
  • More importantly, levels of TNF-alpha strongly correlated with those of the three adhesion molecules and were significantly associated with increased risk of death (P=0.03).
  • In addition, children who died from severe malaria showed higher mean levels of all measured factors compared to those who recovered, with significant differences observed with sICAM-1 (P<0.001) and sE-selectin (P=0.002).
  • Taken together, these results confirm the role of TNF-alpha and the three adhesion molecules in pathogenic processes associated with severe malaria in children, and suggest an association between sICAM-1 and severe malarial anemia.
  • [MeSH-major] Cell Adhesion Molecules / blood. Malaria, Falciparum / immunology. Malaria, Falciparum / physiopathology. Plasmodium falciparum / pathogenicity. Severity of Illness Index. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Animals. Cameroon / epidemiology. Child. Child, Preschool. E-Selectin / blood. Female. Humans. Infant. Intercellular Adhesion Molecule-1 / blood. Malaria, Cerebral / epidemiology. Malaria, Cerebral / immunology. Malaria, Cerebral / parasitology. Malaria, Cerebral / physiopathology. Male. Solubility. Up-Regulation. Vascular Cell Adhesion Molecule-1 / blood

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  • (PMID = 17397790.001).
  • [ISSN] 0001-706X
  • [Journal-full-title] Acta tropica
  • [ISO-abbreviation] Acta Trop.
  • [Language] eng
  • [Grant] United States / FIC NIH HHS / TW / 5D43 TW01264
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / E-Selectin; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1
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9. Farkas A, Tonel G, Nestle FO: Interferon-alpha and viral triggers promote functional maturation of human monocyte-derived dendritic cells. Br J Dermatol; 2008 May;158(5):921-9
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  • [Title] Interferon-alpha and viral triggers promote functional maturation of human monocyte-derived dendritic cells.
  • BACKGROUND: Type I interferons (IFNs) play an important role in the pathogenesis of many autoimmune disorders including psoriasis.
  • In the presence of IFN-alpha and granulocyte/macrophage colony-stimulating factor (GM-CSF), monocytes differentiate into dendritic cells (DCs) referred to as IFN-DCs.
  • OBJECTIVES: Recently, it was shown that single-stranded RNA (ssRNA) triggers TLR7 and TLR8; therefore we studied ssRNA, as a surrogate for ssRNA viruses and their impact on IFN-DCs.
  • METHODS: We established culture conditions for IFN-DCs, generated from plastic adherent monocytes using GM-CSF plus IFN-alpha.
  • The ability of IFN-DCs to stimulate allogeneic T-cell proliferation was evaluated in a mixed leucocyte reaction.
  • RESULTS: We found that IFN-DCs express mRNA for TLR7 and TLR8 and that ssRNA stimulation significantly improves their costimulatory molecule expression, stabilizes their phenotype and enhances their capacity to stimulate naive T-cell proliferation.
  • In contrast, ssRNA stimulation led to a significant production of IL-12p70, IL-1beta, IL-6 and tumour necrosis factor alpha.
  • CONCLUSIONS: Our study sheds light on a potential role for IFN-alpha and viral infections in triggering DC populations in psoriasis.
  • These results provide additional data for the better understanding of human autoimmune and antiviral responses and may also have implications for strategies developing cancer immunotherapy.

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  • (PMID = 18371115.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / AR040065-17; United States / NIAMS NIH HHS / AR / R01 AR040065-17
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interferon-alpha; 0 / RNA, Messenger; 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS152059; NLM/ PMC2829135
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10. Trent JT, Kerdel FA: Tumor necrosis factor alpha inhibitors for the treatment of dermatologic diseases. Dermatol Nurs; 2005 Apr;17(2):97-107
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  • [Title] Tumor necrosis factor alpha inhibitors for the treatment of dermatologic diseases.
  • Tumor necrosis factor alpha (TNFalpha) is involved in cell differentiation, mitogenesis, cytotoxic responses, inflammation, immunomodulation, and wound healing.
  • Because of its numerous roles, it was thought that inhibition of TNF may aid in the treatment of certain dermatologic diseases such as psoriasis, hidradentitis suppurativa, pyoderma gangrenosum, Behcet 's syndrome, and graft versus host disease.
  • The efficacy of these agents has proven impressive and short-term side effects have been few and relatively benign.

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  • (PMID = 15916184.001).
  • [ISSN] 1060-3441
  • [Journal-full-title] Dermatology nursing
  • [ISO-abbreviation] Dermatol Nurs
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Dermatologic Agents; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; OP401G7OJC / Etanercept
  • [Number-of-references] 57
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11. Carlisle DL, Liu X, Hopkins TM, Swick MC, Dhir R, Siegfried JM: Nicotine activates cell-signaling pathways through muscle-type and neuronal nicotinic acetylcholine receptors in non-small cell lung cancer cells. Pulm Pharmacol Ther; 2007;20(6):629-41
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  • [Title] Nicotine activates cell-signaling pathways through muscle-type and neuronal nicotinic acetylcholine receptors in non-small cell lung cancer cells.
  • Nicotinic acetylcholine receptors (nAChR) are expressed on non-neuronal cell types, including normal bronchial epithelial cells, and nicotine has been reported to cause Akt activation in cultured normal airway cells.
  • This study documents mRNA and protein expression of subunits known to form a muscle-type nAChR in non-small cell lung cancer (NSCLC) cell lines.
  • In one NSCLC examined, mRNA and protein for a heteropentamer neuronal-type alpha3beta2 nAChR was detected in addition to a muscle-type receptor.
  • Protein for the alpha5 nAChR was also detected in NSCLC cells.
  • Although, mRNA for the alpha7 nAChR subunit was observed in all cell lines, alpha7 protein was not detectable by immunoblot in NSCLC cell extracts.
  • Immunohistochemistry (IHC) of NSCLC primary tissues from 18 patients demonstrated protein expression of nAChR alpha1 and beta1 subunits, but not alpha7 subunit, in lung tumors, indicating preferential expression of the muscle-type receptor.
  • In addition, the beta1 subunit showed significantly increased expression in lung tumors as compared to non-tumor bronchial tissue.
  • The alpha1 subunit also showed evidence of high expression in lung tumors.
  • Inhibition was observed at 100 nM alpha-bungarotoxin (alpha-BTX) or 10 microM hexamethonium (HEX); maximal inhibition was achieved using a combination of alpha-BTX and HEX.
  • Akt was also phosphorylated in NSCLC cells after exposure to nicotine; this effect was inhibited by the PI3K inhibitor LY294002 and antagonists to the neuronal-type nAChR, but not to the muscle-type receptor.
  • Nicotine triggered influx of calcium in the 273T NSCLC cell line, suggesting that L-type calcium channels were activated.
  • 273T cells also showed greater activation of p44/42 MAPK than of Akt in response to nicotine.
  • Cultures treated with nicotine and the EGFR tyrosine kinase inhibitor gefitinib showed a significant increase in the number of surviving cells compared to gefitinib alone.
  • These data indicate that the muscle-type nAChR, rather than the alpha7 type, is highly expressed in NSCLC and leads to downstream activation of the p44/42 MAPK pathway.
  • Neuronal-type receptors are also present and functional, as evidenced by antagonist studies, although, the expression levels are lower than muscle-type nAChR.
  • Nicotine may play a role in regulating survival of NSCLC cells and endogenous acetylcholine released locally in the lung and/or chronic nicotine exposure might play a role in NSCLC development.
  • [MeSH-major] Ganglionic Stimulants / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Nicotine / pharmacology. Nicotinic Agonists / pharmacology. Protein Subunits / genetics. Receptors, Nicotinic / genetics
  • [MeSH-minor] Acetylcholine / metabolism. Calcium Channels, L-Type / drug effects. Calcium Channels, L-Type / metabolism. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Phosphorylation. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Signal Transduction / drug effects. alpha7 Nicotinic Acetylcholine Receptor

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  • (PMID = 17015027.001).
  • [ISSN] 1094-5539
  • [Journal-full-title] Pulmonary pharmacology & therapeutics
  • [ISO-abbreviation] Pulm Pharmacol Ther
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA090440
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CHRNA1 protein, human; 0 / CHRNB1 protein, human; 0 / Calcium Channels, L-Type; 0 / Chrna7 protein, human; 0 / Ganglionic Stimulants; 0 / Nicotinic Agonists; 0 / Protein Subunits; 0 / RNA, Messenger; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 6M3C89ZY6R / Nicotine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; N9YNS0M02X / Acetylcholine
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12. Yamazaki M, Fukushima H, Shin M, Katagiri T, Doi T, Takahashi T, Jimi E: Tumor necrosis factor alpha represses bone morphogenetic protein (BMP) signaling by interfering with the DNA binding of Smads through the activation of NF-kappaB. J Biol Chem; 2009 Dec 18;284(51):35987-95
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  • [Title] Tumor necrosis factor alpha represses bone morphogenetic protein (BMP) signaling by interfering with the DNA binding of Smads through the activation of NF-kappaB.
  • Bone morphogenetic proteins (BMPs) induce not only bone formation in vivo but also osteoblast differentiation of mesenchymal cells in vitro.
  • Tumor necrosis factor alpha (TNFalpha) inhibits both osteoblast differentiation and bone formation induced by BMPs.
  • In this study, we found that TNFalpha inhibited the alkaline phosphatase activity and markedly reduced BMP2- and Smad-induced reporter activity in MC3T3-E1 cells.
  • These results suggest that TNFalpha inhibits BMP signaling by interfering with the DNA binding of Smads through the activation of NF-kappaB.
  • [MeSH-major] Bone Morphogenetic Protein 2 / metabolism. Cell Nucleus / metabolism. Signal Transduction / physiology. Smad Proteins / metabolism. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Animals. Cell Line. Mice. Mice, Knockout. Nitriles / pharmacology. Sulfones / pharmacology

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  • (PMID = 19854828.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-(4-methylphenylsulfonyl)-2-propenenitrile; 0 / Bmp2 protein, mouse; 0 / Bone Morphogenetic Protein 2; 0 / Nitriles; 0 / Rela protein, mouse; 0 / Smad Proteins; 0 / Sulfones; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2791026
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13. Bartolomé RA, Wright N, Molina-Ortiz I, Sánchez-Luque FJ, Teixidó J: Activated G(alpha)13 impairs cell invasiveness through p190RhoGAP-mediated inhibition of RhoA activity. Cancer Res; 2008 Oct 15;68(20):8221-30
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  • [Title] Activated G(alpha)13 impairs cell invasiveness through p190RhoGAP-mediated inhibition of RhoA activity.
  • The GTPase RhoA is a downstream target of heterotrimeric G(13) proteins and plays key roles in cell migration and invasion.
  • Here, we show that expression in human melanoma cells of a constitutively active, GTPase-deficient Galpha(13) form (G(alpha)(13)QL) or lysophosphatidylcholine (LPC)-promoted signaling through G(alpha)(13)-coupled receptors led to a blockade of chemokine-stimulated RhoA activation and cell invasion that was rescued by active RhoA.
  • Melanoma cells expressing G(alpha)(13)QL or cells stimulated with LPC displayed an increase in p190RhoGAP activation, and defects in RhoA activation and invasion were recovered by knocking down p190RhoGAP expression, thus identifying this GTPase-activating protein (GAP) protein as a downstream G(alpha)(13) target that is responsible for these inhibitory responses.
  • In addition, defective stress fiber assembly and reduced migration speed underlay inefficient invasion of G(alpha)(13)QL melanoma cells.
  • Importantly, G(alpha)(13)QL expression in melanoma cells led to impairment in lung metastasis associated with prolonged survival in SCID mice.
  • The data indicate that G(alpha)(13)-dependent downstream effects on RhoA activation and invasion tightly depend on cell type-specific GAP activities and that G(alpha)(13)-p190RhoGAP signaling might represent a potential target for intervention in melanoma metastasis.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, G12-G13 / physiology. Guanine Nucleotide Exchange Factors / physiology. Melanoma / pathology. Repressor Proteins / physiology. rhoA GTP-Binding Protein / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Chemokine CXCL12 / pharmacology. GTP-Binding Protein alpha Subunits, Gi-Go / physiology. Humans. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Lysophosphatidylcholines / pharmacology. Mice. Mice, SCID. Neoplasm Invasiveness. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction. Swiss 3T3 Cells. Thromboxane A2 / physiology

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  • (PMID = 18922893.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARHGAP35 protein, human; 0 / Chemokine CXCL12; 0 / Guanine Nucleotide Exchange Factors; 0 / Lysophosphatidylcholines; 0 / Proto-Oncogene Proteins c-vav; 0 / Repressor Proteins; 0 / VAV2 protein, human; 57576-52-0 / Thromboxane A2; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, G12-G13; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.2 / rhoA GTP-Binding Protein
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14. Kota RS, Ramana CV, Tenorio FA, Enelow RI, Rutledge JC: Differential effects of lipoprotein lipase on tumor necrosis factor-alpha and interferon-gamma-mediated gene expression in human endothelial cells. J Biol Chem; 2005 Sep 2;280(35):31076-84
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  • [Title] Differential effects of lipoprotein lipase on tumor necrosis factor-alpha and interferon-gamma-mediated gene expression in human endothelial cells.
  • In vascular diseases, such as atherosclerosis, inflammation plays an important role in the pathogenesis of the disease.
  • We examined the role of LPL in modulating tumor necrosis factor-alpha (TNF-alpha)- and interferon-gamma (IFN-gamma)-mediated inflammatory cytokine signal transduction pathways in human aortic endothelial cells (HAECs).
  • LPL significantly suppressed TNF-alpha-induced gene expression, and this suppression was reversed by tetrahydrolipstatin and heparinase.
  • The anti-inflammatory response of LPL in suppressing TNF-alpha-induced gene expression was a result of its inhibition of NF-kappaB activity by the abrogation of IkappaB-alpha degradation and phosphorylation of the p65 subunit.
  • [MeSH-major] Endothelial Cells / physiology. Gene Expression Regulation. Interferon-gamma / metabolism. Lipoprotein Lipase / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Aorta / cytology. Cholesterol, VLDL / metabolism. Culture Media, Serum-Free. Cytokines / metabolism. DNA-Binding Proteins / metabolism. E-Selectin / metabolism. Enzyme Inhibitors / metabolism. Heparin Lyase / metabolism. Humans. Intercellular Adhesion Molecule-1 / genetics. Intercellular Adhesion Molecule-1 / metabolism. Lactones / metabolism. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / metabolism. STAT1 Transcription Factor. Signal Transduction / physiology. Trans-Activators / metabolism. Vascular Cell Adhesion Molecule-1 / metabolism

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  • (PMID = 15994321.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL55667; United States / NHLBI NIH HHS / HL / HL58660; United States / NHLBI NIH HHS / HL / HL70816; United States / NHLBI NIH HHS / HL / HL78615
  • [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 / Cholesterol, VLDL; 0 / Culture Media, Serum-Free; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / E-Selectin; 0 / Enzyme Inhibitors; 0 / Lactones; 0 / NF-kappa B; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / Trans-Activators; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 82115-62-6 / Interferon-gamma; 95M8R751W8 / orlistat; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.1.34 / Lipoprotein Lipase; EC 4.2.2.7 / Heparin Lyase
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15. Haugaard SB, Andersen O, Pedersen SB, Dela F, Deacon CF, Holst JJ, Iversen J, Madsbad S: Glucose-stimulated prehepatic insulin secretion is associated with circulating alanine, triglyceride, glucagon, lactate and TNF-alpha in patients with HIV-lipodystrophy. HIV Med; 2006 Apr;7(3):163-72
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  • [Title] Glucose-stimulated prehepatic insulin secretion is associated with circulating alanine, triglyceride, glucagon, lactate and TNF-alpha in patients with HIV-lipodystrophy.
  • The prehepatic insulin secretion rate was estimated by deconvolution of C-peptide concentrations, and insulin sensitivity (SIRd) was estimated by the glucose clamp technique.
  • The disposition index (Di=ISREG0-10 min x SIRd) was calculated to estimate the beta-cell response relative to insulin sensitivity.
  • RESULTS: FISR was increased by 69% (P<0.001), whereas median Di was decreased by 75% (P<0.01), primarily as a result of a reduction of SI(Rd) by 60% (P<0.001) in LIPO patients compared with controls.
  • Four LIPO patients displayed high FISR [+3 standard deviations (SD), P<0.001], high ISREG0-10 min (+3 SD, P<0.001) and low SIRd (P<0.01), suggesting an intact B-cell capacity to compensate insulin resistance; six LIPO patients exhibited high FISR (+3SD, P<0.001), low ISREG0-10min (-1 SD, P=0.01), and low SIRd (P<0.01), suggesting depletion of readily releasable insulin stores; the remaining eight LIPO patients and controls displayed identical FISR and ISREG0-10 min.
  • Increased concentrations of the nonglucose insulin secretagogues triglyceride (+124%), alanine (+35%) and glucagon (+88%), and also lactate (+96%) and tumour necrosis factor (TNF)-alpha (+62%) were observed in the 10 LIPO patients with aberrations in FISR and ISREG0-10 min compared with the remaining HIV-infected patients (all P<0.05).
  • CONCLUSION: Plasma triglyceride, alanine, glucagon, lactate and TNF-alpha may be associated with alterations in the first-phase prehepatic insulin secretion response to intravenous glucose in normoglycaemic lipodystrophic HIV-infected patients.
  • [MeSH-major] Glucose. HIV-1. HIV-Associated Lipodystrophy Syndrome / metabolism. Insulin / secretion. Insulin Resistance
  • [MeSH-minor] Adult. Alanine / blood. C-Peptide / analysis. Case-Control Studies. Glucagon / blood. Glucose Clamp Technique. Humans. Infusions, Intravenous. Insulin-Secreting Cells / secretion. Lactates / blood. Male. Middle Aged. Stimulation, Chemical. Triglycerides / blood. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16494630.001).
  • [ISSN] 1464-2662
  • [Journal-full-title] HIV medicine
  • [ISO-abbreviation] HIV Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / C-Peptide; 0 / Insulin; 0 / Lactates; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 9007-92-5 / Glucagon; IY9XDZ35W2 / Glucose; OF5P57N2ZX / Alanine
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16. Volante M, Saviozzi S, Rapa I, Ceppi P, Cappia S, Calogero R, Novello S, Borasio P, Papotti M, Scagliotti GV: Epidermal growth factor ligand/receptor loop and downstream signaling activation pattern in completely resected nonsmall cell lung cancer. Cancer; 2007 Sep 15;110(6):1321-8
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  • [Title] Epidermal growth factor ligand/receptor loop and downstream signaling activation pattern in completely resected nonsmall cell lung cancer.
  • BACKGROUND: In recent years, molecular insights shed light on the role of the epidermal growth factor receptor (EGFR) in nonsmall cell lung cancer (NSCLC), and new therapeutic agents, such as the EGFR tyrosine kinase inhibitors, were tested successfully, with responsiveness to those agents more likely in those patients with specific EGFR gene alterations.
  • The objective of the current study was to investigate the protein profiles of EGFR, c-erb-B2, transforming growth factor alpha (TGF-alpha) (one of the EGFR ligands commonly expressed in NSCLC), and some downstream molecules, potentially to detect a subset of tumors with an activated autocrine loop that is responsible for higher intracellular signaling.
  • METHODS: One hundred twelve consecutive patients with resected NSCLC were analyzed by immunohistochemistry for EGFR, the c-erb-B2 receptor, TGF-alpha, and pivotal molecules downstream from EGFR activation.
  • RESULTS: EGFR, c-erb-B2, TGF-alpha and downstream molecule expression, per se, was not correlated significantly with any clinicopathologic variables, with the exception of a significant correlation between squamous histology and EGFR and between adenocarcinoma and TGF-alpha.
  • However, nearly 30% of NSCLCs demonstrated coexpression of both TGF-alpha and EGFR, and this molecular status was associated positively with a statistically significant expression of phosphatidylinositol 3 kinase and an inversely with mitogen-activated protein kinase expression.
  • CONCLUSIONS: The presence of a subgroup of NSCLCs with an activated autocrine loop may help to explain the mechanisms that lead to the relative ineffectiveness of the EGFR tyrosine kinase inhibitor and may support new clinical trials to define whether the subgroup of patients with these tumors reasonably may benefit from higher doses of such inhibitors or from the simultaneous inhibition of EGFR downstream signaling targets.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / surgery. Lung Neoplasms / metabolism. Lung Neoplasms / surgery. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Aged. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Italy. Male. Middle Aged. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Receptor, ErbB-2 / metabolism. Retrospective Studies. Signal Transduction. Transforming Growth Factor alpha / metabolism

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  • [Copyright] (c) 2007 American Cancer Society.
  • (PMID = 17647268.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor alpha; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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17. Li M, Li H, Li C, Zhou S, Guo L, Liu H, Jiang W, Liu X, Li P, McNutt MA, Li G: Alpha fetoprotein is a novel protein-binding partner for caspase-3 and blocks the apoptotic signaling pathway in human hepatoma cells. Int J Cancer; 2009 Jun 15;124(12):2845-54
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  • [Title] Alpha fetoprotein is a novel protein-binding partner for caspase-3 and blocks the apoptotic signaling pathway in human hepatoma cells.
  • Although there is increasing evidence that alpha fetoprotein (AFP) may function as regulatory factor in the growth of tumor cells, the precise mechanism is still unclear.
  • Our results showed that low doses of TNF-related apoptosis-inducing ligand (TRAIL) elevated the activity of caspase-8, but not caspase-3.
  • Caspase-3 colocalized and interacted with AFP in the cytoplasm of Bel 7402 cells, and translocated into nuclei in association with the occurrence of apoptosis while cells were under cotreatment with all-trans retinoic acid (ATRA) or TRAIL.
  • Knockdown of AFP increased the sensitivity of Bel 7402 cells to TRAIL, and thereby, triggered caspase-3 signaling.
  • The effect of AFP on caspase-3 was further confirmed by transfection of the AFP gene into HLE cells (AFP negative).
  • Therefore, it is possible that the combination of AFP gene silencing together with ATRA/TRAIL cotreatment will benefit the enhancement of the chemotherapeutic efficiency of these agents on tumors.
  • [MeSH-major] Apoptosis / physiology. Carcinoma, Hepatocellular / metabolism. Caspase 3 / metabolism. Liver Neoplasms / metabolism. Signal Transduction. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Blotting, Western. Caspase 8 / metabolism. Cell Proliferation / drug effects. Electrophoresis, Polyacrylamide Gel. Flow Cytometry. Fluorescence Resonance Energy Transfer. Humans. Immunoprecipitation. Protein Transport. RNA, Small Interfering / pharmacology. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • [Copyright] Copyright 2008 UICC.
  • (PMID = 19267404.001).
  • [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 / Antineoplastic Agents; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / alpha-Fetoproteins; 5688UTC01R / Tretinoin; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8
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18. Lin CC, Hwang JM, Tsai MT, Su WW, Chen LM, Lai TY, Hsu HH, Yen SK, Huang CY, Liu JY: Protein kinase C alpha location and the expression of phospho-MEK and MDR1 in hepatitis virus-related hepatocellular carcinoma biopsies. Chin J Physiol; 2010 Apr 30;53(2):112-8
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  • [Title] Protein kinase C alpha location and the expression of phospho-MEK and MDR1 in hepatitis virus-related hepatocellular carcinoma biopsies.
  • The purpose of this study was to elucidate the function of protein kinase C (PKC) alpha in human hepatocellular carcinoma (HCC).
  • Expression of PKCalpha, phospho-MEK and MDR1 was significantly increased in the region of HCC location compared with the non-tumor location.
  • The HCC tissues were classified as cytosolic type, where PKCalpha was deposited in the cytoplasm in > 50% of cells, or membranous type for others.
  • The results showed that the higher expression levels of phospho-MEK and MDR1 in HCC location were significantly associated with those patients whose cells were of the membranous type.
  • The results indicate that elevated expression of MDR1 in HCC patients with non-HCV infection may be mediated through PKC signaling pathway.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Hepatitis B / complications. Hepatitis C / complications. Liver Neoplasms / metabolism. Mitogen-Activated Protein Kinase Kinases / metabolism. P-Glycoprotein / metabolism. Protein Kinase C-alpha / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Cell Membrane / metabolism. Cytoplasm / metabolism. Female. Humans. Male. Middle Aged. Retrospective Studies. Signal Transduction / physiology

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  • (PMID = 21793318.001).
  • [ISSN] 0304-4920
  • [Journal-full-title] The Chinese journal of physiology
  • [ISO-abbreviation] Chin J Physiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / P-Glycoprotein; EC 2.7.11.13 / Protein Kinase C-alpha; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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19. Pozharisskiĭ KM, Leenman EE, Arzumanov AA: [Achievements in morphological diagnosis of prostatic cancer: alpha-methylacyl-coenzyme-A-racemase--a new marker of malignant cell transformation]. Arkh Patol; 2005 Sep-Oct;67(5):15-9
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  • [Title] [Achievements in morphological diagnosis of prostatic cancer: alpha-methylacyl-coenzyme-A-racemase--a new marker of malignant cell transformation].
  • Gene P504S is considered as the most specific for prostatic carcinoma and its protein (alpha-methylacyl coenzyme A racemaze (AMACR/P504S) is higly sensitive and specific marker not only for adenocarcinoma cells but also for preceding changes - prostatic intraepithelial neoplasm (PIN).
  • AMACR/P504S seems to be the first marker of malignant transformation and tumor progression.
  • Use of immunohistochemical method for revealing this marker together with methods of basal prostatic cells observation (cytokeratin of a high molecular weight, cytokeratin 5/6, p63) improves morphological diagnosis of prostatic carcinoma, particularly on the material of needle biopsies.
  • This combination allows one to identify neoplastic nature of some difficult lesions.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic. Prostatic Intraepithelial Neoplasia / diagnosis. Prostatic Neoplasms / diagnosis. Racemases and Epimerases / analysis

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  • (PMID = 16323473.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] Editorial; English Abstract
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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20. Crane-Godreau MA, Wira CR: Effects of estradiol on lipopolysaccharide and Pam3Cys stimulation of CCL20/macrophage inflammatory protein 3 alpha and tumor necrosis factor alpha production by uterine epithelial cells in culture. Infect Immun; 2005 Jul;73(7):4231-7
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  • [Title] Effects of estradiol on lipopolysaccharide and Pam3Cys stimulation of CCL20/macrophage inflammatory protein 3 alpha and tumor necrosis factor alpha production by uterine epithelial cells in culture.
  • We have previously demonstrated that rat uterine epithelial cells (UEC) produce CCL20/macrophage inflammatory protein 3 alpha (MIP3alpha) and tumor necrosis factor alpha (TNF-alpha) in response to live and heat-killed Escherichia coli and to the pathogen-associated molecular patterns (PAMP) lipopolysaccharide (LPS) and Pam3Cys.
  • To determine whether estradiol (E2) modulates PAMP-induced CCL20/MIP3alpha and TNF-alpha secretion, primary cultures of rat UEC were incubated with E2 for 24 h and then treated with LPS or Pam3Cys or not treated for an additional 12 h.
  • E2 inhibited the constitutive secretion of TNF-alpha and CCL20/MIP3alpha into culture media.
  • In contrast, and at the same time, E2 lowered the TNF-alpha response to both PAMP.
  • To determine whether estrogen receptors (ER) mediated the effects of E2, epithelial cells were incubated with E2 and/or ICI 182,780, a known ER antagonist.
  • ICI 182,780 had no effect on E2 inhibition of constitutive TNF-alpha and CCL20/MIP3alpha secretion.
  • In contrast, ICI 182,780 reversed the stimulatory effect of E2 on LPS- and/or Pam3Cys-induced CCL20/MIP3alpha secretion as well as partially reversed the inhibitory effect of E2 on TNF-alpha production by epithelial cells.
  • Overall, these results indicate that E2 regulates the production of TNF-alpha and CCL20/MIP3alpha by UEC in the absence as well as presence of PAMP.
  • Since CCL20/MIP3alpha has antimicrobial activity and is chemotactic for immune cells, these studies suggest that regulation of CCL20/MIP3alpha and TNF-alpha by E2 and PAMP may have profound effects on innate and adaptive immune responses to microbial challenge in the female reproductive tract.

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  • (PMID = 15972514.001).
  • [ISSN] 0019-9567
  • [Journal-full-title] Infection and immunity
  • [ISO-abbreviation] Infect. Immun.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI-13541; United States / NIAID NIH HHS / AI / R01 AI013541; United States / NIAID NIH HHS / AI / R37 AI013541; United States / NIAID NIH HHS / AI / P01 AI051877; United States / NIAID NIH HHS / AI / AI-51877
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccl20 protein, rat; 0 / Chemokine CCL20; 0 / Chemokines, CC; 0 / Lipopolysaccharides; 0 / Lipoproteins; 0 / Macrophage Inflammatory Proteins; 0 / Tumor Necrosis Factor-alpha; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; 87420-41-5 / 2,3-bis(palmitoyloxy)-2-propyl-1-palmitoylcysteine; K848JZ4886 / Cysteine
  • [Other-IDs] NLM/ PMC1168574
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21. Kanda H, Ishii K, Ogura Y, Imamura T, Kanai M, Arima K, Sugimura Y: Naftopidil, a selective alpha-1 adrenoceptor antagonist, inhibits growth of human prostate cancer cells by G1 cell cycle arrest. Int J Cancer; 2008 Jan 15;122(2):444-51
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  • [Title] Naftopidil, a selective alpha-1 adrenoceptor antagonist, inhibits growth of human prostate cancer cells by G1 cell cycle arrest.
  • Alpha-1 adrenoceptor antagonists are generally prescribed for benign prostate hyperplasia with lower urinary tract symptoms.
  • Naftopidil, a selective alpha-1 adrenoceptor antagonist, is frequently used in Japan because it has fewer side effects.
  • Here we demonstrate for the first time that naftopidil has growth inhibitory effect in androgen-sensitive and -insensitive human prostate cancer cell lines.
  • The concentrations causing 50% inhibition (IC50) of cancer cell growth were 22.2 +/- 4.0 microM in androgen-sensitive LNCaP cells and 33.2 +/- 1.1 microM in androgen-insensitive PC-3 cells.
  • FACS analysis revealed that cell growth inhibition by naftopidil was due to the arrest of the G1 cell cycle.
  • Expressions of p27(kip1) and p21(cip1) were significantly increased in LNCaP cells treated with naftopidil.
  • In PC-3 cells, naftopidil induced p21(cip1) but not p27(kip1).
  • In vivo, oral administration of naftopidil to nude mice inhibited the growth of PC-3 tumors as compared to vehicle-treated controls.
  • These results suggest that naftopidil may be useful in the chemoprevention of prostate cancer and the intervention of hormone refractory prostate cancer.
  • [MeSH-major] Adrenergic alpha-1 Receptor Antagonists. G1 Phase / drug effects. Naphthalenes / pharmacology. Piperazines / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Adrenergic alpha-Antagonists / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation. Cell Separation. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Flow Cytometry. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Male. Mice. Mice, Nude. Neoplasm Transplantation. Receptors, Adrenergic, alpha-1 / metabolism

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  • [Copyright] Copyright 2007 Wiley-Liss, Inc.
  • (PMID = 17918159.001).
  • [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 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Intracellular Signaling Peptides and Proteins; 0 / Naphthalenes; 0 / Piperazines; 0 / Receptors, Adrenergic, alpha-1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; R9PHW59SFN / naftopidil
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22. Meilleur MA, Akpovi CD, Pelletier RM, Vitale ML: Tumor necrosis factor-alpha-induced anterior pituitary folliculostellate TtT/GF cell uncoupling is mediated by connexin 43 dephosphorylation. Endocrinology; 2007 Dec;148(12):5913-24
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  • [Title] Tumor necrosis factor-alpha-induced anterior pituitary folliculostellate TtT/GF cell uncoupling is mediated by connexin 43 dephosphorylation.
  • The anterior pituitary folliculostellate (FS) cells are key elements of the paracrine control of the pituitary function.
  • These cells are the source and the target of growth factors and cytokines, and are connected to other pituitary cells via Cx43-mediated gap junctions.
  • Here, we show that acute treatment of the FS TtT/GF cell line with TNF-alpha caused a transient cell uncoupling that was accompanied by the dephosphorylation of Cx43 in Ser368.
  • These TNF-alpha-evoked effects were dependent on protein phosphatase 2A (PP2A) and protein kinase C (PKC) activities.
  • TNF-alpha did not affect total cell Cx43-PP2A catalytic subunit interaction, but it did induce PP2A catalytic subunit recruitment to the Triton X-100 insoluble subcellular fraction, in which Cx43-gap junction plaques are recovered.
  • Cx43 did not interact with the conventional PKC-alpha, but it did interact with the atypical PKC-zeta.
  • Moreover, this interaction was weakened by TNF-alpha.
  • The temporary closure of gap junctions during acute TNF-alpha challenge may constitute a protective mechanism to limit or confine the spread of inflammatory signals among the FS cells.
  • [MeSH-major] Connexin 43 / metabolism. Pituitary Gland, Anterior / drug effects. Signal Transduction / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Blotting, Western. Cell Communication / drug effects. Cell Line. Gap Junctions / drug effects. Gap Junctions / metabolism. Isoenzymes / metabolism. Mice. Microscopy, Fluorescence. Phosphoprotein Phosphatases / metabolism. Phosphorylation / drug effects. Protein Binding. Protein Kinase C / metabolism. Protein-Serine-Threonine Kinases / metabolism. Time Factors. Tyrosine / metabolism

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  • (PMID = 17872368.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Connexin 43; 0 / Isoenzymes; 0 / Tumor Necrosis Factor-alpha; 42HK56048U / Tyrosine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.13 / Protein Kinase C; EC 3.1.3.16 / Phosphoprotein Phosphatases
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23. Fiorentino S, Chopin M, Dastot H, Boissel N, Reboul M, Legrès L, Janin A, Aplan P, Sigaux F, Regnault A: Disruption of T cell regulatory pathways is necessary for immunotherapeutic cure of T cell acute lymphoblastic leukemia in mice. Eur Cytokine Netw; 2005 Dec;16(4):300-8
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  • [Title] Disruption of T cell regulatory pathways is necessary for immunotherapeutic cure of T cell acute lymphoblastic leukemia in mice.
  • In recent years, the outcome has been globally improved by current therapies, but it remains poor in patients with high, persistent residual disease following the first course of chemotherapy, prompting evaluation of the possible beneficial effects of immunotherapy protocols.
  • In this study, we hypothesized that the disruption of two immunoregulatory pathways controlling the auto-reactive T cell response might synergize with dendritic cell-based immunotherapy of the disease, which is considered to be poorly immunogenic.
  • In this study, we used TAL1xLMO1 leukemia cells adoptively transferred in mice, to generate murine leukemia with poorly immunogenic cells as a model for human T-ALL.
  • We compared the efficiency of a classical, dendritic cell-based immunotherapy (injection of dendritic cells loaded with tumor-derived antigenic products), to a combined treatment associating injection of antigen-loaded dendritic cells and disruption of the two immunoregulatory pathways: CD25+ suppressive T cells and cytotoxic T lymphocyte-associated antigens (CTLA-4).
  • We show that this combined treatment resulted in cure, concomitantly with in vivo generation of immune memory, and TNF-alpha secretion.
  • This study demonstrates that the disruption of these two immunoregulatory pathways synergized with immunostimulation by dendritic cells loaded with tumor-derived antigens, and paves the way for the testing of this combination in clinical trials.
  • [MeSH-major] Immunotherapy, Adoptive. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Signal Transduction / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Antigens, CD / metabolism. Antigens, Neoplasm / administration & dosage. CTLA-4 Antigen. Cell Line, Tumor. Dendritic Cells / immunology. Dendritic Cells / metabolism. Dendritic Cells / transplantation. Disease Models, Animal. Immunologic Memory. Interleukin-2 Receptor alpha Subunit / biosynthesis. Lymphocyte Depletion. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. T-Lymphocytes, Regulatory / immunology. T-Lymphocytes, Regulatory / metabolism. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 16464745.001).
  • [ISSN] 1148-5493
  • [Journal-full-title] European cytokine network
  • [ISO-abbreviation] Eur. Cytokine Netw.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Ctla4 protein, mouse; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Tumor Necrosis Factor-alpha
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24. Singh RR, Barnes CJ, Talukder AH, Fuqua SA, Kumar R: Negative regulation of estrogen receptor alpha transactivation functions by LIM domain only 4 protein. Cancer Res; 2005 Nov 15;65(22):10594-601
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  • [Title] Negative regulation of estrogen receptor alpha transactivation functions by LIM domain only 4 protein.
  • LIM domain only 4 (LMO4), a member of the LIM-only family of transcriptional coregulatory proteins, consists of two LIM protein-protein interaction domains that enable it to function as a linker protein in multiprotein complexes.
  • Here, we have identified estrogen receptor alpha (ERalpha) and its corepressor, metastasis tumor antigen 1 (MTA1), as two novel binding partners of LMO4.
  • Interestingly, LMO4 exhibited binding with both ERalpha and MTA1 and existed as a complex with ERalpha, MTA1, and histone deacetylases (HDAC), implying that LMO4 was a component of the MTA1 corepressor complex.
  • These findings suggested that LMO4 was an integral part of the molecular machinery involved in the negative regulation of ERalpha transactivation function in breast cells.
  • Because LMO4 is up-regulated in human breast cancers, repression of ERalpha transactivation functions by LMO4 might contribute to the process of breast cancer progression by allowing the development of ERalpha-negative phenotypes, leading to increased aggressiveness of breast cancer cells.
  • [MeSH-major] Estrogen Receptor alpha / physiology. Homeodomain Proteins / metabolism. Transcription Factors / metabolism. Transcriptional Activation / physiology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Cell Line, Tumor. Chromatin / genetics. Chromatin / metabolism. Estrogen Receptor beta / metabolism. Gene Expression Regulation, Neoplastic / physiology. Histone Deacetylases / metabolism. Humans. LIM Domain Proteins. Repressor Proteins / metabolism

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  • (PMID = 16288053.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA098823; United States / NCI NIH HHS / CA / CA90970
  • [Publication-type] 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 / Adaptor Proteins, Signal Transducing; 0 / Chromatin; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / LMO4 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors; EC 3.5.1.- / Mta1 protein, human; EC 3.5.1.98 / Histone Deacetylases
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25. Shan L, Aster JC, Sklar J, Sunday ME: Notch-1 regulates pulmonary neuroendocrine cell differentiation in cell lines and in transgenic mice. Am J Physiol Lung Cell Mol Physiol; 2007 Feb;292(2):L500-9
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  • [Title] Notch-1 regulates pulmonary neuroendocrine cell differentiation in cell lines and in transgenic mice.
  • The notch gene family encodes transmembrane receptors that regulate cell differentiation by interacting with surface ligands on adjacent cells.
  • Previously, we demonstrated that tumor necrosis factor-alpha (TNF) induces neuroendocrine (NE) cell differentiation in H82, but not H526, undifferentiated small cell lung carcinoma lines.
  • We now test the hypothesis that TNF mediates NE cell differentiation in part by altering Notch gene expression.
  • First, using RT-PCR, we determined that TNF treatment of H82, but not H526, transiently decreases notch-1 mRNA in parallel with induction of gene expression for the NE-specific marker DOPA decarboxylase (DDC).
  • After 7 days of Notch-1 antisense treatment, neural cell adhesion molecule (NCAM) immunoreactivity is induced in H82 but not H526.
  • Third, we generated transgenic mice bearing notch-1 driven by the neural/NE-specific calcitonin promoter, which express activated Notch-1 in developing lung epithelium.
  • Newborn NotchCal mouse lungs have high levels of hes1 mRNA, reflecting increased activated Notch, compared with wild-type.
  • NotchCal lungs have decreased CGRP-positive NE cells, decreased protein gene product 9.5 (PGP9.5)-positive NE cells, and decreased gastrin-releasing peptide (GRP), CGRP, and DDC mRNA levels compared with normal littermates.
  • Cumulatively, these observations provide further support for a role for Notch-1 signaling in regulating pulmonary NE cell differentiation.
  • [MeSH-major] Cell Differentiation. Lung / cytology. Neurosecretory Systems / cytology. Receptor, Notch1 / metabolism
  • [MeSH-minor] Animals. Animals, Newborn. Calcitonin / genetics. Carcinoma, Small Cell / genetics. Carcinoma, Small Cell / pathology. Cell Line, Tumor. Dopa Decarboxylase / genetics. Gastrin-Releasing Peptide / genetics. Gastrin-Releasing Peptide / metabolism. Gene Expression / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Mice. Mice, Transgenic. Neural Cell Adhesion Molecules / metabolism. Oligonucleotides, Antisense / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Signal Transduction / drug effects. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 17028268.001).
  • [ISSN] 1040-0605
  • [Journal-full-title] American journal of physiology. Lung cellular and molecular physiology
  • [ISO-abbreviation] Am. J. Physiol. Lung Cell Mol. Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01-HL-44984
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Tumor Necrosis Factor-alpha; 80043-53-4 / Gastrin-Releasing Peptide; 9007-12-9 / Calcitonin; EC 4.1.1.- / Dopa Decarboxylase
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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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  • (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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  • (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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  • (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.
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  • (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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  • (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.
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  • (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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  • (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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  • (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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  • (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.
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  • (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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  • (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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  • (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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  • (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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • (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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  • (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
  •  go-up   go-down


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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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