Visit our Expo - Redox and Inflammation signaling 2012

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Session X : Cell death in cancer Poster X, 21 Human soluble TRAIL/Apo2L induces apoptosis in chemotherapy refractory nodal diffuse large B-cell lymphomas. Saskia AGM Cillessen1, Chris JLM Meijer1, Gert J Ossenkoppele2, Kitty CM Castricum1, August H Westra2, Petra Niesten1, Jettie JF Muris1, Hoite F Nijdam3, Klaas G van der Hem4, Marcel Flens5, Erik Hooijberg1, Joost J Oudejans1 Department of Clinical Pathology1 and Hematology2, VU University Medical Center, Amsterdam. Department of Otolaryngology, Westfries Gasthuis, Hoorn3, Department of Internal Medicine4 and Clinical Pathology5, Zaans Medical Center de Heel, Zaandam. The Netherlands. Email: SAGM.Cillessen@vumc.nl Part of Diffuse Large B-Cell Lymphomas (DLBCL) is resistant to chemotherapy. Human soluble (hs) TRAIL/Apo2L might be an alternative form of therapy for these lymphomas. In isolated lymphoma cells of DLBCL and B-cell lines we investigated whether hsTRAIL/Apo2L induces apoptosis in lymphomas that are resistant to chemotherapy induced cell death. Twelve out of twenty-two DLBCL samples including seven chemotherapy refractory lymphomas were sensitive for hsTRAIL/Apo2L. hsTRAIL/Apo2L induced apoptosis was preferentially observed in DLBCL samples and B-cell lines that were relatively or completely resistant to Etoposide induced apoptosis. Furthermore, hsTRAIL/Apo2L induced apoptosis in DLBCL and B-cell lines showing high expression levels of inhibitors of the caspase 9 mediated pathway Bcl-2 and/or XIAP. In hsTRAIL/Apo2L sensitive cells expression of the TRAIL receptor R1 and/or R2 and absence of R3 and R4 was observed. We conclude that hsTRAIL/Apo2L induces apoptosis in part of chemotherapy refractory nodal DLBCL and that disruption of the caspase 9 mediated pathway and expression of Bcl-2 and XIAP does not confer resistance to hsTRAIL/Apo2L induced apoptosis in DLBCL and B-cell lines. Thus, based on our results hsTRAIL/Apo2L appears to be a valuable alternative treatment for patients with chemotherapy refractory DLBCL. - 354 -
Session X : Cell death in cancer Poster X, 22 In the absence of Insulin-like Growth Factor (IGF)-1 signaling, Interferon-gamma (IFNg) inhibits the growth of human malignant T cells Laura Conti1,2, Angela Longo1, Gabriella Regis1,2, Mirella Giovarelli1,2, Roberto Chiarle1 and Francesco Novelli1,2. 1Center for Experimental Research and Medical Studies (CERMS), San Giovanni Battista Hospital-Molinette, via Santena 5, 10126 Turin, Italy, and 2Department of Medicine and Experimental Oncology, Section of Pathology, University of Turin, C.so Raffaello 30, 10125 Turin, Italy. E-mail: laura.conti@unito.it. IGF-1 is a growth factor that promotes the survival and proliferation of many tumors and cell types, and several approaches to target IGF-1 signaling have resulted in the induction of apoptosis in a broad range of tumor cells. However, we have found that human malignant T cells, which are insensitive to the antiproliferative and apoptotic effects of IFN-g, still grow in the absence of IGF-1 signaling. T cell refractoriness to the IFN-g/Signal Transducer and Activator of Transcription (STAT) 1 pathway mainly rests on internalization of the IFN-g Receptor 2 (IFN-gR2) signaling chain, which is critically induced by IGF-1. Here we show that retrovirus-mediated gene transfer of a dominant negative IGF-1 Receptor (IGF-1R DN) inhibits IFN-gR2 internalization and induces its cell surface accumulation. This results in a strong and sustained IFN-g-induced STAT1 activation and consequently in the high expression of pro-apoptotic molecules that render malignant T cells susceptible to the antiproliferative and apoptotic effects of IFN-g, both in vitro and in vivo. These data indicate that inhibition of IGF-1 signaling associated with IFN-g administration could be a useful approach to inhibit the growth of neoplastic T cells resistant to each treatment on its own. - 355 -
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- 1 - Luxembourg, January 25th to 2
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Table of content PREFACE ..........
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Preface In 1998, we organized the f
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Acknowledgments This meeting has be
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Group B (15h00 - 17h00) Session V.
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- 11 - Exhibition
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Visit our Expo (in alphabetical ord
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Thursday January 26th, 2006 (Early
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Thursday January 26th, 2006 (Evenin
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Regulation of inflammation and gluc
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Saturday January 28th, 2006 (Early
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Oral presentations (by alphabetical
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4: : Lottin S, Vercoutter-Edouart A
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the B-Raf/mitogen-activated/extrace
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Albertini MC, Accorsi A, Citterio B
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AP-1-dependent gene expression in s
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Jaks and cytokine receptors - an in
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The Role of Met-Gab1 Signalling in
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The mammalian tumor suppressor Scri
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SIGNAL TRANSDUCTION BY STRESS-ACTIV
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Title to be announced Caroline Dive
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Mechanisms of DNA methylation in ma
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Blocking the "4 Integrin-Paxillin I
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Regulation of NF-kB-dependent trans
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The immunomodulator AS101 induces g
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Signaling pathways leading to the a
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Boute, N., Jockers, R. and Issad, T
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Jespsen JS, Sorensen MD and Wengel
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8. Nishikawa, H., Kawai, K., Tanaka
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9) Proteome analysis of rat pancrea
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MicroRNA is an anti-apoptotic facto
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Resveratrol inhibits phorbol ester-
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Cross-talk between angiotensin II a
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Multiple role of histamine H 1 rece
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PI3K Targeting by the Beta-GBP Cyto
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D.P. Chopra, R.E. Menard, J. Janusz
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[2] Meijer, L., Flajolet, M. and Gr
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[4] Niemand, C., Nimmesgern, A., Ha
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Oncogenic signaling by mutant p53 M
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activity of the Peroxisome Prolifer
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Restauration of SHIP-1 activity in
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Hypoxia Signaling. Impact on Tumor
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5. Sokolov EI, Zykov KA, Pukhalsky
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HOW ANTITOXIC AND ANTICANCER AGENTS
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Listeria monocytogenes induced Rac1
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Epigenetic Regulation of Stem Cell
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Survey on in vitro cell death induc
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Distinct roles of IRF-3 and IRF-7 i
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Redox-Sensitive Transcription Facto
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Epigenic control of MHC2TA transcri
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Attenuation of MSK1-driven NF-kB ge
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Talking to chromatin: Silencers Sil
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Ubiquitin ligase Smurf1 controls os
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Workshop presentations (by alphabet
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Ambion MicroRNAs (miRNAs) are small
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Organizer: BIOBASE GmbH Date: Janua
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Reliable and efficient gene Knock-d
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Exploring ubiquitin signaling with
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Poster presentations Poster are cla
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Session I : protein domains Poster
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Session II. Receptor signaling and
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Session II : Receptor signaling and
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Session III. Protein kinase cascade
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Session III : Protein kinase cascad
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Session IV. Protein kinase inhibito
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IV. Protein kinase inhibitors: insi
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IV. Protein kinase inhibitors: insi
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V. Phosphatases as key cell signali
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VI. Proteasome degradation pathways
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VI. Proteasome degradation pathways
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Session VII. Stem cell specific cel
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VIII. Inflammation specific signali
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Session XI : Cell death and cardiov
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Session XI: Cell death and cardiova
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Session XII : Cell death and neurod
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Session XIII : Cell signaling pathw
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Session XIV : Transcriptional and t
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Session XV : Reactive oxygen specie
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Session XVI : Chemopreventive agent
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Session XVII : Cell signaling in he
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Dr. Nassera Aouali L-1526 Luxembour
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Dr. Giordano Bianchi Clinic of inte
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Mrs. Isabel Burghardt Laboratory of
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Dr. Jochen Hefl Division of Signal
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Mr. Jan Jepsen 2100 Copenhagen DNK
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Pr. Young Min Kim Division of Biolo
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Mr. Christoph Lahtz AG Tumorgenetik
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Mr. Gustav Nilsonne Department of L
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