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Session X : Cell death in cancer Poster X, 3 Comaprative Proteomics of Ovarian Epithelial Tumors ! Hee Jung An, Nam Hoon Cho, Park, Choi YP, Kang S, Ding O, Kim DS Dept of Pathology, Bundang CHA Medical Hosiptal Dept of Pathology, Yonsei Univresity College of Medicine Brain Korea 21 Project for Medical Science, Yonsei University!! ! We analyzed twelve ovarian epithelial tumors using 2D PAGE-based comparative proteomics to construct intra- and inter-tumoral distance map trees, and to discover surrogate biomarkers indicative of an ovarian tumor. The analysis was performed after laser microdissection of 12 fresh-frozen tissue samples, including 4 serous, 5 mucinous and 3 endometrioid tumors, with correlation with their histopathological characteristics. Ovarian epithelial tumors and normal tissues showed an apparent separation on the distance map tree. Mucinous carcinomas were closest to the normal group, whereas serous carcinomas were located furthest from the normal group. All mucinous tumors with aggressive histology were separated from the LMP group. The benign-looking cysts adjacent to the IEC showed an expression pattern identical to that of the IEC area. The extent of change on the lineages leading to the mucinous and serous carcinoma was 1.98-fold different. The overall gene expression profiles of serous or endometrioid carcinomas appeared to be less affected by grade or stage than by histologic type. The surrogate biomarkers screened in ovarian tumors and found to be significantly upregulated in comparison to normal tissues were as follows: NM23, annexin-1, protein phosphatase-1, ferritin light chain, proteasome alpha-6, and NAGK (N-acetyl glucosamine kinase). In conclusion, ovarian mucinous tumors are distinct from other ovarian epithelial tumors. LMP mucinous tumors showing histologically aggressive features belong to mucinous carcinoma on the proteomic basis. - 336 -
Session X : Cell death in cancer Poster X, 4 Endosulfan inhibits cell growth and apoptosis through activation of ERK1/2 and AKT signaling pathways S. Antherieu 1, N. Ledirac 1, P. Lenormand 2 and R. Rahmani 1 1 INRA UMR-1112, Equipe de Toxicologie Cellulaire et Moléculaire, et Génomique, Sophia-Antipolis, France, e-mail: antherieu@antibes.inra.fr 2 CNRS UMR-6543, Centre Antoine Lacassagne, Nice, France. Endosulfan is an organochlorine insecticide reported to be a potential carcinogen in humans. This insecticide was previously described to alterate MAP kinases signaling pathways and suspected to affect cell growth and differentiation in keratinocytes. In the present study, we assessed the mitogenic and apoptogenic potentials of endosulfan in HaCaT keratinocytes. We first confirmed its mutagenicity by using the AMES assay, which demonstrated that unchanged endosulfan rather than metabolites, was at the origin of mutagenic effects (negative results in the presence of S9 hepatic fractions). Moreover, we showed that endosulfan led to a persistent ERK1/2 phosphorylation with an accumulation of the phosphorylated form both in cytosol and nucleus. This sustained activation is responsible for a decreased cell proliferation, since untreated cells reached confluency after 3 days, whereas confluency is reached after 4 days in endosulfan-treated cells. These data were also confirmed by BrdU incorporation which was strongly decreased after insecticide treatment. In addition, reactive oxygen species (ROS) has been shown to be involved in endosulfaninduced ERK1/2 activation; we demonstrated that blockade of this oxidative stress by NAC (N-acetylcystein) strongly prevented inhibition of proliferation by endosulfan. These results clearly showed that endosulfan-induced ROS were involved in cell growth decrease. Finally, endosulfan apoptogenic potential was investigated and a reduction of caspases 3/7 activation and PARP cleavage was evidenced. This inhibition of apoptosis is probably correlated to endosulfan-induced AKT pathway, since a 3-fold induction of phospho-AKT was observed after 1 h of treatment. On the whole, this study demonstrates that endosulfan is a mutagenic agent, responsible of a ROS-induced proliferation decrease and apoptosis inhibition. These processes in turn prevent elimination of altered cells and therefore may contribute to carcinogenesis. - 337 -
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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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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. Mark Ginsberg Mail code 0726 92
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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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Mrs. Rasa Merzvinskyte Department o
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Mr. Gustav Nilsonne Department of L
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Mrs. Christel Péqueux Tumour and D
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Dr. Gabriella Regis Tumor Immunolog
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Pr. Moncef ZOUALI Centre Viggo Pete
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