Visit our Expo - Redox and Inflammation signaling 2012

More documents

Recommendations

Info

Session XII : Cell death and neurodegenerative diseases Poster XII, 22 Cas III-ia Induces Autophagy and Apoptotic Death in Glioma C6 Cells In Vitro and In Vivo. Cristina Trejo-Solís1, Guadalupe Palencia1, Lucrecia Márquez-Rosado2, Dolores Jiménez-Farfán3, Aurora Sánchez1, Arturo Cruz-Salgado1, Isabel Gracia-Mora4, Lena Ruiz-Ramírez4 and Julio Sotelo1. 1Departamento de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía “MVS”, México, DF. 2Departamento de Biología Celular, Centro de investigación y Estudios Avanzados del IPN, México, DF. 3 Departamento de Neuroinmunología, Instituto de Odontología, UNAM, México, DF. 4Departamento de Química y Medicina Nuclear, UNAM, México, DF. In this reaserch, we investigated the effects of casiopeina III-ia (Cas III-ia)- a new copper compound that exhibits antineoplastic activity- on glioma C6 cells under both in vitro and in vivo conditions, in an attempt to identify potential therapeutic agents against maliganant glioma. The exposure of C6 to Cas III-ia significantly inhibited cell proliferation, increased reactive oxygen species (ROS) formation, and induced cell death. In cultured C6 cells, Cas III-ia caused the accumulation of autophagic vacuoles, formation of LC3-II, and nuclear translocation of AIF and Endonuclease G in all tested concentrations. At higher concentration were observed, loss of mitochondrial transmembrane potential, over-expression of Beclin 1, LAMP3, Bax and Bid, phosphorylation of JNK and ERK, and nuclear translocation of AP-1. Administration of N-acetyl-L—cystein (an antioxidant) resulted in significative inhibition of anti-neoplastic effect of Cas III-ia on C6 glioma cells. These results suggest that Cas III-ia induced death cell by autophagy and caspase independient apoptosis. In addition, treatment of glioma C6- positive rats with Cas III-ia reduced tumor volumen as well as mitotic and cell proliferation indexes, while it increased the apoptotic index. Our findings support the use of cas III-ia for the treatment of malignant gliomas. This work was supported by CONACYT grant U41997-MA1. - 480 -
Session XII : Cell death and neurodegenerative diseases Poster XII, 23 Targeting the IGF-IR for Therapy in Metastatic Human Neuroblastoma Cynthia M. van Golen, Ph.D. 1, Tracy S. Schwab, Ph.D. 1, Bhumsoo Kim, Ph.D.1, Mary Soules1, Sang Su Oh1, Kevin Fung, M.D. 2, Kenneth L van Golen, Ph.D. 3 and Eva L Feldman, M.D., Ph.D. 1. 1Neurology, University of Michigan, Ann Arbor, MI, 48109, 2Otorhinolaryngology, University of Michigan, Ann Arbor, MI, 48109, and 3Internal Medicine, Hematology and Oncology Division, University of Michigan, Ann Arbor, MI, 48109. Neuroblastoma (NBL), the second most common pediatric extracranial tumor, produces metastases in bone resulting in a survival rate of less than 7%. Therefore, understanding how bony metastases form is critical for improving patient survival. Our laboratory has shown that Type I insulin-like growth factor receptor (IGF-IR) expression and activation are present in advanced stage NBL tumors and regulate NBL cell proliferation, motility, invasion, and survival. Bone expresses large amounts of IGF ligands, and the IGF system is required for normal bone physiology. Therefore, we addressed in the current study the role of the IGF system in NBL metastasis to bone. Upon reaching the bone marrow through the circulation, NBL cells must adhere to the bone marrow endothelium, extravasate into the bone microenvironment, and destroy bone tissue to allow for tumor growth. We show high-IGF- IR-expressing NBL cells migrate across a human bone marrow endothelial cell layer toward bone stromal cells, which produce IGF-I, and then adhere tightly to these stromal cells. Transendothelial migration is blocked by both a small molecule inhibitor and a monoclonal neutralizing antibody against the IGF-IR. Intratibial injection of human NBL cells expressing high levels of the IGF-IR, either endogenously or through transfection of an IGF-IR expression construct, leads to tumor formation, osteolytic lesions, and additional secondary tumors in other organs. Intraventricular injection of high-IGF-IR-expressing NBL cells also leads to tumor formation within bone and osteolysis. Osteolytic lesions form when osteoclasts differentiate and become activated in response to tumor cells. When high IGF-IR expressing NBL cells are injected intratibially, increased numbers of multinucleated tartrateresistant acid phosphatase (TRAP) positive cells are detected, suggesting an increase in osteoclast differentiation. In vivo, micro-CT analysis of the bone demonstrates that high-IGF- IR expressing NBL cells promote osteolysis of 81% of trabecular bone by 3 weeks and over 97% of trabecular bone by 4 weeks, with resorption pits also evident within the cortical bone. Conditioned media from high IGF-IR-expressing NBL cells are also capable of supporting osteoclast differentiation in vitro within 10 d. These data suggest that IGF-IR expression in NBL cells in part determines their ability to form osteolytic metastatic tumors within bone; therefore, targeted treatment against the receptor may prove efficacious in treating advanced stage NBL. Targeting the IGF-IR for therapy has recently gained attention in numerous tumors, leading to pharmaceutical production of a number of inhibitors. We are currently testing several of these inhibitors for both in vitro and in vivo efficacy. This work was supported by the Program for Understanding Neurological Diseases (PFUND), the Juvenile Diabetes Research Foundation Center for the Study of Complications in Diabetes, NIH RO1 NS36778, and NIH RO1 NS38849. - 481 -
Page 1 and 2:
- 1 - Luxembourg, January 25th to 2
Page 3 and 4:
Table of content PREFACE ..........
Page 5 and 6:
Preface In 1998, we organized the f
Page 7 and 8:
Acknowledgments This meeting has be
Page 9 and 10:
Group B (15h00 - 17h00) Session V.
Page 11 and 12:
- 11 - Exhibition
Page 13 and 14:
Visit our Expo (in alphabetical ord
Page 15 and 16:
Thursday January 26th, 2006 (Early
Page 17 and 18:
Thursday January 26th, 2006 (Evenin
Page 19 and 20:
Regulation of inflammation and gluc
Page 21 and 22:
Saturday January 28th, 2006 (Early
Page 23 and 24:
Oral presentations (by alphabetical
Page 25 and 26:
4: : Lottin S, Vercoutter-Edouart A
Page 27 and 28:
the B-Raf/mitogen-activated/extrace
Page 29 and 30:
Albertini MC, Accorsi A, Citterio B
Page 31 and 32:
AP-1-dependent gene expression in s
Page 33 and 34:
Jaks and cytokine receptors - an in
Page 35 and 36:
The Role of Met-Gab1 Signalling in
Page 37 and 38:
The mammalian tumor suppressor Scri
Page 39 and 40:
SIGNAL TRANSDUCTION BY STRESS-ACTIV
Page 41 and 42:
Title to be announced Caroline Dive
Page 43 and 44:
Mechanisms of DNA methylation in ma
Page 45 and 46:
Blocking the "4 Integrin-Paxillin I
Page 47 and 48:
Regulation of NF-kB-dependent trans
Page 49 and 50:
The immunomodulator AS101 induces g
Page 51 and 52:
Signaling pathways leading to the a
Page 53 and 54:
Boute, N., Jockers, R. and Issad, T
Page 55 and 56:
Jespsen JS, Sorensen MD and Wengel
Page 57 and 58:
8. Nishikawa, H., Kawai, K., Tanaka
Page 59 and 60:
9) Proteome analysis of rat pancrea
Page 61 and 62:
MicroRNA is an anti-apoptotic facto
Page 63 and 64:
Resveratrol inhibits phorbol ester-
Page 65 and 66:
Cross-talk between angiotensin II a
Page 67 and 68:
Multiple role of histamine H 1 rece
Page 69 and 70:
PI3K Targeting by the Beta-GBP Cyto
Page 71 and 72:
D.P. Chopra, R.E. Menard, J. Janusz
Page 73 and 74:
[2] Meijer, L., Flajolet, M. and Gr
Page 75 and 76:
[4] Niemand, C., Nimmesgern, A., Ha
Page 77 and 78:
Oncogenic signaling by mutant p53 M
Page 79 and 80:
activity of the Peroxisome Prolifer
Page 81 and 82:
Restauration of SHIP-1 activity in
Page 83 and 84:
Hypoxia Signaling. Impact on Tumor
Page 85 and 86:
5. Sokolov EI, Zykov KA, Pukhalsky
Page 87 and 88:
HOW ANTITOXIC AND ANTICANCER AGENTS
Page 89 and 90:
Listeria monocytogenes induced Rac1
Page 91 and 92:
Epigenetic Regulation of Stem Cell
Page 93 and 94:
Survey on in vitro cell death induc
Page 95 and 96:
Distinct roles of IRF-3 and IRF-7 i
Page 97 and 98:
Redox-Sensitive Transcription Facto
Page 99 and 100:
Epigenic control of MHC2TA transcri
Page 101 and 102:
Attenuation of MSK1-driven NF-kB ge
Page 103 and 104:
Talking to chromatin: Silencers Sil
Page 105 and 106:
Ubiquitin ligase Smurf1 controls os
Page 107 and 108:
Workshop presentations (by alphabet
Page 109 and 110:
Ambion MicroRNAs (miRNAs) are small
Page 111 and 112:
Organizer: BIOBASE GmbH Date: Janua
Page 113 and 114:
Reliable and efficient gene Knock-d
Page 115 and 116:
Exploring ubiquitin signaling with
Page 117 and 118:
Poster presentations Poster are cla
Page 119 and 120:
Session I : protein domains Poster
Page 121 and 122:
Page 123 and 124:
Page 125 and 126:
Notes Notes - 125 -
Page 127 and 128:
Session II. Receptor signaling and
Page 129 and 130:
Session II : Receptor signaling and
Page 131 and 132:
Page 133 and 134:
Page 135 and 136:
Page 137 and 138:
Page 139 and 140:
Page 141 and 142:
Page 143 and 144:
Page 145 and 146:
Page 147 and 148:
Page 149 and 150:
Page 151 and 152:
Page 153 and 154:
Page 155 and 156:
Page 157 and 158:
Page 159 and 160:
Page 161 and 162:
Page 163 and 164:
Page 165 and 166:
Page 167 and 168:
Page 169 and 170:
Page 171 and 172:
Page 173 and 174:
Page 175 and 176:
Page 177 and 178:
Page 179 and 180:
Page 181 and 182:
Notes Notes - 181 -
Page 183 and 184:
Session III. Protein kinase cascade
Page 185 and 186:
Session III : Protein kinase cascad
Page 187 and 188:
Page 189 and 190:
Page 191 and 192:
Page 193 and 194:
Page 195 and 196:
Page 197 and 198:
Page 199 and 200:
Page 201 and 202:
Page 203 and 204:
Page 205 and 206:
Page 207 and 208:
Page 209 and 210:
Page 211 and 212:
Page 213 and 214:
Page 215 and 216:
Page 217 and 218:
Page 219 and 220:
Page 221 and 222:
Page 223 and 224:
Page 225 and 226:
Page 227 and 228:
Page 229 and 230:
Page 231 and 232:
Page 233 and 234:
Page 235 and 236:
Page 237 and 238:
Page 239 and 240:
Page 241 and 242:
Page 243 and 244:
Page 245 and 246:
Page 247 and 248:
Page 249 and 250:
Page 251 and 252:
Page 253 and 254:
Page 255 and 256:
Notes Notes - 255 -
Page 257 and 258:
Session IV. Protein kinase inhibito
Page 259 and 260:
IV. Protein kinase inhibitors: insi
Page 261 and 262:
IV. Protein kinase inhibitors: insi
Page 263 and 264:
Notes - 263 -
Page 265 and 266:
- 265 -
Page 267 and 268:
V. Phosphatases as key cell signali
Page 269 and 270:
Page 271 and 272:
Page 273 and 274:
Notes - 273 -
Page 275 and 276:
- 275 -
Page 277 and 278:
VI. Proteasome degradation pathways
Page 279 and 280:
VI. Proteasome degradation pathways
Page 281 and 282:
Session VII. Stem cell specific cel
Page 283 and 284:
Notes - 283 -
Page 285 and 286:
VIII. Inflammation specific signali
Page 287 and 288:
Page 289 and 290:
Page 291 and 292:
Page 293 and 294:
Page 295 and 296:
Page 297 and 298:
Page 299 and 300:
Page 301 and 302:
Page 303 and 304:
Page 305 and 306:
Page 307 and 308:
Page 309 and 310:
Page 311 and 312:
Page 313 and 314:
Page 315 and 316:
Page 317 and 318:
Page 319 and 320:
Page 321 and 322:
Notes - 321 -
Page 323 and 324:
- 323 -
Page 325 and 326:
Session IX. Novel compounds targeti
Page 327 and 328:
Page 329 and 330:
Page 331 and 332:
Page 333 and 334:
Session X : Cell death in cancer -
Page 335 and 336:
Session X : Cell death in cancer Po
Page 337 and 338:
Page 339 and 340:
Page 341 and 342:
Page 343 and 344:
Page 345 and 346:
Page 347 and 348:
Page 349 and 350:
Page 351 and 352:
Page 353 and 354:
Page 355 and 356:
Page 357 and 358:
Page 359 and 360:
Page 361 and 362:
Page 363 and 364:
Page 365 and 366:
Page 367 and 368:
Page 369 and 370:
Page 371 and 372:
Page 373 and 374:
Page 375 and 376:
Page 377 and 378:
Page 379 and 380:
Page 381 and 382:
Page 383 and 384:
Page 385 and 386:
Page 387 and 388:
Page 389 and 390:
Page 391 and 392:
Page 393 and 394:
Page 395 and 396:
Page 397 and 398:
Page 399 and 400:
Page 401 and 402:
Page 403 and 404:
Page 405 and 406:
Page 407 and 408:
Page 409 and 410:
Page 411 and 412:
Page 413 and 414:
Page 415 and 416:
Page 417 and 418:
Page 419 and 420:
Page 421 and 422:
Page 423 and 424:
Page 425 and 426:
Page 427 and 428:
Page 429 and 430: Session X : Cell death in cancer Po
Page 443 and 444: Notes Notes - 443 -
Page 445 and 446: Session XI : Cell death and cardiov
Page 447 and 448: Session XI: Cell death and cardiova
Page 457 and 458: Notes - 457 -
Page 459 and 460: Session XII : Cell death and neurod
Page 479: Session XII : Cell death and neurod
Page 485 and 486: Notes - 485 -
Page 487 and 488: - 487 -
Page 489 and 490: Session XIII : Cell signaling pathw
Page 501 and 502: Notes Notes - 501 -
Page 503 and 504: Session XIV : Transcriptional and t
Page 531 and 532:
Session XIV : Transcriptional and t
Page 533 and 534:
Page 535 and 536:
Page 537 and 538:
Page 539 and 540:
Page 541 and 542:
Page 543 and 544:
Page 545 and 546:
Page 547 and 548:
Page 549 and 550:
Page 551 and 552:
Page 553 and 554:
Page 555 and 556:
Page 557 and 558:
Page 559 and 560:
Page 561 and 562:
Page 563 and 564:
Page 565 and 566:
Page 567 and 568:
Page 569 and 570:
Page 571 and 572:
Page 573 and 574:
Page 575 and 576:
Page 577 and 578:
Page 579 and 580:
Page 581 and 582:
Page 583 and 584:
Notes Notes - 583 -
Page 585 and 586:
Session XV : Reactive oxygen specie
Page 587 and 588:
Page 589 and 590:
Page 591 and 592:
Notes - 591 -
Page 593 and 594:
Session XVI : Chemopreventive agent
Page 595 and 596:
Page 597 and 598:
Page 599 and 600:
Page 601 and 602:
Page 603 and 604:
Page 605 and 606:
Page 607 and 608:
Session XVII : Cell signaling in he
Page 609 and 610:
Page 611 and 612:
Page 613 and 614:
Page 615 and 616:
Page 617 and 618:
Page 619 and 620:
Page 621 and 622:
Page 623 and 624:
Page 625 and 626:
Page 627 and 628:
Page 629 and 630:
Page 631 and 632:
Page 633 and 634:
Page 635 and 636:
Page 637 and 638:
Page 639 and 640:
Page 641 and 642:
Page 643 and 644:
Page 645 and 646:
Page 647 and 648:
Page 649 and 650:
Page 651 and 652:
Page 653 and 654:
Page 655 and 656:
Page 657 and 658:
Page 659 and 660:
Page 661 and 662:
Page 663 and 664:
Page 665 and 666:
Page 667 and 668:
Page 669 and 670:
Notes - 669 -
Page 671 and 672:
- 671 -
Page 673 and 674:
- 673 -
Page 675 and 676:
Dr. Nassera Aouali L-1526 Luxembour
Page 677 and 678:
Dr. Giordano Bianchi Clinic of inte
Page 679 and 680:
Mrs. Isabel Burghardt Laboratory of
Page 681 and 682:
Pr. Czeslaw Cierniewski 92-215 Lodz
Page 683 and 684:
Mr. Igotz Delgado Biochemistry 4894
Page 685 and 686:
Mrs. Anissa Fergani INSERM U-692 67
Page 687 and 688:
Dr. Mark Ginsberg Mail code 0726 92
Page 689 and 690:
Dr. Jochen Hefl Division of Signal
Page 691 and 692:
Mr. Jan Jepsen 2100 Copenhagen DNK
Page 693 and 694:
Pr. Young Min Kim Division of Biolo
Page 695 and 696:
Mr. Christoph Lahtz AG Tumorgenetik
Page 697 and 698:
Pr. Etta Livneh 84105 Beer Sheva IS
Page 699 and 700:
Mrs. Rasa Merzvinskyte Department o
Page 701 and 702:
Mr. Gustav Nilsonne Department of L
Page 703 and 704:
Mrs. Christel Péqueux Tumour and D
Page 705 and 706:
Dr. Gabriella Regis Tumor Immunolog
Page 707 and 708:
Dr. Carsten Scheller 97078 Wuerzbur
Page 709 and 710:
Mr. Yoo-Cheol Song Laboratory of Gy
Page 711 and 712:
Dr. Lucia Maria Valatro Laboratori
Page 713 and 714:
Mrs. Jessica Wagener 40225 Duesseld
Page 715:
Pr. Moncef ZOUALI Centre Viggo Pete
show all

Visit our Expo - Redox and Inflammation signaling 2012

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?