Annual Meeting Proceedings Part 1 - American Society of Clinical ...

More documents

Recommendations

Info

430s Leukemia, Myelodysplasia, and Transplantation 6556 General Poster Session (Board #16G), Mon, 1:15 PM-5:15 PM Maintenance therapy with arsenic after induction in an alternative and long-term case for the prevention of recurrence of acute promyelocytic leukemia during the period between November 2005 and December 2011. Presenting Author: Mozaffar Aznab, Kermanshah University of Medicine, Kermanshah, Iran Background: Arsenic trioxide has been used in the first line treatment of acute promyelocytic leukemia and also for recurrence after ATRA and chemotherapy. In this study, it we used it in induction of remission and maintenance therapy Methods: Between November 2005 to December 2011, 42 patients admitted in our department with APL diagnosis. There were 27 male and 15 women with a median age of 28 years. Arsenic trioxide started at 0.15 mg/kg intravenous infusion till patient’s bone marrows achieve to complete remission. Then, after 28 days rest, we did consolidation with Arsenic trioxide with the same dosage for 28 more days. We continued treatment with 14 days courses of Arsenic trioxide every 3-4 months for 2 years, as maintenance therapy Results: Four patients died during the first 20 days of treatment. Thirty-eight patients achieved to remission. Two patients refused to continue treatment after achieving to remission and excluded from this study. Thirty-six patients finished whole treatment. After a median follow-up of 54 months, 4 patients died due to disease relapse and one patient relapsed and initiated treatment with Arsenic and ATRA. Five patients faced leukocytosis over 100,000/ml. In these cases we were obligated to discontinue Arsenic for 3-4 days and did chemotherapy by Danourobicin for 2 days. Totally 8 patients died during remission induction and long-term follow up. One year, 3 and 5 years RFS were 97%, 87.1% and 79.4 respectively and we didn’t observe any relapse for patients who remained in remission after 5 years. Finally, 31 patients are alive and free of disease. The overall survival was 79.5% for our cohort. Conclusions: Arsenic trioxide is an effective treatment as the first line therapy for new cases of APL and long term therapy with will reduce the risk of diseases recurrence without any major toxicity in long time. 6558 General Poster Session (Board #17A), Mon, 1:15 PM-5:15 PM Response rates in patients with relapsed/refractory acute myeloid leukemia with FLT3-ITD mutation using 5-azacitadine plus sorafenib. Presenting Author: Mona Lisa Alattar, University of Texas at Houston Health Science Center, Houston, TX Background: The outcome of patients with relapsed acute myeloid leukemia (AML) with FLT3-ITD mutation is poor. Sorafenib is an inhibitor of FLT-3 kinase activity in nanomolar concentrations. We conducted this phase II study to evaluate the efficacy and tolerability of the combination of Sorafenib and 5-Aza for the treatment of patients with refractory or relapsed AML with the particular emphasis on those with FLT3-ITD mutation. Methods: Patients were eligible if they had relapsed or refractory AML and were 18 years of age or older. They received 5-Aza 75 mg/m2 daily x 7 together with Sorafenib 200 mg BID X 28 days; cycles were repeated in approximately 1-month intervals. Responses were assessed after first cycle and then at the discretion of the treating physician at the time of the best peripheral blood response. Results: 32 patients with AML with a median age of 61 years (range, 24-87) were enrolled. They included 13 (41%) with diploid cytogenetics, 9 (28%) with complex cytogenetics, and 10 (31%) with miscellaneous chromosomal abnormalities. FLT-3-ITD was detected prior to the initiation of treatment in 30/32 patients. Patients had received a median of 2 prior treatments (range, 1-6). 12 (38%) patients had received �3 prior regimens and 11 had failed therapy with a FLT3 kinase inhibitor (6 with AC220, 1 with PKC412, and 5 with sorafenib, either as monotherapy or with plerixafor); 2 had failed 2 prior FLT3 inhibitors. 10 patients were inevaluable as they never received therapy or discontinued it before response assessment at one month. The overall CR/CRi rate among the 22 evaluable patients is 50%, including 9 (41%) with CRi and 2 (9%) with CR; with a median of 3 (range, 1-9) treatment cycles. The median time to achieving CR/CRi was 3 months (range, 1-4) and the median duration of CR/CRi was 3 months (range, �1–5.5). Three patients proceeded to allogeneic stem cell transplant. The most common study drug-related adverse events were rash and fatigue with no deaths attributable to study medications. Conclusions: Combination of 5-Aza and Sorafenib is promising for the treatment of patients with relapsed and refractory AML with FLT-3-ITD mutation and may allow them to proceed to stem cell transplant. 6557 General Poster Session (Board #16H), Mon, 1:15 PM-5:15 PM Effect of ROR1-targeting small molecules on chronic lymphocytic leukemia (CLL) cells. Presenting Author: Hakan Mellstedt, Karolinska University Hospital Solna, Stockholm, Sweden Background: There is a great interest to develop targeting drugs for CLL, both MAbs and small molecules, to improve the outcome for the disease. ROR1, a receptor tyrosine kinase, is overexpressed on CLL cells but not on normal cells. ROR1 is constitutively phosphorylated and siRNA transfection induces leukemic cell death. The aim of the study is to produce small molecules inhibiting the cytoplasmic tyrosine kinase activity of ROR1, which could induce specific killing of leukemic cells. Methods: A highthroughput screening assay in 384-format has been developed measuring phosphorylation of a substrate peptide by human recombinant intracellular ROR-1 kinase domain. A collection of 80.000 small molecules has been screened generating two chemical series. Novel leads have been synthesized and structure-activity-relationship has been developed using the assay. Results: Three compounds were selected (KAN0173631, KAN0438063, KAN0438175T). Freshly isolated leukemic CLL cells were used as targets in addition to PBMC from healthy donors to test cytotoxicity. The three compounds induced specific apoptosis of CLL cells (Annexin V/PI and MTT) both at 24 and 48h. Efficacy index (EI), i.e. killing of leukemic cells in relation to normal PBMC was favourable. The most promising drug KAN0438063 had an EI of 40 i.e. killed 40 times more CLL cells than PBMC at an IC50 of 10�M. The compounds induced PARP cleavage and cleavage of caspases 8 and 9 as well as down regulation of Mcl-1 and Bcl-xl (Western Blot). ROR1 was dephosphorylated (Western Blot). The selective apoptotic effect was compared to other small molecules targeting non- ROR1 structures in CLL (PCI-32765, CAL-101, R406, R788, STK- 156485, STK-156133) and our compounds were significantly more effective (EI) (p�0.001). Conclusions: We have developed effective and selective series of compounds targeting ROR1 with promising ADMET properties. ROR1 targeting small molecules might also be effective for other tumor cells expressing ROR1 as has been noted for e.g. pancreatic carcinoma cells. Our model molecules will be further optimized and tested in animal tumor models. These molecules represent the first small molecules targeting ROR1 – a “survival factor” in CLL. 6559 General Poster Session (Board #17B), Mon, 1:15 PM-5:15 PM Post hoc analysis of relationship between baseline white blood cell count and survival outcome in a randomized phase III trial of decitabine in older patients with newly diagnosed acute myeloid leukemia. Presenting Author: Chris Arthur, Royal North Shore Hospital, St. Leonards, Australia Background: In a large phase III trial (N�485), patients (pts) �65y with newly diagnosed acute myeloid leukemia (AML) received 1-h IV infusion of decitabine (DAC) 20 mg/m2 for 5 consecutive days every 4 wk or treatment choice (TC) with supportive care or cytarabine 20 mg/m2 subcutaneous injection for 10 consecutive days every 4 wk (NCT00260832; Kantarjian et al. JCO, in press). Enrolled pts had white blood cell (WBC) count �40 x109 /L; baseline WBC counts were relatively low (median [range] DAC: 3.1 x109 /L [0.3-127.0]; TC: 3.7 x109 /L [0.5-80.9]). This post hoc analysis assessed baseline WBC count and survival outcome. Methods: Overall survival (OS) and progression-free survival (PFS) were summarized by baseline WBC subgroups (�1, 1-5, �5 x109 /L). Results: Mature survival data (2010) were based on intent-to-treat (ITT) population (446 deaths: TC, n�227; DAC, n�219). OS was 5.0 mo for TC vs 7.7 mo for DAC (nominal P�.037). For each WBC subgroup, differences in OS for TC vs DAC were not significant (NS), but hazard ratios (HR) favored DAC for all subgroups (Table). There was a significant difference in PFS in favor of DAC for patients with baseline WBC 1–5 x109 /L (P�.005; HR�0.67) and �5 x109 /L (P�.027; HR�0.71). Conclusions: These data are consistent with overall results, with a trend toward improved outcome with DAC regardless of baseline WBC count in older pts with newly diagnosed AML. Further analyses are warranted. Outcome WBC x10 9 /L TC Median, a mo Event/n OS All pts 5.0 227/243 �1 4.9 20/22 1-5 5.9 106/115 �5 4.3 94/99 PFS All pts 2.1 221/243 �1 2.2 20/22 1-5 2.9 110/115 �5 2.1 98/99 DAC Median, a mo Event/n 7.7 219/242 8.6 22/25 9.5 104/119 6.3 88/93 3.7 221/242 5.5 24/25 3.8 111/119 3.4 89/93 Nominal P value b HR (95% CI) c P�.037 HR�0.82 (0.68, 0.99) P�NS HR�0.85 (0.42, 1.70) P�NS HR�0.78 (0.58, 1.03) P�NS HR�0.82 (0.60, 1.10) P�.003 HR�0.75 (0.62, 0.91) P�NS HR�1.05 (0.56, 1.97) P�.005 HR�0.67 (0.51, 0.89) P�.027 HR� 0.71 (0.53, 0.97) a Kaplan-Meier product limit estimates. b 2-sided log-rank test. c Stratified Cox regression model (age and cytogenetic risk as strata; treatment group as covariate). HR �1 means advantage for DAC. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
6560 General Poster Session (Board #17C), Mon, 1:15 PM-5:15 PM Increased risk of MDS/AML post radiation treatment for breast cancer: Analysis of SEER data 2001-2008. Presenting Author: Henry G. Kaplan, Swedish Cancer Institute, Seattle, WA Background: Ionizing radiation is a known cause of myeloid leukemia, but it is not known whether therapeutic doses for breast cancer (BC) pose risk. We hypothesized that BC radiation treatment is associated with increased risk of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML)) as seen in a previously conducted institutional cohort study. Methods: We used 2001-2008 Surveillance, Epidemiology and End Results (SEER) database records to identify a cohort of first primary BC patients treated with radiation who were unlikely to be treated with chemotherapy (stage 0 and estrogen receptor positive (ER�) stage I). We identified subsequent MDS/AML diagnoses in the BC cohort, using SEER to query appropriate ICD-O-3 codes. We compared observed MDS/AML rates in the BC cohort to expected rates, estimated for first primary MDS/AML in the entire population, and calculated observed/expected rate ratios with 95% confidence intervals (CI). Results: We estimated an increased overall risk of MDS/AML in the breast cancer cases treated with radiation compared to the general population (RR�4.23, 95% CI 3.41, 5.18). The relative risk was higher for stage I ER� breast cancer cases �65 years of age (RR�7.75, 95% CI 5.18, 11.05) than for stage 0 cases �65 years of age (RR�3.65, 95% CI 1.57, 7.05). Among women 65 years and older, there was a more modest increased risk, only seen for stage 1 ER� breast cancer cases (RR�1.52) (table). Conclusions: Our results suggest that radiation treatment for breast cancer is associated with increased risk of MDS/AML. The effect appears to be age-dependent. Expected and observed MDS/AML incidence rates in breast cancer cases with radiation treatment (per 100,000 person years). Expected rate Person years Observed rate (n�cases) Rate ratio (95% CI) Stage 0, age
Page 1:
Volume 30, Issue 15S, Part I of II
Page 4 and 5:
Editor: Michael A. Carducci, MD Man
Page 6 and 7:
Volume 30, Issue 15S Supplement to
Page 8 and 9:
Letter from the Editor The 2012 ASC
Page 10 and 11:
JOURNAL of CLINICAL ONCOLOGY ......
Page 12 and 13:
ASCO Conflict of Interest Policy an
Page 14 and 15:
2s Special Awards also “normalize
Page 17 and 18:
2012 ASCO Annual Meeting Proceeding
Page 19 and 20:
500 Oral Abstract Session, Sun, 8:0
Page 21 and 22:
508 Clinical Science Symposium, Sat
Page 23 and 24:
516 Poster Discussion Session (Boar
Page 25 and 26:
Page 27 and 28:
Page 29 and 30:
540 General Poster Session (Board #
Page 31 and 32:
549^ General Poster Session (Board
Page 33 and 34:
Page 35 and 36:
Page 37 and 38:
Page 39 and 40:
Page 41 and 42:
Page 43 and 44:
Page 45 and 46:
Page 47 and 48:
Page 49 and 50:
Page 51 and 52:
Page 53 and 54:
Page 55 and 56:
TPS647 General Poster Session (Boar
Page 57 and 58:
Page 59 and 60:
Page 61 and 62:
LBA1000 Oral Abstract Session, Tue,
Page 63 and 64:
1008 Oral Abstract Session, Tue, 9:
Page 65 and 66:
1016 Poster Discussion Session (Boa
Page 67 and 68:
Page 69 and 70:
Page 71 and 72:
1040 General Poster Session (Board
Page 73 and 74:
Page 75 and 76:
Page 77 and 78:
Page 79 and 80:
Page 81 and 82:
Page 83 and 84:
Page 85 and 86:
Page 87 and 88:
Page 89 and 90:
Page 91 and 92:
Page 93 and 94:
Page 95 and 96:
TPS1138 General Poster Session (Boa
Page 97 and 98:
Page 99 and 100:
1504 Oral Abstract Session, Mon, 8:
Page 101 and 102:
Page 103 and 104:
Page 105 and 106:
Page 107 and 108:
Page 109 and 110:
Page 111 and 112:
Page 113 and 114:
Page 115 and 116:
Page 117 and 118:
Page 119 and 120:
Page 121 and 122:
Page 123 and 124:
Page 125 and 126:
Page 127 and 128:
2000 Oral Abstract Session, Sun, 8:
Page 129 and 130:
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:
Developmental Therapeutics—Clinic
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:
Page 183 and 184:
Page 185 and 186:
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:
LBA3500^ Oral Abstract Session, Sun
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:
LBA4000 Oral Abstract Session, Sat,
Page 253 and 254:
4008 Oral Abstract Session, Sat, 3:
Page 255 and 256:
Page 257 and 258:
Page 259 and 260:
Page 261 and 262:
Page 263 and 264:
Page 265 and 266:
Page 267 and 268:
Page 269 and 270:
Page 271 and 272:
Page 273 and 274:
Page 275 and 276:
Page 277 and 278:
Page 279 and 280:
Page 281 and 282:
Page 283 and 284:
Page 285 and 286:
Page 287 and 288:
Page 289 and 290:
Page 291 and 292:
Page 293 and 294:
4516 Oral Abstract Session, Tue, 9:
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:
Page 323 and 324:
Page 325 and 326:
Page 327 and 328:
Page 329 and 330:
Page 331 and 332:
Page 333 and 334:
Page 335 and 336:
Page 337 and 338:
Page 339 and 340:
LBA5000 Oral Abstract Session, Sat,
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:
5504^ Oral Abstract Session, Sun, 8
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: 5592 General Poster Session (Board
Page 393 and 394: TPS5600 General Poster Session (Boa
Page 395 and 396: 6004 Oral Abstract Session, Sat, 3:
Page 397 and 398: 6012 Clinical Science Symposium, Su
Page 399 and 400: 6020 Poster Discussion Session (Boa
Page 429 and 430: 6504 Oral Abstract Session, Mon, 8:
Page 441: 6552 General Poster Session (Board
Page 463 and 464: TPS6640 General Poster Session (Boa
Page 465 and 466: Lung Cancer—Non-small Cell Local-
Page 493 and 494:
Page 495 and 496:
Page 497 and 498:
Page 499 and 500:
Page 501 and 502:
Page 503 and 504:
Page 505 and 506:
Page 507 and 508:
Page 509 and 510:
Page 511 and 512:
Page 513 and 514:
Page 515 and 516:
Page 517 and 518:
Page 519 and 520:
Page 521 and 522:
Page 523 and 524:
Page 525 and 526:
Page 527 and 528:
Page 529 and 530:
Page 531 and 532:
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:
9016 Clinical Science Symposium, Tu
Page 585 and 586:
Page 587 and 588:
Page 589 and 590:
Page 591 and 592:
Page 593 and 594:
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:
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:
9520 Clinical Science Symposium, Mo
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:
10004 Oral Abstract Session, Mon, 3
Page 645 and 646:
10012 Poster Discussion Session (Bo
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:
TPS10100 General Poster Session (Bo
Page 669 and 670:
10504 Oral Abstract Session, Mon, 8
Page 671 and 672:
Page 673 and 674:
Page 675 and 676:
Page 677 and 678:
Page 679 and 680:
Page 681 and 682:
Page 683 and 684:
Page 685 and 686:
Page 687 and 688:
Page 689 and 690:
Page 691 and 692:
Page 693 and 694:
Page 695 and 696:
Page 697 and 698:
Page 699 and 700:
Page 701:
TPS10634 General Poster Session (Bo
Page 704 and 705:
Author Index Note: Numerals refer t
Page 706 and 707:
Alexanian, Raymond 8093 Alexeev, Bo
Page 708 and 709:
Arkenau, Hendrik-Tobias 2540, 3000,
Page 710 and 711:
Ballen, Karen K. 6606, 6617, 6618,
Page 712 and 713:
Ben-Aharon, Irit 548, 2556, e13080
Page 714 and 715:
Blancas, Isabel e11535, e11545, e21
Page 716 and 717:
Brandes, Johann Christoph 7048, 106
Page 718 and 719:
Cakir, Betul 9567 Calabek, Bernadet
Page 720 and 721:
Ceraulo, Domenica 4017 Cerbone, Lin
Page 722 and 723:
Chinen, Ludmilla T.D. e16046 Chinen
Page 724 and 725:
Come, Steven E. 9071, 9100 Comis, S
Page 726 and 727:
Dahlheimer, Tambra 2546 Dahmane, El
Page 728 and 729:
DeLacure, Mark D. e16052 Delage, Ju
Page 730 and 731:
Domingo, Gelenis 6568, 6575, 6588 D
Page 732 and 733:
El Sherbeiny, Esam e15129 El-Deiry,
Page 734 and 735:
Fayad, Luis 6501, 8067 Fayette, Jer
Page 736 and 737:
Foroni, Chiara e11546 Foroni, Letiz
Page 738 and 739:
Gang, Wu 7091, e14511 Gangaram, Anj
Page 740 and 741:
Gimenez Capitan, Ana 4068, 10596, e
Page 742 and 743:
Granowetter, Linda 9537 Grant, Barb
Page 744 and 745:
Hainsworth, John D. 618, 1018, 1086
Page 746 and 747:
Heerschap, Arend e13111 Heersink, M
Page 748 and 749:
Hong, Seung-Mo 3568 Hong, Sook Hee
Page 750 and 751:
Im, Young-Hyuck 598^, 644, TPS649,
Page 752 and 753:
Ji, Yongling e17527 Jia, Jingquan e
Page 754 and 755:
Kaparelou, Maria 583 Kapaun, Christ
Page 756 and 757:
Kim, Chan Kyu e14688 Kim, Chang Won
Page 758 and 759:
Komatsu, Yoshihiro e14689 Komatsu,
Page 760 and 761:
Laack, Nadia N. 2032, e14507 Laadem
Page 762 and 763:
Lee, Ji-Hyun TPS3114, 6100 Lee, Jih
Page 764 and 765:
Lim, Kian-Huat e14584 Lim, Kiat Hon
Page 766 and 767:
Loupakis, Fotios 3518, 3540, 3546,
Page 768 and 769:
Man, Shan e11061, e15177^ Manaloor,
Page 770 and 771:
Mathieu-Nicot, Florence e19623 Math
Page 772 and 773:
Mergenthaler, Hans-Guenther e15026
Page 774 and 775:
Molero, Xavier e21035 Moles-Moreau,
Page 776 and 777:
Munoz-Sanchez, MM e19590 Munsell, M
Page 778 and 779:
Ng, Daniel e15050 Ng, Dawn Marie e1
Page 780 and 781:
Oguri, Senri 5556 Oh, Do Youn 1003
Page 782 and 783:
Palassini, Elena 10026, 10053, 1006
Page 784 and 785:
Peisker, Uwe 10600 Peker, Deniz e18
Page 786 and 787:
Piwnica-Worms, Helen 3047 Pizzo, Fa
Page 788 and 789:
Rabinowits, Guilherme 5501, 5582, 9
Page 790 and 791:
Reyes-Rivera, Irmarie CRA3503 Reyna
Page 792 and 793:
Rose, Steven C. 3590 Rosell, Rafael
Page 794 and 795:
Sakata, Shinya e18059 Sakata, Yuh 3
Page 796 and 797:
Schenkein, David P. 6606 Schepp, Wo
Page 798 and 799:
Sha, Dan 3564 Sha, Huifang e13528 S
Page 800 and 801:
Silva, Jose D. 5567 Silva, Milton J
Page 802 and 803:
Sousa, Carlos Eduardo Pires 643 Sou
Page 804 and 805:
Su, Xinying 4124 Su, Yu-Chieh e1600
Page 806 and 807:
Tan, Chee Seng 1064, e19523 Tan, Ch
Page 808 and 809:
Tillmanns, Todd D. 5014, e15514 Til
Page 810 and 811:
Uchiyama, Tomotaka e21108 Udovitsa,
Page 812 and 813:
Videtic, Gregory M.M. e14611, e1466
Page 814 and 815:
Wang, Yuan e15124 Wang, Yunfei 547
Page 816 and 817:
Wischnewsky, Manfred 1078 Wischnik,
Page 818 and 819:
Yasuda, Hiromi e14029 Yasuda, Hiroy
Page 820:
Zhang, Xinmin e16022 Zhang, Xu Dong
show all

Annual Meeting Proceedings Part 1 - American Society of Clinical ...

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

Delete template?

Save as template?