NcXHF

Recommendations

Info

LEUKEMIA, MYELODYSPLASIA, AND TRANSPLANTATION Progress in Myeloproliferative Neoplasms: Biology to Bedside CHAIR Alison R. Moliterno, MD The Johns Hopkins Hospital Baltimore, MD SPEAKERS Jean-Jacques Kiladjian, MD, PhD Hôpital Saint-Louis Paris, France Michael W. Deininger, MD, PhD University of Utah Huntsman Cancer Institute Salt Lake City, UT
RECOGNIZING AND MANAGING HIGH-RISK CML Diagnosing and Managing Advanced Chronic Myeloid Leukemia Michael W. Deininger, MD, PhD OVERVIEW Clinical staging of chronic myeloid leukemia (CML) distinguishes between chronic phase (CP-CML), accelerated phase (AP-CML), and blastic phase (BP-CML), reflecting its natural history in the absence of effective therapy. Morphologically, transformation from CP-CML to AP/BP-CML is characterized by a progressive or sudden loss of differentiation. Multiple different somatic mutations have been implicated in transformation from CP-CML to AP/BC-CML, but no characteristic mutation or combination of mutations have emerged. Gene expression profiles of AP-CML and BP-CML are similar, consistent with biphasic evolution at the molecular level. Gene expression of tyrosine kinase inhibitor (TKI)–resistant CP-CML and second CP-CML resemble AP/BP-CML, suggesting that morphology alone is a poor predictor of biologic behavior. At the clinical level, progression to AP/BP-CML or resistance to first-line TKI therapy distinguishes a good risk condition with survival close to the general population from a disease likely to reduce survival. Progression while receiving TKI therapy is frequently caused by mutations in the target kinase BCR-ABL1, but progression may occur in the absence of explanatory BCR-ABL1 mutations, suggesting involvement of alternative pathways. Identifying patients in whom milestones of TKI response fail to occur or whose disease progress while receiving therapy requires appropriate molecular monitoring. Selection of salvage TKI depends on prior TKI history, comorbidities, and BCR-ABL1 mutation status. Despite the introduction of novel TKIs, therapy of AP/BP-CML remains challenging and requires accepting modalities with substantial toxicity, such as hematopoietic stem cell transplantation (HSCT). It is thought that CML is initiated when a hematopoietic stem cell acquires the t(9;22)(q11;34) reciprocal translocation, which the cytogenetic correlate is the Philadelphia chromosome (Ph). Based on the increase in CML incidence in survivors of the atomic bombings on Japan, the latency between this initial event to the clinical manifestation is estimated to be approximately 8 years. 1 Whether or not a clonal genetic lesion predates the acquisition of Ph or whether additional genetic abnormalities are required to produce CP- CML is a matter of debate. However, recent next-generation sequencing studies suggest both scenarios are possible. 2 Without effective therapy, CP-CML invariably progresses to an acute leukemia termed BP-CML, sometimes through an intermediate stage referred to as AP-CML. BP-CML may have a myeloid (70%), B-lymphoid (20%), or mixed phenotype (10%). 3 Observations from the 1920s, when therapeutic options were limited to splenic irradiation and arsenic trioxide, suggest that the natural duration of CP-CML may be approximately 2.5 years. In the developed world, the vast majority of patients are diagnosed in the chronic phase, frequently when an abnormal complete blood count leads to a diagnostic workup. Presentation with AP/BP-CML is more common in countries with lower socioeconomic status, probably reflecting delays in diagnosis as a result of insuffıcient access to medical care. The term “advanced CML” is not clearly defıned and variably used to include AP/BP-CML only or also CP-CML resistant to standard therapy. DEFINING ADVANCED CHRONIC MYELOID LEUKEMIA: CHRONIC PHASE, ACCELERATED PHASE, AND BLASTIC PHASE Several different classifıcation systems have been developed to defıne the phases of CML based on morphologic and clinical criteria, including the International Bone Marrow Transplant Registry (IBMTR), The University of Texas MD Anderson Cancer Center (MDACC), and World Health Organization (WHO) classifıcations (Table 1). The simultaneous use of different systems has generated considerable confusion, as different classifıcations may assign patients to different disease phases and some of the criteria lack a precise defınition. For example, the WHO defınition of AP-CML uses increasing white blood cells and spleen size unresponsive to therapy as defıning criteria. Another important discrepancy is the bone marrow or blood blast percentage that defınes BP-CML. Whereas the WHO classifıcation uses 20% or greater as the cutoff (in line with acute myeloid leukemia [AML]), MDACC and IBMTR classifıcations use 30% or greater. The MDACC criteria defıning AP-CML were prospectively validated as independent prognostic variables, and From the Huntsman Cancer Institute, Division of Hematology and Hematologic Malignancies, University of Utah, Salt Lake City, UT. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Michael W. Deininger, MD, PhD, Huntsman Cancer Institute, Room 4280, 2000 Circle of Hope, Salt Lake City, UT 84112-5550; email: michael.deininger@hci.utah.edu. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e381
Page 1 and 2:
AMERICAN SOCIETY OF CLINICAL ONCOLO
Page 3:
American Society of Clinical Oncolo
Page 6 and 7:
Controversies in Neoadjuvant Therap
Page 8 and 9:
Clinical Trials of Precision Medici
Page 10 and 11:
Managing Ovarian Cancer in the Olde
Page 12 and 13:
Updates in the Multimodality Manage
Page 14 and 15:
PEDIATRIC ONCOLOGY Real-Time Molecu
Page 16 and 17:
2015 ASCO Annual Meeting Disclosure
Page 18 and 19:
2015 Educational Book Expert Panel
Page 20 and 21:
James Marshall, PhD Roswell Park Ca
Page 22 and 23:
2015 Annual Meeting Supporters* MIS
Page 24 and 25:
David Yurman Corporate Allies Conqu
Page 26 and 27:
INVITED ARTICLES This year’s invi
Page 28 and 29:
WONG, CAPASSO, AND ECKHARDT 3 3 sc
Page 30 and 31:
WONG, CAPASSO, AND ECKHARDT terize
Page 32 and 33:
WONG, CAPASSO, AND ECKHARDT for mul
Page 34 and 35:
STEPHEN T. SONIS portantly, patient
Page 36 and 37:
STEPHEN T. SONIS elements of a clus
Page 38 and 39:
STEPHEN T. SONIS Defıning the clin
Page 40 and 41:
STEPHEN T. SONIS predict oral mucos
Page 42 and 43:
HUSSAIN AND DIPAOLA TABLE 1. U.S. F
Page 44 and 45:
HUSSAIN AND DIPAOLA mizing use of p
Page 46 and 47:
INVITED ARTICLES DIAGNOSTICS The Fu
Page 48 and 49:
EDWARD S. KIM TABLE 1. Selected Umb
Page 50 and 51:
EDWARD S. KIM platform that plans t
Page 52 and 53:
INVITED ARTICLES HEAD AND NECK CANC
Page 54 and 55:
GROSS AND COHEN treatments are poor
Page 56 and 57:
GROSS AND COHEN 22. Ratner M. Pharm
Page 58 and 59:
GILBERT ET AL tional scholars, lead
Page 60 and 61:
GILBERT ET AL ment of physician com
Page 62 and 63:
GILBERT ET AL greater understanding
Page 64 and 65:
INVITED ARTICLES GASTROINTESTINAL C
Page 66 and 67:
ENG ET AL colorectal cancer. Indeed
Page 68 and 69:
INVITED ARTICLES BREAST CANCER I Wi
Page 70 and 71:
WILLIAM M. SIKOV gational treatment
Page 72 and 73:
DELUCHE, ONESTI, AND ANDRE Precisio
Page 74 and 75:
DELUCHE, ONESTI, AND ANDRE the path
Page 76 and 77:
DELUCHE, ONESTI, AND ANDRE combine
Page 78 and 79:
SALAMA AND CHMURA Surgery or Ablati
Page 80 and 81:
SALAMA AND CHMURA TABLE 1. Frequenc
Page 82 and 83:
SALAMA AND CHMURA per patient was 8
Page 84 and 85:
SALAMA AND CHMURA 4. Fisher B. Labo
Page 86 and 87:
BREAST CANCER Controversies in Neoa
Page 88 and 89:
WHITE AND DEMICHELE KEY POINTS
Page 90 and 91:
WHITE AND DEMICHELE growing body of
Page 92 and 93:
WHITE AND DEMICHELE signed with app
Page 94 and 95:
BREAST CANCER Individualizing the A
Page 96 and 97:
OLDER WOMEN WITH EARLY-STAGE BREAST
Page 98 and 99:
Page 100 and 101:
Page 102 and 103:
Page 104 and 105:
IMMUNITY IN TRIPLE-NEGATIVE BREAST
Page 106 and 107:
Page 108 and 109:
Page 110 and 111:
MOLECULAR SUBTYPES AND NEW TARGETS
Page 112 and 113:
Page 114 and 115:
Page 116 and 117:
Page 118 and 119:
Page 120 and 121:
ADJUVANT AND NEOADJUVANT THERAPY FO
Page 122 and 123:
Page 124 and 125:
Page 126 and 127:
Page 128 and 129:
CANCER PREVENTION, GENETICS, AND EP
Page 130 and 131:
ADDRESSING BARRIERS TO BREAST CANCE
Page 132 and 133:
Page 134 and 135:
Page 136 and 137:
Page 138 and 139:
DECISION MAKING IN THE CONTEXT OF B
Page 140 and 141:
Page 142 and 143:
Page 144 and 145:
Page 146 and 147:
SCHIFFMAN, FISHER, AND GIBBS econom
Page 148 and 149:
SCHIFFMAN, FISHER, AND GIBBS High-r
Page 150 and 151:
SCHIFFMAN, FISHER, AND GIBBS could
Page 152 and 153:
SCHIFFMAN, FISHER, AND GIBBS due to
Page 154 and 155:
Page 156 and 157:
CAN DIET AND LIFESTYLE PREVENT BREA
Page 158 and 159:
Page 160 and 161:
Page 162 and 163:
Page 164 and 165:
REFORMING THE BUY-AND-BILL CHEMOTHE
Page 166 and 167:
Page 168 and 169:
Page 170 and 171:
CARE DELIVERY AND PRACTICE MANAGEME
Page 172 and 173:
THE PATIENT-CENTERED MEDICAL HOME c
Page 174 and 175:
THE PATIENT-CENTERED MEDICAL HOME F
Page 176 and 177:
THE PATIENT-CENTERED MEDICAL HOME F
Page 178 and 179:
THE PATIENT-CENTERED MEDICAL HOME c
Page 180 and 181:
INTEGRATING ICD-10 IN YOUR PRACTICE
Page 182 and 183:
Page 184 and 185:
Page 186 and 187:
Page 188 and 189:
CENTRAL NERVOUS SYSTEM TUMORS Brain
Page 190 and 191:
AHLUWALIA AND WINKLER TARGETING ANG
Page 192 and 193:
AHLUWALIA AND WINKLER cancer brain
Page 194 and 195:
AHLUWALIA AND WINKLER However, the
Page 196 and 197:
AHLUWALIA AND WINKLER in patients w
Page 198 and 199:
MEHTA AND AHLUWALIA of SRS for brai
Page 200 and 201:
MEHTA AND AHLUWALIA for patients ol
Page 202 and 203:
MEHTA AND AHLUWALIA 14. Atalar B, M
Page 204 and 205:
MAWRIN, CHUNG, AND PREUSSER Biology
Page 206 and 207:
MAWRIN, CHUNG, AND PREUSSER Fibrobl
Page 208 and 209:
MAWRIN, CHUNG, AND PREUSSER grade a
Page 210 and 211:
MAWRIN, CHUNG, AND PREUSSER Disclos
Page 212 and 213:
MAWRIN, CHUNG, AND PREUSSER 72. Sur
Page 214 and 215:
DEVELOPMENTAL THERAPEUTICS AND TRAN
Page 216 and 217:
ESTEVA, MILLER, AND TEICHER TARGETS
Page 218 and 219:
ESTEVA, MILLER, AND TEICHER gle che
Page 220 and 221:
ESTEVA, MILLER, AND TEICHER TABLE 2
Page 222 and 223:
ESTEVA, MILLER, AND TEICHER 21. Ans
Page 224 and 225:
Page 226 and 227:
STUART M. LICHTMAN include a Geriat
Page 228 and 229:
STUART M. LICHTMAN an outcome of ca
Page 230 and 231:
BARRIOS, WERUTSKY, AND MARTINEZ-MES
Page 232 and 233:
Page 234 and 235:
Page 236 and 237:
Page 238 and 239:
Page 240 and 241:
MANDREKAR, DAHLBERG, AND SIMON FIGU
Page 242 and 243:
MANDREKAR, DAHLBERG, AND SIMON FIGU
Page 244 and 245:
MANDREKAR, DAHLBERG, AND SIMON know
Page 246 and 247:
Page 248 and 249:
DIENSTMANN, SALAZAR, AND TABERNERO
Page 250 and 251:
Page 252 and 253:
Page 254 and 255:
Page 256 and 257:
RIMAWI, DE ANGELIS, AND SCHIFF FIGU
Page 258 and 259:
RIMAWI, DE ANGELIS, AND SCHIFF TABL
Page 260 and 261:
RIMAWI, DE ANGELIS, AND SCHIFF tent
Page 262 and 263:
RIMAWI, DE ANGELIS, AND SCHIFF phas
Page 264 and 265:
CHRISTINE M. LOVLY TKIs have been t
Page 266 and 267:
CHRISTINE M. LOVLY EGFR TKIs appear
Page 268 and 269:
CHRISTINE M. LOVLY MAP2K1, which en
Page 270 and 271:
CHRISTINE M. LOVLY patients with ad
Page 272 and 273:
Page 274 and 275:
DAMODARAN, BERGER, AND ROYCHOWDHURY
Page 276 and 277:
Page 278 and 279:
Page 280 and 281:
Page 282 and 283:
ZARDAVAS AND PICCART-GEBHART TABLE
Page 284 and 285:
ZARDAVAS AND PICCART-GEBHART TABLE
Page 286 and 287:
ZARDAVAS AND PICCART-GEBHART triple
Page 288 and 289:
ZARDAVAS AND PICCART-GEBHART mutati
Page 290 and 291:
MICHAEL A. POSTOW Managing Immune C
Page 292 and 293:
MICHAEL A. POSTOW diarrhea symptoms
Page 294 and 295:
MICHAEL A. POSTOW tion. One of thes
Page 296 and 297:
MICHAEL A. POSTOW nitis during ipil
Page 298 and 299:
GASTROINTESTINAL (COLORECTAL) CANCE
Page 300 and 301:
PRECISION THERAPY FOR RECTAL CANCER
Page 302 and 303:
PRECISION THERAPY FOR RECTAL CANCER
Page 304 and 305:
GASTROINTESTINAL (COLORECTAL) CANCE
Page 306 and 307:
MARWAN FAKIH was offset by a detrim
Page 308 and 309:
MARWAN FAKIH TABLE 1. Biologicals i
Page 310 and 311:
MARWAN FAKIH TABLE 3. EGFR Targetin
Page 312 and 313:
MARWAN FAKIH TABLE 6. EGFR Targetin
Page 314 and 315:
MARWAN FAKIH 5-fluorouracil (FOLFIR
Page 316 and 317:
PUNT, SIMKENS, AND KOOPMAN 5-FU/LV
Page 318 and 319:
PUNT, SIMKENS, AND KOOPMAN TABLE 1.
Page 320 and 321:
PUNT, SIMKENS, AND KOOPMAN 35. Veno
Page 322 and 323:
CERCEK, CUSACK, AND RYAN Treatment
Page 324 and 325:
CERCEK, CUSACK, AND RYAN leagues pe
Page 326 and 327:
GASTROINTESTINAL (NONCOLORECTAL) CA
Page 328 and 329:
ABOU-ALFA ET AL sess liver function
Page 330 and 331:
ABOU-ALFA ET AL tinuing liver injur
Page 332 and 333:
ABOU-ALFA ET AL mors including HCC,
Page 334 and 335:
ABOU-ALFA ET AL HCC (Anti-Programme
Page 336 and 337:
AHN ET AL Making Sense of Current a
Page 338 and 339:
AHN ET AL Pancreatic cancer has bee
Page 340 and 341:
AHN ET AL Disclosures of Potential
Page 342 and 343:
Page 344 and 345:
EGIDIO DEL FABBRO tion of precachex
Page 346 and 347:
EGIDIO DEL FABBRO FIGURE 3. Mechani
Page 348 and 349:
EGIDIO DEL FABBRO II RCT of ghrelin
Page 350 and 351:
EGIDIO DEL FABBRO 22. Tan BH, Birds
Page 352 and 353:
Page 354 and 355:
THE SPECTRUM OF NEUROENDOCRINE TUMO
Page 356 and 357:
Page 358 and 359:
Page 360 and 361:
Page 362 and 363:
Page 364 and 365:
Page 366 and 367:
CHALLENGING THE TREATMENT PARADIGM
Page 368 and 369:
Page 370 and 371:
Page 372 and 373:
Page 374 and 375:
Page 376 and 377:
STAGE I TESTICULAR GERM CELL CANCER
Page 378 and 379:
STAGE I TESTICULAR GERM CELL CANCER
Page 380 and 381:
GERM CELL TUMORS: LOOKING TO THE FU
Page 382 and 383:
Page 384 and 385:
Page 386 and 387:
SALVAGE CHEMOTHERAPY Salvage Therap
Page 388 and 389:
SALVAGE CHEMOTHERAPY References 1.
Page 390 and 391:
EARLY CHEMOTHERAPY IN MEN WITH META
Page 392 and 393:
Page 394 and 395:
Page 396 and 397:
Page 398 and 399:
RADIUM 223 AND METASTATIC CASTRATIO
Page 400 and 401:
RADIUM 223 AND METASTATIC CASTRATIO
Page 402 and 403:
IMMUNOTHERAPY FOR PROSTATE TUMORS I
Page 404 and 405:
IMMUNOTHERAPY FOR PROSTATE TUMORS F
Page 406 and 407:
IMMUNOTHERAPY FOR PROSTATE TUMORS T
Page 408 and 409:
IMMUNOTHERAPY FOR PROSTATE TUMORS F
Page 410 and 411:
IMMUNOTHERAPY FOR PROSTATE TUMORS a
Page 412 and 413:
EVOLVING IMMUNOTHERAPY STRATEGIES I
Page 414 and 415:
Page 416 and 417:
Page 418 and 419:
NOVEL IMMUNOTHERAPY AGENTS IN METAS
Page 420 and 421:
Page 422 and 423:
Page 424 and 425:
Page 426 and 427:
PROMISING STRATEGIES IN BLADDER CAN
Page 428 and 429:
Page 430 and 431:
Page 432 and 433:
Page 434 and 435:
GYNECOLOGIC CANCER Cervical Cancer
Page 436 and 437:
MACKAY, WENZEL, AND MILESHKIN In th
Page 438 and 439:
MACKAY, WENZEL, AND MILESHKIN admin
Page 440 and 441:
MACKAY, WENZEL, AND MILESHKIN TABLE
Page 442 and 443:
MACKAY, WENZEL, AND MILESHKIN ing s
Page 444 and 445:
MACKAY, WENZEL, AND MILESHKIN 59. F
Page 446 and 447:
GYNECOLOGIC CANCER Managing Ovarian
Page 448 and 449:
DUSKA, TEW, AND MOORE KEY POINTS A
Page 450 and 451:
DUSKA, TEW, AND MOORE FIGURE 2. Sur
Page 452 and 453:
DUSKA, TEW, AND MOORE FIGURE 3. Che
Page 454 and 455:
DUSKA, TEW, AND MOORE FIGURE 4. Ger
Page 456 and 457:
DUSKA, TEW, AND MOORE 10. Griffıth
Page 458 and 459:
GYNECOLOGIC CANCER Treatment of the
Page 460 and 461:
CHEMOTHERAPY FOR PATIENTS WITH BMOC
Page 462 and 463:
Page 464 and 465:
Page 466 and 467:
Page 468 and 469:
PROGRESS IN HEAD AND NECK SQUAMOUS
Page 470 and 471:
Page 472 and 473:
Page 474 and 475:
HEAD AND NECK CANCER PI3-Kinase: Ge
Page 476 and 477:
ISAACSSON VELHO, CASTRO JR, AND CHU
Page 478 and 479:
Page 480 and 481:
Page 482 and 483:
SHARON H. GIORDANO Comparative Effe
Page 484 and 485:
SHARON H. GIORDANO measured confoun
Page 486 and 487:
SHARON H. GIORDANO These databases
Page 488 and 489:
HEALTH SERVICES RESEARCH AND QUALIT
Page 490 and 491:
INDUSTRY AND ONCOLOGY KEY POINTS F
Page 492 and 493: INDUSTRY AND ONCOLOGY has been “l
Page 494 and 495: INDUSTRY AND ONCOLOGY by (covered)
Page 496 and 497: INDUSTRY AND ONCOLOGY 42. World Hea
Page 498 and 499: CANCER CARE QUALITY: CURRENT STATE
Page 504 and 505: MANAGING OLDER PATIENTS WITH ALL Th
Page 506 and 507: MANAGING OLDER PATIENTS WITH ALL TA
Page 508 and 509: MANAGING OLDER PATIENTS WITH ALL FI
Page 510 and 511: MANAGING OLDER PATIENTS WITH ALL FI
Page 512 and 513: MANAGING OLDER PATIENTS WITH ALL ra
Page 514 and 515: TREATMENT OF PHILADELPHIA CHROMOSOM
Page 522 and 523: CD19 CAR THERAPY FOR ALL FIGURE 1.
Page 524 and 525: CD19 CAR THERAPY FOR ALL 5. Zhou G,
Page 526 and 527: NEW TARGETED THERAPIES FOR iNHL New
Page 528 and 529: NEW TARGETED THERAPIES FOR iNHL TAB
Page 534 and 535: NEW TARGETED THERAPIES FOR iNHL a P
Page 536 and 537: HEMATOPOIETIC CELL TRANSPLANTATION
Page 544 and 545: MICHAEL W. DEININGER TABLE 1. Defin
Page 546 and 547: MICHAEL W. DEININGER the ATP-bindin
Page 548 and 549: MICHAEL W. DEININGER broad range ef
Page 550 and 551: MICHAEL W. DEININGER 30. Hughes T,
Page 552 and 553: PEMMARAJU AND MOLITERNO TABLE 1. Ac
Page 554 and 555: PEMMARAJU AND MOLITERNO drome (BCS)
Page 556 and 557: PEMMARAJU AND MOLITERNO 13. Xing S,
Page 558 and 559: THERAPIES AND INDICATIONS FOR PH-NE
Page 566 and 567: LEUKEMIA, MYELODYSPLASIA, AND TRANS
Page 568 and 569: RECENT UPDATES IN MDS AND MDS/MPNS
Page 582 and 583: LUNG CANCER Beyond Second-Line Trea
Page 584 and 585: BEYOND SECOND-LINE TREATMENT FOR LU
Page 586 and 587: BEYOND SECOND-LINE TREATMENT FOR LU
Page 588 and 589: LUNG CANCER New Therapies for Histo
Page 590 and 591: GERBER, PAIK, AND DOWLATI a tumor t
Page 592 and 593:
GERBER, PAIK, AND DOWLATI squamous
Page 594 and 595:
GERBER, PAIK, AND DOWLATI FIGURE 2.
Page 596 and 597:
GERBER, PAIK, AND DOWLATI TABLE 1.
Page 598 and 599:
GERBER, PAIK, AND DOWLATI gression
Page 600 and 601:
GERBER, PAIK, AND DOWLATI Disclosur
Page 602 and 603:
GERBER, PAIK, AND DOWLATI enzyme in
Page 604 and 605:
GERBER, PAIK, AND DOWLATI receptor
Page 606 and 607:
LILENBAUM, LEIGHL, AND NEUBAUER Exp
Page 608 and 609:
LILENBAUM, LEIGHL, AND NEUBAUER tha
Page 610 and 611:
LILENBAUM, LEIGHL, AND NEUBAUER Ref
Page 612 and 613:
BERNARDO H.L. GOULART The Value of
Page 614 and 615:
BERNARDO H.L. GOULART TABLE 1. Expe
Page 616 and 617:
BERNARDO H.L. GOULART every 6 month
Page 618 and 619:
BERNARDO H.L. GOULART lung-cancer/l
Page 620 and 621:
LUNG CANCER Updates in the Multimod
Page 622 and 623:
WOODARD AND JABLONS section, becaus
Page 624 and 625:
WOODARD AND JABLONS mediastinum is
Page 626 and 627:
WOODARD AND JABLONS FIGURE 1. Molec
Page 628 and 629:
NASSER HANNA Current Standards and
Page 630 and 631:
NASSER HANNA At the 2014 ASCO Annua
Page 632 and 633:
NASSER HANNA culty of this task. Va
Page 634 and 635:
LYMPHOMA AND PLASMA CELL DISORDERS
Page 636 and 637:
NOWAKOWSKI AND CZUCZMAN sociated wi
Page 638 and 639:
NOWAKOWSKI AND CZUCZMAN trial is in
Page 640 and 641:
NOWAKOWSKI AND CZUCZMAN TABLE 2. DH
Page 642 and 643:
NOWAKOWSKI AND CZUCZMAN 15. Aragon-
Page 644 and 645:
DAVID W. SCOTT Cell-of-Origin in Di
Page 646 and 647:
DAVID W. SCOTT FIGURE 1. The Origin
Page 648 and 649:
DAVID W. SCOTT FIGURE 2. Immunohist
Page 650 and 651:
DAVID W. SCOTT FIGURE 3. The Lymph2
Page 652 and 653:
DAVID W. SCOTT 10. Shaffer AL 3rd,
Page 654 and 655:
CHEAH, OKI, AND FANALE Novel Treatm
Page 656 and 657:
CHEAH, OKI, AND FANALE an ongoing G
Page 658 and 659:
CHEAH, OKI, AND FANALE a similar me
Page 660 and 661:
CHEAH, OKI, AND FANALE TABLE 3. Sel
Page 662 and 663:
CHEAH, OKI, AND FANALE eral T cell
Page 664 and 665:
CHEAH, OKI, AND FANALE 77. Cairns R
Page 666 and 667:
STEPHEN ANSELL associated with pati
Page 668 and 669:
STEPHEN ANSELL Disclosures of Poten
Page 670 and 671:
MATEOS AND SAN MIGUEL Smoldering Mu
Page 672 and 673:
MATEOS AND SAN MIGUEL years. This f
Page 674 and 675:
MATEOS AND SAN MIGUEL previously me
Page 676 and 677:
MATEOS AND SAN MIGUEL TABLE 2. Risk
Page 678 and 679:
MATEOS AND SAN MIGUEL 30. Rajkumar
Page 680 and 681:
BHUTANI, LANDGREN, AND USMANI of th
Page 682 and 683:
BHUTANI, LANDGREN, AND USMANI bette
Page 684 and 685:
BHUTANI, LANDGREN, AND USMANI fıne
Page 686 and 687:
BHUTANI, LANDGREN, AND USMANI FIGUR
Page 688 and 689:
BHUTANI, LANDGREN, AND USMANI 15. K
Page 690 and 691:
MOREAU AND TOUZEAU Multiple Myeloma
Page 692 and 693:
MOREAU AND TOUZEAU other effıcacy
Page 694 and 695:
MOREAU AND TOUZEAU was able to indu
Page 696 and 697:
MOREAU AND TOUZEAU Group consensus
Page 698 and 699:
LYMPHOMA AND PLASMA CELL DISORDERS
Page 700 and 701:
MANAGEMENT OF CLL Up-Front Manageme
Page 702 and 703:
MANAGEMENT OF CLL than 17p-/TP53mut
Page 704 and 705:
MANAGEMENT OF CLL could be associat
Page 706 and 707:
MANAGEMENT OF CLL tion by nonmalign
Page 708 and 709:
MANAGEMENT OF CLL fludarabine and c
Page 710 and 711:
MANAGEMENT OF CLL lymphocytic leuke
Page 712 and 713:
PROGNOSTIC FACTORS AND ADJUVANT RAD
Page 714 and 715:
Page 716 and 717:
Page 718 and 719:
MERKEL CELL CARCINOMA Merkel Cell C
Page 720 and 721:
MERKEL CELL CARCINOMA tions in PIK3
Page 722 and 723:
MERKEL CELL CARCINOMA treating MCC
Page 724 and 725:
MERKEL CELL CARCINOMA 32. Leonard J
Page 726 and 727:
MELANOMA/SKIN CANCERS Locoregional
Page 728 and 729:
PERFUSION AND INFUSION IN THE ERA O
Page 730 and 731:
Page 732 and 733:
Page 734 and 735:
NEOADJUVANT THERAPY OF MELANOMA Neo
Page 736 and 737:
NEOADJUVANT THERAPY OF MELANOMA TAB
Page 738 and 739:
NEOADJUVANT THERAPY OF MELANOMA ity
Page 740 and 741:
NEOADJUVANT THERAPY OF MELANOMA 4.
Page 742 and 743:
MELANOMA/SKIN CANCERS Targeted Mole
Page 744 and 745:
SULLIVAN ET AL FIGURE 1. Relevant S
Page 746 and 747:
SULLIVAN ET AL Resistance to BRAF i
Page 748 and 749:
SULLIVAN ET AL TABLE 1. Clinical Tr
Page 750 and 751:
SULLIVAN ET AL 17. Halait H, Demart
Page 752 and 753:
SULLIVAN ET AL NRAS-mutant melanoma
Page 754 and 755:
KLEPIN, RODIN, AND HURRIA Treating
Page 756 and 757:
KLEPIN, RODIN, AND HURRIA plication
Page 758 and 759:
KLEPIN, RODIN, AND HURRIA plan was
Page 760 and 761:
KLEPIN, RODIN, AND HURRIA patient-s
Page 762 and 763:
KLEPIN, RODIN, AND HURRIA 62. Blanc
Page 764 and 765:
PERIPHERAL NEUROTOXICITY IN CANCER
Page 766 and 767:
Page 768 and 769:
Page 770 and 771:
Page 772 and 773:
PARTRIDGE, JACOBSEN, AND ANDERSEN C
Page 774 and 775:
PARTRIDGE, JACOBSEN, AND ANDERSEN c
Page 776 and 777:
PARTRIDGE, JACOBSEN, AND ANDERSEN w
Page 778 and 779:
PARTRIDGE, JACOBSEN, AND ANDERSEN v
Page 780 and 781:
LESLIE R. SCHOVER Sexual Healing in
Page 782 and 783:
LESLIE R. SCHOVER tinuous ADT in pr
Page 784 and 785:
LESLIE R. SCHOVER 12. Potosky AL, H
Page 786 and 787:
CATHERINE H. VAN POZNAK TABLE 1. Wo
Page 788 and 789:
CATHERINE H. VAN POZNAK (tamoxifen,
Page 790 and 791:
CATHERINE H. VAN POZNAK TABLE 3. FD
Page 792 and 793:
CATHERINE H. VAN POZNAK premenopaus
Page 794 and 795:
SHARI GOLDFARB KEY POINTS Brea
Page 796 and 797:
SHARI GOLDFARB and friction with va
Page 798 and 799:
SHARI GOLDFARB importance both duri
Page 800 and 801:
PATIENT AND SURVIVOR CARE Moving Su
Page 802 and 803:
MAYER ET AL TABLE 1. Quality Metric
Page 804 and 805:
MAYER ET AL to enhance the quality
Page 806 and 807:
MAYER ET AL FIGURE 2. (A) Infertili
Page 808 and 809:
MAYER ET AL efıcial suggests that
Page 810 and 811:
PATIENT AND SURVIVOR CARE The Chall
Page 812 and 813:
BRUERA AND PAICE Choice of Opioid a
Page 814 and 815:
BRUERA AND PAICE toxicity and proce
Page 816 and 817:
BRUERA AND PAICE effective. Basic s
Page 818 and 819:
PEDIATRIC ONCOLOGY Real-Time Molecu
Page 820 and 821:
CARROLL, RAETZ, AND MEYER KEY POINT
Page 822 and 823:
CARROLL, RAETZ, AND MEYER most are
Page 824 and 825:
CARROLL, RAETZ, AND MEYER markers a
Page 826 and 827:
PEDIATRIC ONCOLOGY Translating Surv
Page 828 and 829:
REDUCING THE BURDEN OF LATE EFFECTS
Page 830 and 831:
Page 832 and 833:
Page 834 and 835:
Page 836 and 837:
PROFESSIONAL DEVELOPMENT The Challe
Page 838 and 839:
ADVANCES IN WEBSITE INFORMATION RES
Page 840 and 841:
Page 842 and 843:
Page 844 and 845:
Page 846 and 847:
COMMUNICATION AND TECHNOLOGY: IT’
Page 848 and 849:
Page 850 and 851:
Page 852 and 853:
PATIENT-REPORTED OUTCOMES IN ONCOLO
Page 854 and 855:
PATIENT-REPORTED OUTCOMES IN ONCOLO
Page 856 and 857:
PROFESSIONAL DEVELOPMENT Trends, An
Page 858 and 859:
CLINICAL ONCOLOGY PRACTICE 2015 FIG
Page 860 and 861:
CLINICAL ONCOLOGY PRACTICE 2015 (6.
Page 862 and 863:
CLINICAL ONCOLOGY PRACTICE 2015 Pro
Page 864 and 865:
ADJUVANT/NEOADJUVANT MEDICAL THERAP
Page 866 and 867:
Page 868 and 869:
Page 870 and 871:
INDICATIONS FOR ADJUVANT RADIATION
Page 872 and 873:
Page 874 and 875:
Page 876 and 877:
Page 878 and 879:
SARCOMA Latest Advances in Systemic
Page 880 and 881:
SYSTEMIC THERAPY FOR OSTEOSARCOMA A
Page 882 and 883:
SYSTEMIC THERAPY FOR OSTEOSARCOMA A
Page 884 and 885:
RETHINKING TREATMENT FOR CHONDROSAR
Page 886 and 887:
Page 888 and 889:
Page 890 and 891:
Page 892 and 893:
BONE SARCOMAS IN ADULTS local disea
Page 894 and 895:
BONE SARCOMAS IN ADULTS structure a
Page 896 and 897:
SARCOMA Well-Differentiated and Ded
Page 898 and 899:
ABBAS MANJI ET AL ticular region. 7
Page 900 and 901:
ABBAS MANJI ET AL MYXOID (ROUND CEL
Page 902 and 903:
ABBAS MANJI ET AL versus doxorubici
Page 904 and 905:
SHLUSH AND HERSHKOVITZ Clonal Evolu
Page 906 and 907:
SHLUSH AND HERSHKOVITZ FIGURE 1. Ti
Page 908 and 909:
TUMOR BIOLOGY New Strategies to Und
Page 910 and 911:
KNAPP, DHAWAN, AND OSTRANDER in dog
Page 912 and 913:
KNAPP, DHAWAN, AND OSTRANDER TABLE
Page 914 and 915:
KNAPP, DHAWAN, AND OSTRANDER 14. Fe
Page 916 and 917:
SOURBIER, SRINIVASAN, AND LINEHAN M
Page 918 and 919:
SOURBIER, SRINIVASAN, AND LINEHAN F
Page 920 and 921:
SOURBIER, SRINIVASAN, AND LINEHAN T
Page 922:
Author Index Abbas Manji, Gulam ...
show all

NcXHF

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

Delete template?

Save as template?