2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

More documents

Recommendations

Info

continue this randomization based on the different biology of BCP and T-ALL (the reason that the question was asked separately in two parallel trials in the first place). Interestingly, the best reported contemporary results in pediatric T-ALL come from the UKALL 2003 trial, which used essentially a COG ABFM backbone regimen with Capizzi MTX plus asparaginase during IM. 22 The second randomization in AALL0434 is to receive versus not receive six 5-day courses of nelarabine during the first �16 months of therapy. Nelarabine, a prodrug of ara-G, showed substantial clinical activity in phase I/II T-ALL trials, but was associated with significant, often severe, and sometimes fatal CNS toxicity. 23,24 The COG then conducted a pilot study of nelarabine plus BFM-86 type chemotherapy in children with newly diagnosed T-ALL and found encouraging activity but much lower rates of overall and severe toxicity than had been seen in relapsed patients treated in the phase I/II trials. 25 AALL0434 included a pilot safety phase during which only an HR subset of T-ALL patients with a poor response was randomly selected to be treated with/without nelarabine. This safety phase was concluded with no significant differences in toxicity among the patients treated with/without nelarabine, and AALL0434 is now in the efficacy phase in which �90% of patients are randomly selected to be treated with/without nelarabine (all except for a tightly defined low-risk patient subset). 26 VHR ALL A small subset of pediatric ALL patients can be defined as being at very high risk (VHR) of relapse. The definition of this subgroup is constantly evolving, but there is a general consensus that alternative treatment strategies may be indicated for these patients in comparison with treatment given to other patients with HR ALL. As discussed above, the BFM group has termed this group HR and uses intensive multiagent chemotherapy HR blocks, an additional protocol II for these patients, with hematopoietic stem cell transplant (HSCT) in CR1 for the subset with a poor treatment response at end of protocol Ib. The COG AALL0031 pilot study (2002 to 2006) tested an intensive multiagent chemotherapy regimen in children with VHR ALL, which included Ph-positive ALL, hypodiploidy (chromosome number less than 44), poor response to induction therapy (more than 25% marrow blasts at day 29 or 5% to 25% marrow blasts/more than 1% MRD at day 43 after 2 weeks of extended induction therapy), or MLL translocation and an SER (more than 5% blasts at day 15 of induction). 9,27 The results were encouraging for patients with Ph-negative VHR ALL, with a nonsignificant trend toward improved outcome for those treated with HSCT. 27 The study design with all patients receiving identical chemotherapy and those with Ph-positive ALL also receiving imatinib facilitated assessment of imatinib toxicity. Notably, the addition of imatinib was quite safe and did not lead to increased toxicity. 9 More importantly, adding imatinib led to major improvements in early 614 outcome for patients with Ph-positive ALL, with a 3-year EFS rate of 80% � 11% (95% CI, 64% to 90%), which was more than twice that of historic controls treated in the preimatinib era (35% � 4%; p � 0.0001). There was no apparent advantage to HSCT as compared with intensive chemotherapy plus imatinib. These results have been stable with longer follow-up 28 and have led to changes in clinical practice in treatment of children with Ph-positive ALL. The COG has now completed enrollment (2008 to 2012) on a successor Ph-positive ALL trial (AALL0622) that utilized the AALL0031 chemotherapy backbone with imatinib replaced with dasatinib, a more potent second-generation Abl TKI. The study showed that it was safe to add continuous dasatinib treatment (60 mg/m 2 /day) to this intensive chemotherapy regimen; it is still much too early to assess treatment efficacy. In 2012, the COG and European EsPhALL groups will commence enrollment on a joint pilot study (developed in conjunction with Bristol Myers Squibb) that will test the safety and efficacy of dasatinib added to the BFM HR treatment backbone, which has lower cumulative doses of many chemotherapy agents than the AALL0031 regimen. Future Perspectives STEPHEN P. HUNGER The substantial improvements that have occurred in outcome for pediatric HR ALL over the past few decades have been accompanied by recognition that there are a number of different ALL subsets that come under the umbrella term HR ALL. For some subsets, outcomes have been improved by optimizing delivery of chemotherapy agents that have been in widespread clinical use for the past 25 years, as exemplified by the results of COG AALL0232. For other subsets, such as Ph-positive ALL, optimizing traditional cytotoxic chemotherapy agents led to limited improvements in outcome, 29 but introduction of new and/or targeted therapies had a major effect on outcome. 9 It is expected that ongoing genomic studies will lead to recognition of additional VHR ALL subsets defined by the presence of specific sentinel genomic lesions that can potentially be targeted by novel therapies. 30 The rarity of these and other VHR ALL subsets will require increased collaborations between North American and Western European investigators in order to test the efficacy of novel/targeted therapies in these patient subsets. Acknowledgments The author dedicates this manuscript to the memory of Jim Nachman, who passed away unexpectedly, and far too early, in 2011. Jim developed the ABFM regimen; played a major role in developing productive, fruitful interactions between the CCG/ COG and BFM groups; and shaped the design of most COG ALL trials of the past 25 years. He was widely recognized as an international leader in pediatric oncology clinical research and as a mentor to many investigators. The author and the rest of the pediatric oncology community miss his advice, his infectious enthusiasm, his laugh and politically incorrect sense of humor, and most of all his friendship.
ABFM THERAPY FOR PEDIATRIC ALL Author’s Disclosures of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role Stephen P. Hunger Bristol-Myers Squibb (U); Genzyme (U) 1. Ries LA, Smith MA, Gurney JG, et al (eds). Cancer Incidence and Survival among Children and Adolescents: United States SEER Program 1975-1995. Bethesda, MD: National Cancer Institute; 1999. 2. Hunger SP, Lu X, Devidas M, et al. Improved survival for children and adolescents from 1990-2005: a report from the Children’s Oncology Group. J Clin Oncol. In press. 3. Schultz KR, Pullen DJ, Sather HN, et al. Risk- and response-based classification of childhood B-precursor acute lymphoblastic leukemia: a combined analysis of prognostic markers from the Pediatric Oncology Group (POG) and Children’s Cancer Group (CCG). Blood. 2007;109:926-935. 4. Smith M, Arthur D, Camitta B, et al. Uniform approach to risk classification and treatment assignment for children with acute lymphoblastic leukemia. J Clin Oncol. 1996;14:18-24. 5. Borowitz MJ, Devidas M, Hunger SP, et al. Clinical significance of minimal residual disease in childhood acute lymphoblastic leukemia and its relationship to other prognostic factors: a Children’s Oncology Group study. Blood. 2008;111:5477-5485. 6. Conter V, Bartram CR, Valsecchi MG, et al. Molecular response to treatment redefines all prognostic factors in children and adolescents with B-cell precursor acute lymphoblastic leukemia: results in 3184 patients of the AIEOP-BFM ALL 2000 study. Blood. 2010;115:3206-3214. 7. Nachman JB, Sather HN, Sensel MG, et al. Augmented post-induction therapy for children with high-risk acute lymphoblastic leukemia and a slow response to initial therapy. N Engl J Med. 1998;338:1663-1671. 8. Riehm H, Gadner H, Welte K. The West-Berlin therapy study of acute lymphoblastic leukemia in childhood—report after 6 years (author’s transl). Klin Padiatr. 1977;189:89-102. 9. Schultz KR, Bowman WP, Aledo A, et al. Improved early event-free survival with imatinib in Philadelphia chromosome-positive acute lymphoblastic leukemia: a Children’s Oncology Group study. J Clin Oncol. 2009;27: 5175-5181. 10. Henze G, Langermann HJ, Bramswig J, et al. The BFM 76/79 acute lymphoblastic leukemia therapy study (author’s transl). Klin Padiatr. 1981; 193:145-154. 11. Conter V, Valsecchi MG, Silvestri D, et al. Pulses of vincristine and dexamethasone in addition to intensive chemotherapy for children with intermediate-risk acute lymphoblastic leukaemia: a multicentre randomised trial. Lancet. 2007;369:123-131. 12. Stanulla M, Schrappe M. Treatment of childhood acute lymphoblastic leukemia. Semin Hematol. 2009;46:52-63. 13. Tubergen DG, Gilchrist GS, O’Brien RT, et al. Improved outcome with delayed intensification for children with acute lymphoblastic leukemia and intermediate presenting features: a Childrens Cancer Group phase III trial. J Clin Oncol. 1993;11:527-537. 14. Hunger SP, Winick NJ, Sather HN, et al. Therapy of low-risk subsets of childhood acute lymphoblastic leukemia: when do we say enough? Pediatr Blood Cancer. 2005;45:876-880. 15. Bostrom BC, Sensel MR, Sather HN, et al. Dexamethasone versus prednisone and daily oral versus weekly intravenous mercaptopurine for patients with standard-risk acute lymphoblastic leukemia: a report from the Children’s Cancer Group. Blood. 2003;101:3809-3817. 16. Matloub Y, Bostrom BC, Hunger SP, et al. Escalating intravenous methotrexate improves event-free survival in children with standard-risk acute lymphoblastic leukemia: a report for the Children’s Oncology Group. Blood. 2011;118:243-251. Stock Ownership Honoraria Amgen (B); Bristol-Myers Squibb (I); Merck (B); Pfizer (B) REFERENCES Research Funding Expert Testimony Bristol-Myers Squibb; Genzyme (U) Other Remuneration 17. Gaynon PS, Steinherz PG, Bleyer WA, et al. Improved therapy for children with acute lymphoblastic leukemia and unfavorable presenting features: a follow-up report of the Childrens Cancer Group Study CCG-106. J Clin Oncol. 1993;11:2234-2242. 18. Gaynon PS, Desai AA, Bostrom BC, et al. Early response to therapy and outcome in childhood acute lymphoblastic leukemia: a review. Cancer. 1997; 80:1717-1726. 19. Seibel NL, Steinherz PG, Sather HN, et al. Early postinduction intensification therapy improves survival for children and adolescents with highrisk acute lymphoblastic leukemia: a report from the Children’s Oncology Group. Blood. 2008;111:2548-2555. 20. Larsen EC, Salzer WL, Devidas M, et al. Comparison of high-dose methotrexate (HD-MTX) with Capizzi methotrexate plus asparaginase (C- MTX/ASNase) in children and young adults with high-risk acute lymphoblastic leukemia (HR-ALL): a report from the Children’s Oncology Group study AALL0232. J Clin Oncol. 2011;29:6s (suppl; abstr 3). 21. Winick NJ, Salzer WL, Devidas M, et al. Dexamethasone (DEX) versus prednisone (PRED) during induction for children with high risk acute lymphoblastic leukemia (HR-ALL): a report from the Children’s Oncology Group study AALL0232. J Clin Oncol 2011;29:586s (suppl; abstr 9504). 22. Vora A, Wade R, Mitchell CD, et al. Improved outcome for children and young adults with T-cell acute lymphoblastic leukaemia (ALL): results of the United Kingdome Medical Research Council (MRC) Trial UKALL 2003. Blood (ASH Annual Meeting Abstracts). 2008;112:908. 23. Kurtzberg J, Ernst TJ, Keating MJ, et al. Phase I study of 506U78 administered on a consecutive 5-day schedule in children and adults with refractory hematologic malignancies. J Clin Oncol. 2005;23:3396-3403. 24. Berg SL, Blaney SM, Devidas M, et al. Phase II study of nelarabine (compound 506U78) in children and young adults with refractory T-cell malignancies: a report from the Children’s Oncology Group. J Clin Oncol. 2005;23:3376-3382. 25. Dunsmore K, Devidas M, Borowitz MJ, et al. Nelarabine in combination with intensive modified BFM AALL00P2: a pilot study for the treatment of high-risk T-ALL a report from the Children’s Oncology Group. J Clin Oncol. 2008;26:539s (suppl; abstr 10002). 26. Winter SS, Devidas M, Wood BL, et al. Nelerabine may be safely incorporated into a phase III study for newly diagnosed T-lineage acute lymphoblastic leukemia: a report from the Children’s Oncology Group. Blood (ASH Annual Meeting Abstracts). 2010;116:865a. 27. Schultz KR, Bowman WP, Slayton WB, et al. Philadelphia chromosome negative (Ph-) very high risk (VHR) acute lymphoblastic leukemia (ALL) in children and adolescents: the impact of intensified chemotherapy on early event free survival (EFS) in Children’s Oncology Group study AALL0031. Blood (ASH Annual Meeting Abstracts). 2008;112:911. 28. Schultz KR, Bowman WP, Aledo A, et al. Continuous dosing imatinib with intensive chemotherapy gives equivalent outcomes to allogeneic BMT for Philadelphia chromosome-positive (Ph�) acute lymphoblastic leukemia (ALL) with longer term follow up: Updated results of Children’s Oncology Group (COG) AALL0031. Pediatr Blood Cancer. 2010;54:788. 29. Aricò M, Schrappe M, Hunger SP, et al. Clinical outcome of children with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leukemia treated between 1995 and 2005. J Clin Oncol. 2010;28:4755-4761. 30. Hunger SP, Raetz EA, Loh ML, et al. Improving outcomes for high-risk ALL: translating new discoveries into clinical care. Pediatr Blood Cancer. 2001;56:984-993. 615
Page 1 and 2:
AMERICAN SOCIETY OF CLINICAL ONCOLO
Page 3 and 4:
American Society of Clinical Oncolo
Page 5 and 6:
American Society of Clinical Oncolo
Page 7 and 8:
New Looks and Challenges for Cooper
Page 9 and 10:
Genitourinary Cancer Best Use of Im
Page 11 and 12:
Research and Standard of Care: Lung
Page 13 and 14:
Practice Management and Information
Page 15 and 16:
2012 ASCO Annual Meeting Disclosure
Page 17 and 18:
Matti S. Aapro, MD Clinique De Geno
Page 19 and 20:
Hedy Lee Kindler, MD The University
Page 21 and 22:
Douglas E. Wood, MD University of W
Page 23 and 24:
Mary Lou Smith, JD, MBA Research Ad
Page 25 and 26:
ASCO and Conquer Cancer Foundation
Page 27 and 28:
Letter from the Editor The theme of
Page 29 and 30:
Adjuvant Therapy for Older Women wi
Page 31 and 32:
TREATMENT FOR OLDER WOMEN WITH BREA
Page 33 and 34:
Page 35 and 36:
Page 37 and 38:
MANAGEMENT OF T1 BREAST CANCERS the
Page 39 and 40:
MANAGEMENT OF T1 BREAST CANCERS Tab
Page 41 and 42:
MANAGEMENT OF T1 BREAST CANCERS Tab
Page 43 and 44:
MANAGEMENT OF T1 BREAST CANCERS 93.
Page 45 and 46:
MANAGEMENT OF T1 BREAST CANCERS 1 c
Page 47 and 48:
ADJUVANT ENDOCRINE THERAPY reductio
Page 49 and 50:
ADJUVANT ENDOCRINE THERAPY which ra
Page 51 and 52:
ADJUVANT ENDOCRINE THERAPY assay is
Page 53 and 54:
A DICKENS TALE OF THE TREATMENT OF
Page 55 and 56:
TREATMENT OF ADVANCED BREAST CANCER
Page 57 and 58:
Page 59 and 60:
Page 61 and 62:
Page 63 and 64:
Page 65 and 66:
A FRESH LOOK AT DUCTAL CARCINOMA IN
Page 67 and 68:
DCIS: OPPORTUNITIES AND UNCHARTED W
Page 69 and 70:
DCIS: OPPORTUNITIES AND UNCHARTED W
Page 71 and 72:
Ductal Carcinoma In Situ, and the I
Page 73 and 74:
DCIS AND INFLUENCE OF RISK FACTORS
Page 75 and 76:
KEY QUESTIONS IN THE LOCO-REGIONAL
Page 77 and 78:
POSTMASTECTOMY RADIATION AND PARTIA
Page 79 and 80:
The Appropriate Extent of Surgery f
Page 81 and 82:
SURGERY FOR EARLY-STAGE BREAST CANC
Page 83 and 84:
BIOLOGY AND LOCAL THERAPY DECISIONS
Page 85 and 86:
Clinical and Imaging Surveillance F
Page 87 and 88:
SURVEILLANCE FOLLOWING BREAST CANCE
Page 89 and 90:
SURVEILLANCE FOLLOWING BREAST CANCE
Page 91 and 92:
Advanced Imaging Techniques for the
Page 93 and 94:
IMAGING TECHNIQUES FOR BREAST CANCE
Page 95 and 96:
IMAGING TECHNIQUES FOR BREAST CANCE
Page 97 and 98:
Update of the Oxford Overview: New
Page 99 and 100:
UPDATE OF THE OXFORD OVERVIEW Fig.
Page 101 and 102:
Page 103 and 104:
Page 105 and 106:
UPDATE OF THE OXFORD OVERVIEW Overv
Page 107 and 108:
Gene Patents and Personalized Medic
Page 109 and 110:
GENE PATENTS AND EFFECTS ON PERSONA
Page 111 and 112:
Chemoprevention for Breast Cancer:
Page 113 and 114:
CHEMOPREVENTION FOR BREAST CANCER T
Page 115 and 116:
CHEMOPREVENTION FOR BREAST CANCER C
Page 117 and 118:
CONTROVERSIES IN PROSTATE CANCER: P
Page 119 and 120:
PROSTATE CANCER RISK REDUCTION men
Page 121 and 122:
PROSTATE CANCER RISK REDUCTION Auth
Page 123 and 124:
PSA SCREENING: HARMS WITHOUT CLEAR
Page 125 and 126:
PSA SCREENING: HARMS WITHOUT CLEAR
Page 127 and 128:
GLIOBLASTOMA: TAKING THE STANDARD O
Page 129 and 130:
GLIOBLASTOMA: BIOLOGY, GENETICS AND
Page 131 and 132:
Page 133 and 134:
Page 135 and 136:
FUTURE DIRECTIONS IN GBM THERAPY pr
Page 137 and 138:
FUTURE DIRECTIONS IN GBM THERAPY Ch
Page 139 and 140:
ESTABLISHING TREATMENTS FOR GLIOBLA
Page 141 and 142:
Page 143 and 144:
Page 145 and 146:
Current Concepts in Brain Tumor Ima
Page 147 and 148:
CONCEPTS IN BRAIN TUMOR IMAGING tum
Page 149 and 150:
CONCEPTS IN BRAIN TUMOR IMAGING Aut
Page 151 and 152:
PERSPECTIVES ON HEADLINE-MAKING NEW
Page 153 and 154:
TTF THERAPY IN GLIOBLASTOMA Fig. 1.
Page 155 and 156:
TTF THERAPY IN GLIOBLASTOMA istics.
Page 157 and 158:
TTF THERAPY IN GLIOBLASTOMA because
Page 159 and 160:
Limitations of Adaptive Clinical Tr
Page 161 and 162:
LIMITATIONS OF ADAPTIVE CLINICAL TR
Page 163 and 164:
LIMITATIONS OF ADAPTIVE CLINICAL TR
Page 165 and 166:
Capturing the Patient Perspective:
Page 167 and 168:
PATIENT-REPORTED OUTCOMES AS TRIAL
Page 169 and 170:
PATIENT-REPORTED OUTCOMES AS TRIAL
Page 171 and 172:
NEW LOOKS AND CHALLENGES FOR COOPER
Page 173 and 174:
NCI NATIONAL CLINICAL TRIALS NETWOR
Page 175 and 176:
Successful Integration of Cooperati
Page 177 and 178:
COG: GIVING NEW MEANING TO COOPERAT
Page 179 and 180:
A Critical Review of the Enrollment
Page 181 and 182:
BLACK PATIENTS AND CANCER CLINICAL
Page 183 and 184:
BLACK PATIENTS AND CANCER CLINICAL
Page 185 and 186:
Trastuzumab Emtansine (T-DM1): Hitc
Page 187 and 188:
T-DM1 AND THERAPEUTIC ANTIBODIES ag
Page 189 and 190:
TARGETING CD30 IN HODGKIN LYMPHOMA
Page 191 and 192:
TARGETING CD30 IN HODGKIN LYMPHOMA
Page 193 and 194:
EARLY DRUG DEVELOPMENT: CASTING A W
Page 195 and 196:
Table 1. Response Rates in Expanded
Page 197 and 198:
Drug Development in the Era of Pers
Page 199 and 200:
that the core pathway is not comple
Page 201 and 202:
This situation is not surprising, g
Page 203 and 204:
Practical Management of Immune-Rela
Page 205 and 206:
the anterior pituitary axis is invo
Page 207 and 208:
TARGETING CRITICAL MOLECULAR ABERRA
Page 209 and 210:
Abl suppression; and 3) the early e
Page 211 and 212:
50% 50% 100% Change in Tumor Size m
Page 213 and 214:
vanced solid tumors, even if they a
Page 215 and 216:
Targeting Molecular Aberrations in
Page 217 and 218:
date. With the advent of gene expre
Page 219 and 220:
consortium to facilitate the testin
Page 221 and 222:
ETHICAL CHALLENGES OF HEALTH CARE R
Page 223 and 224:
HEALTH CARE REFORM AND ONCOLOGY dev
Page 225 and 226:
HEALTH CARE REFORM AND ONCOLOGY aut
Page 227 and 228:
INTERNATIONAL VARIATION IN UNDERSTA
Page 229 and 230:
midcareer physician; in one cross-s
Page 231 and 232:
Table 1. Recommendations for Person
Page 233 and 234:
stances (e.g., stage of career, fam
Page 235 and 236:
elationship” is also acknowledged
Page 237 and 238:
Conclusion In more individualistic
Page 239 and 240:
The Oncologist’s Duty to Provide
Page 241 and 242:
an external observer, but to the pe
Page 243 and 244:
MEDICAL ERRORS IN CANCER CARE: PREV
Page 245 and 246:
DISCLOSING MEDICAL ERRORS Disclosur
Page 247 and 248:
DISCLOSING MEDICAL ERRORS Author’
Page 249 and 250:
PREVENTING MEDICAL ERRORS more diff
Page 251 and 252:
“PERSONALIZED” ONCOLOGY FOR COL
Page 253 and 254:
0.001), progression-free survival (
Page 255 and 256:
mately 40% of patients with colorec
Page 257 and 258:
Table 1. Tumor Marker Utility Gradi
Page 259 and 260:
treatment (tx) for metastatic color
Page 261 and 262:
The Interventional Radiologist Role
Page 263 and 264:
effect. The most common drug that h
Page 265 and 266:
gone forever, no further therapy is
Page 267 and 268:
is irrelevant if it is already rese
Page 269 and 270:
Resection and Thermal Ablation of L
Page 271 and 272:
Author’s Disclosures of Potential
Page 273 and 274:
Minimally Invasive Surgery of Recta
Page 275 and 276:
outcomes; local, wound-site, and di
Page 277 and 278:
Authors’ Disclosures of Potential
Page 279 and 280:
CAO/ARO 04 study—which added oxal
Page 281 and 282:
STAGE III COLON CANCER: WHAT WORKS,
Page 283 and 284:
Table 1. Comparison of Fluoropyrimi
Page 285 and 286:
tients with stages II and III color
Page 287 and 288:
ized by high fruit, vegetable, poul
Page 289 and 290:
Exercise Change trial: a randomized
Page 291 and 292:
A New Direction for Pancreatic Canc
Page 293 and 294:
Table 1. FOLFIRINOX versus Gemcitab
Page 295 and 296:
The Southwest Oncology Group (SWOG)
Page 297 and 298:
A Matter of Timing: Is There a Role
Page 299 and 300:
an OS benefit with radiation therap
Page 301 and 302:
a dose of 50.4 Gy to 59.4 Gy of rad
Page 303 and 304:
more commonly given for APC, specia
Page 305 and 306:
subcutaneous bolus or infusion. Hal
Page 307 and 308:
patients are cared for completely w
Page 309 and 310:
Varying Lymphadenectomies for Gastr
Page 311 and 312:
Table 1. Regional Lymph Nodes of th
Page 313 and 314:
Conclusion There are clear differen
Page 315 and 316:
Will Disease Heterogeneity Help Def
Page 317 and 318:
prematurely due to poor accrual. 18
Page 319 and 320:
Adjuvant Treatments for Localized A
Page 321 and 322:
ADJUVANT TREATMENT FOR GASTRIC CANC
Page 323 and 324:
LIVER-DIRECTED THERAPEUTIC OPTIONS
Page 325 and 326:
ated with unique dose distributions
Page 327 and 328:
HCC, with encouraging outcomes in e
Page 329 and 330:
tion. Advanced computer-based image
Page 331 and 332:
a 5-year survival rate of 70% follo
Page 333 and 334:
THE MANAGEMENT OF LESS COMMON BUT C
Page 335 and 336:
Fig 1. PubMed publications and clin
Page 337 and 338:
of therapeutic options, patient sel
Page 339 and 340:
less informative than the GRETCH an
Page 341 and 342:
Table 3. New Agents/Regimens under
Page 343 and 344:
combined with concurrent transarter
Page 345 and 346:
to optimize the use of erlotinib by
Page 347 and 348:
Optimal Use of Imaging to Guide Tre
Page 349 and 350:
enhancement seen. Furthermore, the
Page 351 and 352:
CASTRATION-RESISTANT PROSTATE CANCE
Page 353 and 354:
Fig. 1. FDA regulatory approvals in
Page 355 and 356:
Prognostic, Predictive, and Surroga
Page 357 and 358:
adhesion molecule and further chara
Page 359 and 360:
and treatment options are expanding
Page 361 and 362:
KIDNEY CANCER BIOLOGY AND THERAPEUT
Page 363 and 364:
Prognostic Factors in Advanced RCC
Page 365 and 366:
cell immunotherapy in which a small
Page 367 and 368:
New Developments in Urothelial Canc
Page 369 and 370:
Novel Approaches in Advanced Urothe
Page 371 and 372:
10. Albers P, Park SI, Niegisch G,
Page 373 and 374:
700 at a dose of 400 mg twice daily
Page 375 and 376:
therapy for nonmetastatic prostate
Page 377 and 378:
ADJUVANT THERAPY FOR OLDER PATIENTS
Page 379 and 380:
Adjuvant Systemic Therapy Adjuvant
Page 381 and 382:
with early-stage breast cancer were
Page 383 and 384:
clinical trials to generate additio
Page 385 and 386:
Adjuvant Treatment of Older Patient
Page 387 and 388:
OLDER PATIENTS WITH LUNG CANCER Fig
Page 389 and 390:
OLDER PATIENTS WITH LUNG CANCER adj
Page 391 and 392:
Considerations and Controversies in
Page 393 and 394:
OLDER PATIENTS WITH ADVANCED CANCER
Page 395 and 396:
Page 397 and 398:
Page 399 and 400:
RECENT CLINICAL HIGHLIGHTS IN GYNEC
Page 401 and 402:
GLOBAL ADVANCES IN GYNECOLOGIC ONCO
Page 403 and 404:
GLOBAL ADVANCES IN GYNECOLOGIC ONCO
Page 405 and 406:
The European Society of Gynaecologi
Page 407 and 408:
ESGO EDUCATIONAL AND RESEARCH ACTIV
Page 409 and 410:
UPFRONT TREATMENT OF OVARIAN CANCER
Page 411 and 412:
ANTIANGIOGENICS AND PARP INHIBITORS
Page 413 and 414:
ANTIANGIOGENICS AND PARP INHIBITORS
Page 415 and 416:
Intraperitoneal Treatment in Ovaria
Page 417 and 418:
INTRAPERITONEAL TREATMENT IN OVARIA
Page 419 and 420:
Dose-Dense Chemotherapy and Neoadju
Page 421 and 422:
CHEMOTHERAPY FOR OVARIAN CANCER Fig
Page 423 and 424:
CHEMOTHERAPY FOR OVARIAN CANCER whi
Page 425 and 426:
UTERINE SARCOMA: CHALLENGING CASES
Page 427 and 428:
HISTOLOGIC FEATURES AND MANAGEMENT
Page 429 and 430:
Page 431 and 432:
Page 433 and 434:
SURGICAL OPTIONS FOR UTERINE SARCOM
Page 435 and 436:
SURGICAL OPTIONS FOR UTERINE SARCOM
Page 437 and 438:
PATIENTS WITH HPV-POSITIVE OROPHARY
Page 439 and 440:
HPV-INDUCED OROPHARYNX CANCER analy
Page 441 and 442:
HPV-INDUCED OROPHARYNX CANCER fract
Page 443 and 444:
Important Early Advances in Squamou
Page 445 and 446:
EARLY ADVANCES IN SCCHN Fig 1. Targ
Page 447 and 448:
Application of Genomic and Proteomi
Page 449 and 450:
GENOMIC AND PROTEOMIC TECHNOLOGIES
Page 451 and 452:
GENOMIC AND PROTEOMIC TECHNOLOGIES
Page 453 and 454:
TREATMENT OF THYROID CANCERS: NEW I
Page 455 and 456:
EVALUATION OF ADVANCED THYROID CANC
Page 457 and 458:
EVALUATION OF ADVANCED THYROID CANC
Page 459 and 460:
Systemic Therapeutic Approaches to
Page 461 and 462:
APPROACHES TO ADVANCED THYROID CANC
Page 463 and 464:
AVOIDING OVERDIAGNOSIS AND OVERTREA
Page 465 and 466:
Table 1. Prevalence of Prostate Can
Page 467 and 468:
Table 3. Potential Risks and Benefi
Page 469 and 470:
Overdiagnosis and Overtreatment of
Page 471 and 472:
een reached by other modeling effor
Page 473 and 474:
east cancer community have FDA-appr
Page 475 and 476:
COSTS OF CANCER CARE: AFFORDABILITY
Page 477 and 478:
REDUCING THE COST OF CANCER CARE Fi
Page 479 and 480:
REDUCING THE COST OF CANCER CARE Th
Page 481 and 482:
REDUCING THE COST OF CANCER CARE de
Page 483 and 484:
Why Hasn’t Genomic Testing Change
Page 485 and 486:
tigators should develop prospective
Page 487 and 488:
MANAGEMENT OF CHRONIC LYMPHOCYTIC L
Page 489 and 490:
PREDICTIVE PARAMETERS IN CLL Table
Page 491 and 492:
PREDICTIVE PARAMETERS IN CLL patien
Page 493 and 494:
Transplant in Chronic Lymphocytic L
Page 495 and 496:
WHEN TO OFFER TRANSPLANTATION IN CL
Page 497 and 498:
WHEN TO OFFER TRANSPLANTATION IN CL
Page 499 and 500:
NEW DEVELOPMENTS IN MYELOPROLIFERAT
Page 501 and 502:
SMALL-MOLECULE INHIBITORS FOR MPN S
Page 503 and 504:
SMALL-MOLECULE INHIBITORS FOR MPN L
Page 505 and 506:
Insights into the Molecular Genetic
Page 507 and 508:
GENETICS OF MYELOPROLIFERATIVE NEOP
Page 509 and 510:
Page 511 and 512:
Page 513 and 514:
Classification of Myeloproliferativ
Page 515 and 516:
CLASSIFICATION AND PROGNOSIS OF MPN
Page 517 and 518:
CLASSIFICATION AND PROGNOSIS OF MPN
Page 519 and 520:
AROUND THE WORLD IN ALMOST 80 MINUT
Page 521 and 522:
LUNG CANCER IN BRAZIL Fig. 1. Relat
Page 523 and 524:
LUNG CANCER IN BRAZIL Fig. 3. Chara
Page 525 and 526:
LUNG CANCER IN BRAZIL Author’s Di
Page 527 and 528:
LUNG CANCER IN CHINA Fig 1. Chinese
Page 529 and 530:
LUNG CANCER IN CHINA well equipped
Page 531 and 532:
Research and Standard of Care: Lung
Page 533 and 534:
LUNG CANCER IN ROMANIA ● Protecti
Page 535 and 536:
LUNG CANCER IN ROMANIA reimbursemen
Page 537 and 538:
A New Model: Physician-Patient Coll
Page 539 and 540:
PHYSICIAN ENGAGEMENT IN ONLINE PATI
Page 541 and 542:
PHYSICIAN ENGAGEMENT IN ONLINE PATI
Page 543 and 544:
LUNG CANCER SCREENING 101 CHAIR Chr
Page 545 and 546:
LUNG CANCER SCREENING The concern i
Page 547 and 548:
LUNG CANCER SCREENING Fig. 1. Guide
Page 549 and 550:
LUNG CANCER SCREENING Fig. 2. Guide
Page 551 and 552:
LUNG CANCER SCREENING 19. Montes RP
Page 553 and 554:
Molecular Testing of Non-Small Cell
Page 555 and 556:
MOLECULAR TESTING AND NSCLC Fig 1.
Page 557 and 558:
MOLECULAR TESTING AND NSCLC logic d
Page 559 and 560:
THYMOMA AND THYMIC CARCINOMA: UPDAT
Page 561 and 562:
MANAGEMENT OF THYMIC CARCINOMA recu
Page 563 and 564:
MANAGEMENT OF THYMIC CARCINOMA Refe
Page 565 and 566:
The Creation of the International T
Page 567 and 568:
ITMIG AS A MODEL FOR RARE DISEASES
Page 569 and 570:
Thymoma: From Chemotherapy to Targe
Page 571 and 572:
SYSTEMIC TREATMENT OF THYMOMA Study
Page 573 and 574:
SYSTEMIC TREATMENT OF THYMOMA cance
Page 575 and 576:
What Is the Best Strategy for Incor
Page 577 and 578:
TREATMENT OF FOLLICULAR LYMPHOMA Fi
Page 579 and 580:
TREATMENT OF FOLLICULAR LYMPHOMA me
Page 581 and 582:
TREATMENT OF FOLLICULAR LYMPHOMA ou
Page 583 and 584:
TREATMENT OPTIONS IN INDOLENT LYMPH
Page 585 and 586:
Page 587 and 588:
Page 589 and 590:
ROLE OF HCT FOR INDOLENT LYMPHOMA T
Page 591 and 592:
ROLE OF HCT FOR INDOLENT LYMPHOMA T
Page 593 and 594:
ROLE OF HCT FOR INDOLENT LYMPHOMA e
Page 595 and 596:
CONTROVERSIES IN MYELOMA: INDUCTION
Page 597 and 598:
TRANSPLANTATION FOR MYELOMA Alterna
Page 599 and 600:
TRANSPLANTATION FOR MYELOMA compare
Page 601 and 602:
TRANSPLANTATION FOR MYELOMA autolog
Page 603 and 604:
CURRENT STATUS OF MYELOMA THERAPY K
Page 605 and 606:
CURRENT STATUS OF MYELOMA THERAPY F
Page 607 and 608:
CURRENT STATUS OF MYELOMA THERAPY T
Page 609 and 610:
Maintenance Therapy for Myeloma: Ho
Page 611 and 612:
MAINTENANCE THERAPY FOR MULTIPLE MY
Page 613 and 614:
Page 615 and 616:
Page 617 and 618:
NEW OPTIONS, NEW QUESTIONS: HOW TO
Page 619 and 620:
THERAPIES FOR PATIENTS WITH METASTA
Page 621 and 622:
Page 623 and 624:
Page 625 and 626:
ANTIEMETICS: CURRENT STANDARDS, EME
Page 627 and 628:
ANTIEMETICS: ASCO GUIDELINE UPDATE
Page 629 and 630:
Page 631 and 632:
Page 633 and 634:
Page 635 and 636:
Chemotherapy-Induced Nausea and Vom
Page 637 and 638:
INCIDENCE AND PREVALENCE OF CHEMOTH
Page 639 and 640:
New Frontiers in Mucositis By Dougl
Page 641 and 642:
MUCOSAL INJURY CAUSED BY CANCER THE
Page 643 and 644:
Page 645 and 646:
Page 647 and 648:
Short- and Long-term Cardiovascular
Page 649 and 650:
Recent Advances in Cardiotoxicity o
Page 651 and 652:
CARDIOTOXICITY OF ANTICANCER THERAP
Page 653 and 654:
CARDIOTOXICITY OF ANTICANCER THERAP
Page 655 and 656:
The Oncologist as the Patient with
Page 657 and 658: THE ONCOLOGIST AS THE PATIENT OR RE
Page 659 and 660: Prolonged Febrile Neutropenia in th
Page 661 and 662: FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 663 and 664: FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 665 and 666: TREATMENT APPROACHES IN CHILDREN wh
Page 667 and 668: TREATMENT APPROACHES IN CHILDREN th
Page 669 and 670: GENETIC COUNSELING OF THE PATIENT W
Page 671 and 672: CANCER PREDISPOSITION IN CHILDHOOD
Page 679 and 680: HOW TO MANAGE VERY RARE PEDIATRIC C
Page 681 and 682: RARE CANCER IN CHILDREN Registries
Page 683 and 684: Genetic Alterations in Childhood Me
Page 685 and 686: GENETIC ALTERATIONS IN CHILDHOOD ME
Page 687 and 688: Desmoid-Type Fibromatosis in Childr
Page 689 and 690: CHEMOTHERAPY FOR DESMOID TUMOR Tabl
Page 691 and 692: CHEMOTHERAPY FOR DESMOID TUMOR 14.
Page 693 and 694: Targeting the Insulin-Like Growth F
Page 695 and 696: TARGETING THE IGF SYSTEM Fig. 1. Th
Page 697 and 698: TARGETING THE IGF SYSTEM malignanci
Page 699 and 700: Hedgehog Pathway in Pediatric Cance
Page 701 and 702: HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 703 and 704: HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 705 and 706: Development and Refinement of Augme
Page 707: ABFM THERAPY FOR PEDIATRIC ALL than
Page 711 and 712: RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 713 and 714: RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 715 and 716: Role of Doxorubicin in Rhabdomyosar
Page 717 and 718: DOXORUBICIN IN RHABDOMYOSARCOMA 8.
Page 719 and 720: Identification of Novel Biologic Ta
Page 721 and 722: NOVEL TARGETS IN THE TREATMENT OF D
Page 723 and 724: Is Biopsy Safe in Children with New
Page 725 and 726: SAFETY OF DIPG BIOPSY IN CHILDREN F
Page 727 and 728: SAFETY OF DIPG BIOPSY IN CHILDREN 1
Page 729 and 730: CHILDREN WITH DIFFUSE INTRINSIC PON
Page 731 and 732: Communication and Decision Support
Page 733 and 734: COMMUNICATION AND DECISION SUPPORT
Page 739 and 740: Planning for the Future: The Role o
Page 741 and 742: present in the office suite but doe
Page 743 and 744: Summary and Care Plan are provided.
Page 745 and 746: DOING IT RIGHT, AND FOR LESS: IMPLE
Page 747 and 748: CLINICAL PATHWAYS STANDARDIZING PER
Page 749 and 750: CLINICAL PATHWAYS STANDARDIZING PER
Page 751 and 752: The Future of Oncology Care with Pe
Page 753 and 754: quantity. Determining the appropria
Page 755 and 756: THE ASCO QUALITY ONCOLOGY PRACTICE
Page 757 and 758: IMPROVING VALUE OF CARE IN ONCOLOGY
Page 759 and 760:
IMPROVING VALUE OF CARE IN ONCOLOGY
Page 761 and 762:
IMPROVING VALUE OF CARE IN ONCOLOGY
Page 763 and 764:
PHYSICIAN WELLNESS: COPING WITH REP
Page 765 and 766:
also provides insight on how clinic
Page 767 and 768:
good resource for exploring the pri
Page 769 and 770:
of death or following death and inc
Page 771 and 772:
telephone call to the family, sendi
Page 773 and 774:
New Insights in Cross-Cultural Comm
Page 775 and 776:
CROSS-CULTURAL COMMUNICATION Sideba
Page 777 and 778:
THE ONCOLOGIST, THE PATIENT, AND TH
Page 779 and 780:
estimate of the proportion of their
Page 781 and 782:
exactly the same treatment, even th
Page 783 and 784:
How to Decide Whether to Offer and
Page 785 and 786:
NONSTANDARD THERAPIES FOR ADVANCED
Page 787 and 788:
NONSTANDARD THERAPIES FOR ADVANCED
Page 789 and 790:
TARGETED THERAPIES IN TARGETED OR U
Page 791 and 792:
TARGETED THERAPY IN SARCOMA rates a
Page 793 and 794:
TARGETED THERAPY IN SARCOMA seen in
Page 795 and 796:
TARGETED THERAPY IN SARCOMA recepto
Page 797 and 798:
Adjuvant Treatment of Gastrointesti
Page 799 and 800:
ADJUVANT THERAPY IN HIGH-RISK GASTR
Page 801 and 802:
Management of Tyrosine Kinase Inhib
Page 803 and 804:
TKI-RESISTANT GIST Primary Imatinib
Page 805 and 806:
TKI-RESISTANT GIST Table 2. Clinica
Page 807 and 808:
BIOLOGIC PRINCIPLES OF TARGETED COM
Page 809 and 810:
COMBINING TARGETED AGENTS IN CLINIC
Page 811 and 812:
COMBINING TARGETED AGENTS IN CLINIC
Page 813 and 814:
Combination Therapies Building on t
Page 815 and 816:
COMBINATIONS FOR MELANOMA agents th
Page 817 and 818:
MECHANISMS OF RESISTANCE TO TARGETE
Page 819 and 820:
RESISTANCE MECHANISMS TO MAPK INHIB
Page 821 and 822:
RESISTANCE MECHANISMS TO MAPK INHIB
Page 823 and 824:
Mechanisms of Resistance to Targete
Page 825 and 826:
RESISTANCE TO TARGETED THERAPIES IN
Page 827 and 828:
RESISTANCE TO TARGETED THERAPIES IN
Page 829 and 830:
Translating PI3K-Delta Inhibitors t
Page 831 and 832:
THE STORY OF CAL-101 6% of patients
Page 833 and 834:
PI3 Kinase in Cancer: From Biology
Page 835 and 836:
PI3 KINASE IN CANCER Fig. 1. The PI
Page 837 and 838:
PI3 KINASE IN CANCER Fig. 3. In viv
Page 840:
This publication is supported by an
show all

2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

Create successful ePaper yourself

Delete template?

Save as template?