2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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Authors’ Disclosures of Potential Conflicts of Interest Author Melissa M. Hudson* Louis S. Constine* *No relevant relationships to disclose. Employment or Leadership Positions Consultant or Advisory Role 1. Donaldson SS, Kaplan HS. Complications of treatment of Hodgkin’s disease in children. Cancer Treat Rep. 1982;66:977-989. 2. Donaldson SS, Link MP. Combined modality treatment with low-dose radiation and MOPP chemotherapy for children with Hodgkin’s disease. J Clin Oncol. 1987;5:742-749. 3. Bhatia S, Robison LL, Oberlin O, et al. Breast cancer and other second neoplasms after childhood Hodgkin’s disease. N Engl J Med. 1996;334:745- 751. 4. Hancock SL, Tucker MA, Hoppe RT. Factors affecting late mortality from heart disease after treatment of Hodgkin’s disease. JAMA. 1993;270: 1949-1955. 5. Devita VT, Jr., Serpick AA, Carbone PP. Combination chemotherapy in the treatment of advanced Hodgkin’s disease. Ann Intern Med. 1970;73:881- 895. 6. Bonadonna G, Santoro A. ABVD chemotherapy in the treatment of Hodgkin’s disease. Cancer Treat Rev. 1982;9:21-35. 7. Donaldson SS, Whitaker SJ, Plowman PN, et al. Stage I-II pediatric Hodgkin’s disease: Long-term follow-up demonstrates equivalent survival rates following different management schemes. J Clin Oncol. 1990;8:1128- 1137. 8. Dorffel W, Luders H, Ruhl U, et al. Preliminary results of the multicenter trial GPOH-HD 95 for the treatment of Hodgkin’s disease in children and adolescents: Analysis and outlook. Klin Padiatr. 2003;215:139-145. 9. Schwartz CL. Special issues in pediatric Hodgkin’s disease. Eur J Haematol. Suppl 2005;55-62. 10. Donaldson SS, Hudson MM, Lamborn KR, et al. VAMP and low-dose, involved-field radiation for children and adolescents with favorable, earlystage Hodgkin’s disease: Results of a prospective clinical trial. J Clin Oncol. 2002;20:3081-3087. 11. Nachman JB, Sposto R, Herzog P, et al. Randomized comparison of low-dose involved-field radiotherapy and no radiotherapy for children with Hodgkin’s disease who achieve a complete response to chemotherapy. J Clin Oncol. 2002;20:3765-3771. 12. Metzger ML, Weinstein HJ, Hudson MM, et al. Results of a prospective clinical trial of VAMP alone without irradiation for pediatric favorable, early-stage Hodgkin lymphoma patients who achieve an early complete response. J Clin Oncol Proc Am Soc Clin Oncol. 2011;29:585s. 13. Gerres L, Bramswig JH, Schlegel W, et al. The effects of etoposide on testicular function in boys treated for Hodgkin’s disease. Cancer. 1998;83: 2217-2222. 14. Schellong G, Potter R, Bramswig J, et al. High cure rates and reduced long-term toxicity in pediatric Hodgkin’s disease: The German-Austrian multicenter trial DAL-HD-90. The German-Austrian Pediatric Hodgkin’s Disease Study Group. J Clin Oncol. 1999;17:3736-3744. 620 Stock Ownership Honoraria REFERENCES Research Funding HUDSON AND CONSTINE Expert Testimony Other Remuneration 15. Mauz-Korholz C, Hasenclever D, Dorffel W, et al. Procarbazine-free OEPA-COPDAC chemotherapy in boys and standard OPPA-COPP in girls have comparable effectiveness in pediatric Hodgkin’s lymphoma: The GPOH- HD-2002 study. J Clin Oncol. 2010;28:3680-3686. 16. Yahalom J, Mauch P. The involved field is back: Issues in delineating the radiation field in Hodgkin’s disease. Ann Oncol. 2002;13 Suppl 1:79-83. 17. Ruhl U, Albrecht M, Dieckmann K, et al. Response-adapted radiotherapy in the treatment of pediatric Hodgkin’s disease: An interim report at 5 years of the German GPOH-HD 95 trial. Int J Radiat Oncol Biol Phys. 2001;51:1209-1218. 18. Schwartz CL, Constine LS, Villaluna D, et al. A risk-adapted, responsebased approach using ABVE-PC for children and adolescents with intermediate- and high-risk Hodgkin lymphoma: The results of P9425. Blood. 2009;114:2051-2059. 19. Kelly KM, Sposto R, Hutchinson R, et al. BEACOPP chemotherapy is a highly effective regimen in children and adolescents with high-risk Hodgkin lymphoma: A report from the Children’s Oncology Group. Blood. 2011;117: 2596-2603. 20. Colpo A, Hochberg E, Chen YB. Current Status of Autologous Stem Cell Transplantation in Relapsed and Refractory Hodgkin’s Lymphoma. Oncologist. 2012;17:80-90. 21. Majhail NS, Bajorunaite R, Lazarus HM, et al. Long-term survival and late relapse in 2-year survivors of autologous haematopoietic cell transplantation for Hodgkin and non-Hodgkin lymphoma. Br J Haematol. 2009;147: 129-139. 22. Moskowitz AJ, Perales MA, Kewalramani T, et al. Outcomes for patients who fail high dose chemoradiotherapy and autologous stem cell rescue for relapsed and primary refractory Hodgkin lymphoma. Br J Haematol. 2009;146:158-163. 23. Wendland MM, Asch JD, Pulsipher MA, et al. The impact of involved field radiation therapy for patients receiving high-dose chemotherapy followed by hematopoietic progenitor cell transplant for the treatment of relapsed or refractory Hodgkin disease. Am J Clin Oncol. 2006;29:189-195. 24. Koh ES, Tran TH, Heydarian M, et al. A comparison of mantle versus involved-field radiotherapy for Hodgkin’s lymphoma: Reduction in normal tissue dose and second cancer risk. Radiat Oncol. 2007;2:13. 25. Donaldson SS, Link MP, Weinstein HJ, et al. Final results of a prospective clinical trial with VAMP and low-dose involved-field radiation for children with low-risk Hodgkin’s disease. J Clin Oncol. 2007;25:332-337. 26. Tebbi CK, Mendenhall N, London WB, et al. Treatment of stage I, IIA, IIIA1 pediatric Hodgkin disease with doxorubicin, bleomycin, vincristine and etoposide (DBVE) and radiation: A Pediatric Oncology Group (POG) study. Pediatr Blood Cancer. 2006;46:198-202.
Role of Doxorubicin in Rhabdomyosarcoma: Is the Answer Knowable? Overview: The role of doxorubicin in treatment of rhabdomyosarcoma (RMS) has been controversial for 30 years. Despite its known activity in RMS, because of its risk of cardiotoxicity, its use is not justified in low-risk patients who have an excellent chance of cure with vincristine, actinomycin with or without cyclophosphamide, and primary tumor treatment. For patients with intermediate and high risks, the risk/benefit ratio must be carefully considered. In addition, the peak incidence of RMS is in toddlers, with whom the risk of THE ROLE of doxorubicin in the treatment of rhabdomyosarcoma has been controversial for over three decades. The first report of its activity in rhabdomyosarcoma was by Massimo and colleagues in 1969, 1 followed by an early phase II study in children by Tan, which showed that doxorubicin was active against both newly diagnosed and previously treated rhabdomyosarcoma. 2 However, one of the major disadvantages of doxorubicin is its cardiotoxicity, which was recognized early in its use. 3 Risk factors for cardiotoxicity include young age at administration, higher cumulative dose, and radiation fields including the heart. With the peak incidence of rhabdomyosarcoma being in toddlers, and the majority of patients being under age 10 at diagnosis, cardiotoxicity is a factor in the risk/benefit calculation. Low-risk patients (low stage and clinical group, favorable histology) have excellent outcomes— with survival rates of 80% to 90% with VAC (vincristine, actinomycin, cyclophosphamide) or VA (vincristine, actinomycin) and primary tumor treatment alone; in them, the use of doxorubicin with its potential for long-term cardiotoxicity cannot be justified. The goal of this discussion is to review the historic data on use of doxorubicin in rhabdomyosarcoma, as well as to discuss ongoing clinical studies utilizing it. Historical Perspectives North American Experience. Patients with group III and group IV rhabdomyosarcoma were randomly assigned in Intergroup Rhabdomyosarcoma Study (IRS) to receive therapy with VAC and radiation, with or without doxorubicin. The dose of doxorubicin was 60 mg/m 2 , given at 10 to 12 week intervals (alternating with actinomycin) either alone or with continuous daily oral cyclophosphamide. There was no difference in outcome between regimens and the conclusion was that doxorubicin did not improve the outcome of patients with group III or IV disease. 4 It should be noted that the intervals between treatment cycles were much longer in the early RMS studies than treatment intervals are in the current era, and much of the cyclophosphamide was given orally. IRS II, conducted between 1978 and 1984, again evaluated the role of doxorubicin in patients with group III and IV rhabdomyosarcoma, but this time given along with vincristine and intravenous cyclophosphamide as “pulsed” therapy. Patients were randomly assigned between repetitive pulse VAC or repetitive pulse VAC/VDC (D � doxorubicin). 5 Once again, there was no difference in outcomes between the two regimens. By Carola A. S. Arndt, MD cardiotoxicity of anthracyclines is higher. A number of trials both in North America and Europe, which are reviewed in this article, have investigated the role of doxorubicin in RMS, with no conclusive outcomes. In addition, differences in riskgroup assignment on two sides of the Atlantic further complicate comparisons and analyses. The current European EpSSG 2005 study for high-risk RMS (by the European definition) may come closest to giving an answer to the role of doxorubicin in RMS. IRS III, conducted between 1984 and 1991, had a very complex study design. 5 For patients with group II tumors, the major objective was to see whether the addition of doxorubicin to VA and radiation therapy (RT) improved the outcome of favorable histology tumors. Patients were randomly assigned to treatment with VA or VA plus doxorubicin (with RT in both cases). The outcome was better for the patients treated with VA plus doxorubicin (89% vs. 54% 5 years survival, p � 0.03). However, when historic controls from IRS II treated with VA and RT were included, the statistical significance disappeared. Moreover, the VA regimen had a worse outcome on IRS III than the identical therapy on IRS II, further confounding the results. Nevertheless, the paper stated, “In this randomized comparison, there was suggestive statistical evidence that the addition of doxorubicin (30 mg/m 2 /d IV X 2 during weeks 3, 6, 12, 15, 21, and 24) to a basic VA regimen improved clinical outcome.” Patients with group III and group IV tumors were treated with doxorubicin containing regimens that also included other agents in addition to VAC, making the individual contribution of doxorubicin impossible to determine. Patients with clinical group I and II unfavorable histology tumors received pulsed VDC and VAC plus cisplatin, and showed significant improvement in 5-year progression free survival and survival rates compared with similar patients treated less intensively on IRS II (71% � 6% and 80% � 6% versus 59% � 5% and 71% � 5%, respectively; p � 0.002 and 0.01, respectively). However, the regimens were quite complex, making the individual contribution of doxorubicin impossible to determine. In a series of “phase II window” studies for high-risk patients with metastatic disease conducted by the Children’s Oncology Group (COG) between 1988 and 2000, the combination of doxorubicin/ifosfamide and etoposide/ ifosfamide had the highest response rates, although there was no survival difference. 6 So once again, the role of doxorubicin was not able to be determined conclusively. A pilot study utilizing VDC alternating with ifosfamide/ From the Department of Pediatric and Adolescent Medicine, Mayo Clinic Children’s Center, Rochester, MN. Author’s disclosure of potential conflicts of interest are found at the end of this article. Address reprint requests to Carola A. S. Arndt, MD, Mayo Clinic, Mayo Clinic Children’s Center, Department of Pediatric and Adolescent Medicine, 200 First Street SW, Rochester, MN; email: carndt@mayo.edu. © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10 621
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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American Society of Clinical Oncolo
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American Society of Clinical Oncolo
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New Looks and Challenges for Cooper
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Genitourinary Cancer Best Use of Im
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Research and Standard of Care: Lung
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Practice Management and Information
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2012 ASCO Annual Meeting Disclosure
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Matti S. Aapro, MD Clinique De Geno
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Hedy Lee Kindler, MD The University
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Douglas E. Wood, MD University of W
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Mary Lou Smith, JD, MBA Research Ad
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ASCO and Conquer Cancer Foundation
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Letter from the Editor The theme of
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Adjuvant Therapy for Older Women wi
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TREATMENT FOR OLDER WOMEN WITH BREA
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MANAGEMENT OF T1 BREAST CANCERS the
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MANAGEMENT OF T1 BREAST CANCERS Tab
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MANAGEMENT OF T1 BREAST CANCERS Tab
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MANAGEMENT OF T1 BREAST CANCERS 93.
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MANAGEMENT OF T1 BREAST CANCERS 1 c
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ADJUVANT ENDOCRINE THERAPY reductio
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ADJUVANT ENDOCRINE THERAPY which ra
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ADJUVANT ENDOCRINE THERAPY assay is
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A DICKENS TALE OF THE TREATMENT OF
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TREATMENT OF ADVANCED BREAST CANCER
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A FRESH LOOK AT DUCTAL CARCINOMA IN
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DCIS: OPPORTUNITIES AND UNCHARTED W
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DCIS: OPPORTUNITIES AND UNCHARTED W
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Ductal Carcinoma In Situ, and the I
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DCIS AND INFLUENCE OF RISK FACTORS
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KEY QUESTIONS IN THE LOCO-REGIONAL
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POSTMASTECTOMY RADIATION AND PARTIA
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The Appropriate Extent of Surgery f
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SURGERY FOR EARLY-STAGE BREAST CANC
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BIOLOGY AND LOCAL THERAPY DECISIONS
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Clinical and Imaging Surveillance F
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SURVEILLANCE FOLLOWING BREAST CANCE
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SURVEILLANCE FOLLOWING BREAST CANCE
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Advanced Imaging Techniques for the
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IMAGING TECHNIQUES FOR BREAST CANCE
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IMAGING TECHNIQUES FOR BREAST CANCE
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Update of the Oxford Overview: New
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UPDATE OF THE OXFORD OVERVIEW Fig.
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UPDATE OF THE OXFORD OVERVIEW Overv
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Gene Patents and Personalized Medic
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GENE PATENTS AND EFFECTS ON PERSONA
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Chemoprevention for Breast Cancer:
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CHEMOPREVENTION FOR BREAST CANCER T
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CHEMOPREVENTION FOR BREAST CANCER C
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CONTROVERSIES IN PROSTATE CANCER: P
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PROSTATE CANCER RISK REDUCTION men
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PROSTATE CANCER RISK REDUCTION Auth
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PSA SCREENING: HARMS WITHOUT CLEAR
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PSA SCREENING: HARMS WITHOUT CLEAR
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GLIOBLASTOMA: TAKING THE STANDARD O
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GLIOBLASTOMA: BIOLOGY, GENETICS AND
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FUTURE DIRECTIONS IN GBM THERAPY pr
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FUTURE DIRECTIONS IN GBM THERAPY Ch
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ESTABLISHING TREATMENTS FOR GLIOBLA
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Current Concepts in Brain Tumor Ima
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CONCEPTS IN BRAIN TUMOR IMAGING tum
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CONCEPTS IN BRAIN TUMOR IMAGING Aut
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PERSPECTIVES ON HEADLINE-MAKING NEW
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TTF THERAPY IN GLIOBLASTOMA Fig. 1.
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TTF THERAPY IN GLIOBLASTOMA istics.
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TTF THERAPY IN GLIOBLASTOMA because
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Limitations of Adaptive Clinical Tr
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LIMITATIONS OF ADAPTIVE CLINICAL TR
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LIMITATIONS OF ADAPTIVE CLINICAL TR
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Capturing the Patient Perspective:
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PATIENT-REPORTED OUTCOMES AS TRIAL
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PATIENT-REPORTED OUTCOMES AS TRIAL
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NEW LOOKS AND CHALLENGES FOR COOPER
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NCI NATIONAL CLINICAL TRIALS NETWOR
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Successful Integration of Cooperati
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COG: GIVING NEW MEANING TO COOPERAT
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A Critical Review of the Enrollment
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BLACK PATIENTS AND CANCER CLINICAL
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BLACK PATIENTS AND CANCER CLINICAL
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Trastuzumab Emtansine (T-DM1): Hitc
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T-DM1 AND THERAPEUTIC ANTIBODIES ag
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TARGETING CD30 IN HODGKIN LYMPHOMA
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TARGETING CD30 IN HODGKIN LYMPHOMA
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EARLY DRUG DEVELOPMENT: CASTING A W
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Table 1. Response Rates in Expanded
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Drug Development in the Era of Pers
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that the core pathway is not comple
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This situation is not surprising, g
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Practical Management of Immune-Rela
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the anterior pituitary axis is invo
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TARGETING CRITICAL MOLECULAR ABERRA
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Abl suppression; and 3) the early e
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50% 50% 100% Change in Tumor Size m
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vanced solid tumors, even if they a
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Targeting Molecular Aberrations in
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date. With the advent of gene expre
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consortium to facilitate the testin
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ETHICAL CHALLENGES OF HEALTH CARE R
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HEALTH CARE REFORM AND ONCOLOGY dev
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HEALTH CARE REFORM AND ONCOLOGY aut
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INTERNATIONAL VARIATION IN UNDERSTA
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midcareer physician; in one cross-s
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Table 1. Recommendations for Person
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stances (e.g., stage of career, fam
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elationship” is also acknowledged
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Conclusion In more individualistic
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The Oncologist’s Duty to Provide
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an external observer, but to the pe
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MEDICAL ERRORS IN CANCER CARE: PREV
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DISCLOSING MEDICAL ERRORS Disclosur
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DISCLOSING MEDICAL ERRORS Author’
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PREVENTING MEDICAL ERRORS more diff
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“PERSONALIZED” ONCOLOGY FOR COL
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0.001), progression-free survival (
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mately 40% of patients with colorec
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Table 1. Tumor Marker Utility Gradi
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treatment (tx) for metastatic color
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The Interventional Radiologist Role
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effect. The most common drug that h
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gone forever, no further therapy is
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is irrelevant if it is already rese
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Resection and Thermal Ablation of L
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Author’s Disclosures of Potential
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Minimally Invasive Surgery of Recta
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outcomes; local, wound-site, and di
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Authors’ Disclosures of Potential
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CAO/ARO 04 study—which added oxal
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STAGE III COLON CANCER: WHAT WORKS,
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Table 1. Comparison of Fluoropyrimi
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tients with stages II and III color
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ized by high fruit, vegetable, poul
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Exercise Change trial: a randomized
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A New Direction for Pancreatic Canc
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Table 1. FOLFIRINOX versus Gemcitab
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The Southwest Oncology Group (SWOG)
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A Matter of Timing: Is There a Role
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an OS benefit with radiation therap
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a dose of 50.4 Gy to 59.4 Gy of rad
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more commonly given for APC, specia
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subcutaneous bolus or infusion. Hal
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patients are cared for completely w
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Varying Lymphadenectomies for Gastr
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Table 1. Regional Lymph Nodes of th
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Conclusion There are clear differen
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Will Disease Heterogeneity Help Def
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prematurely due to poor accrual. 18
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Adjuvant Treatments for Localized A
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ADJUVANT TREATMENT FOR GASTRIC CANC
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LIVER-DIRECTED THERAPEUTIC OPTIONS
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ated with unique dose distributions
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HCC, with encouraging outcomes in e
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tion. Advanced computer-based image
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a 5-year survival rate of 70% follo
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THE MANAGEMENT OF LESS COMMON BUT C
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Fig 1. PubMed publications and clin
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of therapeutic options, patient sel
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less informative than the GRETCH an
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Table 3. New Agents/Regimens under
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combined with concurrent transarter
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to optimize the use of erlotinib by
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Optimal Use of Imaging to Guide Tre
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enhancement seen. Furthermore, the
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CASTRATION-RESISTANT PROSTATE CANCE
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Fig. 1. FDA regulatory approvals in
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Prognostic, Predictive, and Surroga
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adhesion molecule and further chara
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and treatment options are expanding
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KIDNEY CANCER BIOLOGY AND THERAPEUT
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Prognostic Factors in Advanced RCC
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cell immunotherapy in which a small
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New Developments in Urothelial Canc
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Novel Approaches in Advanced Urothe
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10. Albers P, Park SI, Niegisch G,
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700 at a dose of 400 mg twice daily
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therapy for nonmetastatic prostate
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ADJUVANT THERAPY FOR OLDER PATIENTS
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Adjuvant Systemic Therapy Adjuvant
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with early-stage breast cancer were
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clinical trials to generate additio
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Adjuvant Treatment of Older Patient
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OLDER PATIENTS WITH LUNG CANCER Fig
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OLDER PATIENTS WITH LUNG CANCER adj
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Considerations and Controversies in
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OLDER PATIENTS WITH ADVANCED CANCER
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RECENT CLINICAL HIGHLIGHTS IN GYNEC
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GLOBAL ADVANCES IN GYNECOLOGIC ONCO
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GLOBAL ADVANCES IN GYNECOLOGIC ONCO
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The European Society of Gynaecologi
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ESGO EDUCATIONAL AND RESEARCH ACTIV
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UPFRONT TREATMENT OF OVARIAN CANCER
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ANTIANGIOGENICS AND PARP INHIBITORS
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ANTIANGIOGENICS AND PARP INHIBITORS
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Intraperitoneal Treatment in Ovaria
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INTRAPERITONEAL TREATMENT IN OVARIA
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Dose-Dense Chemotherapy and Neoadju
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CHEMOTHERAPY FOR OVARIAN CANCER Fig
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CHEMOTHERAPY FOR OVARIAN CANCER whi
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UTERINE SARCOMA: CHALLENGING CASES
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HISTOLOGIC FEATURES AND MANAGEMENT
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SURGICAL OPTIONS FOR UTERINE SARCOM
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SURGICAL OPTIONS FOR UTERINE SARCOM
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PATIENTS WITH HPV-POSITIVE OROPHARY
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HPV-INDUCED OROPHARYNX CANCER analy
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HPV-INDUCED OROPHARYNX CANCER fract
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Important Early Advances in Squamou
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EARLY ADVANCES IN SCCHN Fig 1. Targ
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Application of Genomic and Proteomi
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GENOMIC AND PROTEOMIC TECHNOLOGIES
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GENOMIC AND PROTEOMIC TECHNOLOGIES
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TREATMENT OF THYROID CANCERS: NEW I
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EVALUATION OF ADVANCED THYROID CANC
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EVALUATION OF ADVANCED THYROID CANC
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Systemic Therapeutic Approaches to
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APPROACHES TO ADVANCED THYROID CANC
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AVOIDING OVERDIAGNOSIS AND OVERTREA
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Table 1. Prevalence of Prostate Can
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Table 3. Potential Risks and Benefi
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Overdiagnosis and Overtreatment of
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een reached by other modeling effor
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east cancer community have FDA-appr
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COSTS OF CANCER CARE: AFFORDABILITY
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REDUCING THE COST OF CANCER CARE Fi
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REDUCING THE COST OF CANCER CARE Th
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REDUCING THE COST OF CANCER CARE de
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Why Hasn’t Genomic Testing Change
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tigators should develop prospective
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MANAGEMENT OF CHRONIC LYMPHOCYTIC L
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PREDICTIVE PARAMETERS IN CLL Table
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PREDICTIVE PARAMETERS IN CLL patien
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Transplant in Chronic Lymphocytic L
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WHEN TO OFFER TRANSPLANTATION IN CL
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WHEN TO OFFER TRANSPLANTATION IN CL
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NEW DEVELOPMENTS IN MYELOPROLIFERAT
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SMALL-MOLECULE INHIBITORS FOR MPN S
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SMALL-MOLECULE INHIBITORS FOR MPN L
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Insights into the Molecular Genetic
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GENETICS OF MYELOPROLIFERATIVE NEOP
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Classification of Myeloproliferativ
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CLASSIFICATION AND PROGNOSIS OF MPN
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CLASSIFICATION AND PROGNOSIS OF MPN
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AROUND THE WORLD IN ALMOST 80 MINUT
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LUNG CANCER IN BRAZIL Fig. 1. Relat
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LUNG CANCER IN BRAZIL Fig. 3. Chara
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LUNG CANCER IN BRAZIL Author’s Di
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LUNG CANCER IN CHINA Fig 1. Chinese
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LUNG CANCER IN CHINA well equipped
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Research and Standard of Care: Lung
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LUNG CANCER IN ROMANIA ● Protecti
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LUNG CANCER IN ROMANIA reimbursemen
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A New Model: Physician-Patient Coll
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PHYSICIAN ENGAGEMENT IN ONLINE PATI
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PHYSICIAN ENGAGEMENT IN ONLINE PATI
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LUNG CANCER SCREENING 101 CHAIR Chr
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LUNG CANCER SCREENING The concern i
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LUNG CANCER SCREENING Fig. 1. Guide
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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 and 708: ABFM THERAPY FOR PEDIATRIC ALL than
Page 709 and 710: ABFM THERAPY FOR PEDIATRIC ALL Auth
Page 711 and 712: RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 713: RADIOTHERAPY FOR PEDIATRIC HODGKIN
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 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
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2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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