2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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Author’s Disclosures of Potential Conflicts of Interest Author S. Vincent Rajkumar* *No relevant relationships to disclose. Employment or Leadership Positions Consultant or Advisory Role 1. Rajkumar SV. Treatment of Multiple Myeloma. Nature Rev Clin Oncol. 2011;8:479-491. 2. Rajkumar SV. Multiple myeloma: 2012 update on diagnosis, riskstratification, and management. American Journal of Hematology. 2012;87: 78-88. 3. Kyle RA, Rajkumar SV. Criteria for diagnosis, staging, risk stratification and response assessment of multiple myeloma. Leukemia. 2009;23:3-9. 4. Russell SJ, Rajkumar SV. Multiple myeloma and the road to personalised medicine. Lancet Oncol. 2011;12:617-619. 5. Kumar SK, Mikhael JR, Buadi FK, et al. Management of newly diagnosed symptomatic multiple myeloma: updated Mayo stratification of Myeloma and Risk-Adapted Therapy (mSMART) consensus guidelines. Mayo Clinic Proceedings. 2009;84:1095-110. 6. Rajkumar SV, Gahrton G, Bergsagel PL. Approach to the treatment of multiple myeloma: a clash of philosophies. Blood. 2011;118:3205-3211. 7. Rajkumar SV, Jacobus S, Callander NS, et al. Lenalidomide plus high-dose dexamethasone versus lenalidomide plus low-dose dexamethasone as initial therapy for newly diagnosed multiple myeloma: an open-label randomised controlled trial. Lancet Oncol. 2010;11:29-37. 8. Palumbo A, Rajkumar SV, Dimopoulos MA, et al. Prevention of thalidomide- and lenalidomide-associated thrombosis in myeloma. Leukemia. 2008;22:414-423. 9. Harousseau JL, Attal M, Avet-Loiseau H, et al. Bortezomib pPlus dexamethasone is superior to vincristine plus doxorubicin plus dexamethasone as induction treatment prior to autologous stem-cell transplantation in newly diagnosed multiple myeloma: results of the IFM 2005-01 phase III trial. J Clin Oncol. 2010;28:4621-4629. 10. Richardson PG, Weller E, Lonial S, et al. Lenalidomide, bortezomib, and dexamethasone combination therapy in patients with newly diagnosed multiple myeloma. Blood. 2010;116:679-686. 11. Cavo M, Tacchetti P, Patriarca F, et al. Bortezomib with thalidomide plus dexamethasone compared with thalidomide plus dexamethasone as induction therapy before, and consolidation therapy after, double autologous stem-cell transplantation in newly diagnosed multiple myeloma: a randomised phase 3 study. Lancet. 2010;376:2075-2085. 12. Moreau P, Facon T, Attal M, et al. Comparison of reduced-dose bortezomib plus thalidomide plus dexamethasone (vTD) to bortezomib plus dexamethasone (VD) as induction treatment prior to ASCT in de novo multiple myeloma (MM): Results of IFM2007-02 study. J Clin Oncol. 2010;28 (suppl; abstr 8014). 13. Kumar S, Flinn IW, Richardson PG, et al. Novel Three- and Four-Drug Combination Regimens of Bortezomib, Dexamethasone, Cyclophosphamide, and Lenalidomide, for Previously Untreated Multiple Myeloma: Results From the Multi-Center, Randomized, Phase 2 EVOLUTION Study. Abstract presented at ASH Annual Meeting; December 2010; Orlando, FL. 14. Mateos MV, Oriol A, Martínez-López J, et al. Bortezomib, melphalan, and prednisone versus bortezomib, thalidomide, and prednisone as induction therapy followed by maintenance treatment with bortezomib and thalidomide versus bortezomib and prednisone in elderly treated patients with untreated multiple myeloma: a randomized trial. Lancet Oncol. 2010;11:934-941. 15. Palumbo A, Bringhen S, Rossi D, et al. Bortezomib-melphalanprednisone-thalidomide followed by maintenance with bortezomibthalidomide compared with bortezomib-melphalan-prednisone for initial treatment of multiple myeloma: a randomized controlled trial. J Clin Oncol. 2010;28:5101-5109. 16. Moreau P, Pylypenko H, Grosicki S, et al. Subcutaneous versus intra- 514 Stock Ownership Honoraria REFERENCES Research Funding Expert Testimony S. VINCENT RAJKUMAR Other Remuneration venous administration of bortezomib in patients with relapsed multiple myeloma: a randomised, phase 3, non-inferiority study. Lancet Oncol. 2011; 12:431-440. 17. Barlogie B, Anaissie E, van Rhee F, et al. Incorporating bortezomib into upfront treatment for multiple myeloma: early results of total therapy 3. British Journal of Haematology. 2007;138:176-185. 18. Facon T, Mary JY, Hulin C, et al. Melphalan and prednisone plus thalidomide versus melphalan and prednisone alone or reduced-intensity autologous stem cell transplantation in elderly patients with multiple myeloma (IFM 99-06): a randomised trial. Lancet. 2007;370:1209-1218. 19. Hulin C, Facon T, Rodon P, et al. Efficacy of melphalan and prednisone plus thalidomide in patients older than 75 years with newly diagnosed multiple myeloma: IFM 01/01 Trial. J Clin Oncol. 2009;27:3664-3670. 20. Palumbo A, Bringhen S, Caravita T, et al. Oral melphalan and prednisone chemotherapy plus thalidomide compared with melphalan and prednisone alone in elderly patients with multiple myeloma: randomised controlled trial. Lancet. 2006;367:825-831. 21. Waage A, Gimsing P, Fayers P, et al. Melphalan and prednisone plus thalidomide or placebo in elderly patients with multiple myeloma. Blood. 2010;116:1405-1412. 22. Wijermans P, Schaafsma M, Termorshuizen F, et al. Phase III study of the value of thalidomide added to melphalan plus prednisone in elderly patients with newly diagnosed multiple myeloma: the HOVON 49 Study. J Clin Oncol. 2010;28:3160-3166. 23. Beksac M, Haznedar R, Firatli-Tuglular T, et al. Addition of thalidomide to oral melphalan/prednisone in patients with multiple myeloma not eligible for transplantation: results of a randomized trial from the Turkish Myeloma Study Group. Eur J Haematol. 2011;86:16-22. 24. Kapoor P, Rajkumar SV, Dispenzieri A, et al. Melphalan and prednisone versus melphalan, prednisone and thalidomide for elderly and/or transplant ineligible patients with multiple myeloma: A meta-analysis. Leukemia. 2011;25:689-696. 25. Fayers PM, Palumbo A, Hulin C, et al. Thalidomide for previously untreated elderly patients with multiple myeloma: meta-analysis of 1685 individual patient data from 6 randomized clinical trials. Blood. 2011;118: 1239-1247. 26. San Miguel JF, Schlag R, Khuageva NK, et al. Bortezomib plus melphalan and prednisone for initial treatment of multiple myeloma. N Engl J Med. 2008;359:906-917. 27. Nair B, van Rhee F, Shaughnessy JD Jr., et al. Superior results of Total Therapy 3 (2003-33) in gene expression profiling-defined low-risk multiple myeloma confirmed in subsequent trial 2006-66 with VRD maintenance. Blood. 2010;115:4168-4173. 28. van Rhee F, Szymonifka J, Anaissie E, et al. Total therapy 3 for multiple myeloma: Prognostic implications of cumulative dosing and premature discontinuation of VTD maintenance components, bortezomib, thalidomide and dexamethasone, relevant to all phases of therapy. Blood. 2010;116: 1220-1227. 29. Palumbo A, Bringhen S, Liberati AM, et al. Oral melphalan, prednisone, and thalidomide in elderly patients with multiple myeloma: updated results of a randomized controlled trial. Blood. 2008;112:3107-3114. 30. Mateos MV, Richardson PG, Schlag R, et al. Bortezomib plus melphalan and prednisone compared with melphalan and prednisone in previously untreated multiple myeloma: updated follow-up and impact of subsequent therapy in the phase III VISTA trial. J Clin Oncol. 2010;28:2259- 2266.
Maintenance Therapy for Myeloma: How Much, How Long, and at What Cost? By Michel Attal, MD, and Murielle Roussel, MD Overview: Maintenance therapy in multiple myeloma has been under investigation for more than 3 decades and has been without evidence of clear advantage in terms of progression-free survival (PFS) until the mid-2000s. Neither conventional chemotherapy, prednisone, nor interferon-based maintenance regimens offered any benefit after conventional or high-dose therapy. Thalidomide was the first drug, mainly given as maintenance after high dose therapy, to demonstrate clinical benefits in terms of PFS and, in some studies, of overall survival (OS). The role of other novel agents such as lenalidomide and bortezomib as maintenance therapy is emerging. Lenalidomide has been shown to reduce the risk of relapse with longer follow-up needed to see if this will THERAPEUTIC ADVANCES in the treatment of multiple myeloma have improved remission duration and OS. 1 While agents such as thalidomide, bortezomib, and lenalidomide have had a major effect on response rates, most patients with multiple myeloma will ultimately relapse. Further strategies are needed to both improve response depth and prolong response duration in order to induce a clonal extinction and, at last, cure the disease. Maintenance therapy can be defined as any treatment given after completion of induction treatment, for a prolonged period of time, with the goal of extending the duration of response, prolonging PFS and OS, while maintaining a good quality of life. 2,3 In addition, an optimal maintenance treatment should have an acceptable toxicity profile and not compromise treatment at time of relapse. Unfortunately, this strategy remains elusive in multiple myeloma. Early attempts at maintenance therapy with conventional chemotherapy has always failed to prolong PFS and OS 4 and the role of long-term steroids has also been controversial. 5 The effect of alpha-interferon was shown to be modest in terms of prolonging PFS and OS. 6,7 Most investigators concluded that the benefit was small and needed to be balanced against the cost and potential toxicity of prolonged treatment with alpha-interferon. The advent of “novel” agents (thalidomide, bortezomib, and lenalidomide) renewed the concept of maintenance or long-term treatment, even for elderly patients or those not eligible for high dose therapy (HDT). Several phase II and III trials on maintenance therapy are ongoing. Maintenance Therapy with Immunomodulatory Drugs (IMiDs) The IMiDs thalidomide and lenalidomide are the most frequently studied maintenance drugs, given their ease of oral administration and established antimyeloma efficacy (Table 1). Thalidomide and Lenalidomide Prolong Duration of Response after HDT Thalidomide. There are five randomized studies with thalidomide maintenance after HDT that have been published to date; one additional trial was reported during the American Society of Hematology meeting in 2010. 8-13 De- translate into a survival benefit. At present, a number of key questions remain unanswered. What are the optimal dose and duration of those treatments? Is the risk of toxicity and second primary malignancies acceptable? Will the disease be more aggressive at time of relapse? Is the clinical benefit predicted by initial prognostic factors and response to previous therapy? Does maintenance therapy work by further eradication of minimal residual disease or by immunological control of the malignant clone? Ongoing randomized trials are evaluating lenalidomide and bortezomib, both in the transplant and nontransplant settings, to better define the role of these drugs as maintenance in multiple myeloma. spite differences, such as duration of treatment and/or concomitant use of prednisone/prednisolone, thalidomide maintenance was consistently associated with a longer PFS. The benefit with respect to OS, however, was variable. Along with the Arkansas group, the Intergroupe Francophone du Myélome (IFM) was one of the first to show that thalidomide as maintenance after tandem autologous stem cell transplantation (ASCT) was superior to no maintenance or pamidronate alone (IFM 9902 trial 9 ). Continuous thalidomide increased the complete response (CR) and very good partial response (VGPR) rate (67% vs. 55% and 57%, respectively; p � 0.03), the 3-year PFS (52% vs. 36% and 37%, respectively; p � 0.009), and the 4-year OS (87% vs. 77% and 74%, respectively; p � 0.04). The Australian group 10 obtained similar results when comparing thalidomide (for 12 months) plus prednisolone (until progression) with prednisolone alone. The thalidomide-containing arm achieved higher rates of VGPR with increased PFS and OS. Within the total therapy 2 program, 8 thalidomide was given as maintenance until disease progression or intolerance. In the initial report, CR rate and 5-year PFS were notably better in the thalidomide arm (62% vs. 43% and 56% vs. 44%, respectively) but there was no improvement in OS. After relapse, survival was shorter in patients pre-exposed to thalidomide. However, in an updated analysis (with a median follow-up of 72 months), prolonged OS was eventually confirmed even in a subgroup of patients with poor-risk cytogenetics. 14 Lastly, a recently presented meta-analysis of five transplant studies revealed a significant improvement both in PFS (p � 0.001) and OS (p � 0.002) with thalidomide maintenance therapy. 15 Lenalidomide. Given the more favorable efficacy profile, lenalidomide was considered an attractive agent for maintenance. This has prompted several ongoing trials designed to compare continuous treatment until relapse with no maintenance after ASCT. Two large randomized phase III From the Hematology Department, CHU Purpan, Toulouse, France. Authors’ disclosures of potential conflicts of interest are found at the end of this article. Address reprint requests to M. Attal, MD, Hématologie Clinique, CHU Purpan, Place du Dr Baylac, TSA 40031, 31059 Toulouse Cedex 9, France; email: attal.m@chu-toulouse.fr. © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10 515
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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
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 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: CURRENT STATUS OF MYELOMA THERAPY T
Page 611 and 612: MAINTENANCE THERAPY FOR MULTIPLE MY
Page 617 and 618: NEW OPTIONS, NEW QUESTIONS: HOW TO
Page 619 and 620: THERAPIES FOR PATIENTS WITH METASTA
Page 625 and 626: ANTIEMETICS: CURRENT STANDARDS, EME
Page 627 and 628: ANTIEMETICS: ASCO GUIDELINE UPDATE
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 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 673 and 674:
Page 675 and 676:
Page 677 and 678:
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 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 735 and 736:
Page 737 and 738:
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:
Page 761 and 762:
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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