2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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ment, patients should be assessed for blood cell counts and blood chemistry analysis at 3 monthly intervals. Abdominal imaging is recommended every 3 to 6 months during adjuvant imatinib therapy and after cessation of imatinib ther- Author’s Disclosures of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role Jaap Verweij Abbott Laboratories; Boehringer Ingelheim; Enzon; GlaxoSmithKline; InteRNA; Johnson & Johnson; Novartis; Otsuka; Pfizer; Sanofi; Teva 1. Miettinen M, Lasota J. Gastrointestinal stromal tumors: Review on morphology, molecular pathology, prognosis, and differential diagnosis. Arch Pathol Lab Med. 2006;130:1466-1478. 2. Rubin BP, Heinrich MC, Corless CL. Gastrointestinal stromal tumour. Lancet. 2007;369:1731-1741. 3. DeMatteo RP, Lewis JJ, Leung D, et al. Two hundred gastrointestinal stromal tumors: recurrence patterns and prognostic factors for survival. Ann Surg. 2000;231:51-58. 4. Joensuu H, Vehtari A, Riihimäki J, et al. Risk of gastrointestinal stromal tumour recurrence after surgery: an analysis of pooled populationbased cohorts. Lancet Oncology. Epub 2011 December 7. 5. Miettinen M, El-Rifai W, L HLS, et al. Evaluation of malignancy and prognosis of gastrointestinal stromal tumors: a review. Hum Pathol. 2002;33: 478-483. 6. Nilsson B, Bumming P, Meis-Kindblom JM, et al. Gastrointestinal stromal tumors: the incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era—a population-based study in western Sweden. Cancer. 2005;103:821-829. 7. Huang HY, Li CF, Huang WW, et al. A modification of NIH consensus criteria to better distinguish the highly lethal subset of primary localized gastrointestinal stromal tumors: a subdivision of the original high-risk group on the basis of outcome. Surgery. 2007;141:748-756. 8. Goh BK, Chow PK, Yap WM, et al. Which is the optimal risk stratification system for surgically treated localized primary GIST? Comparison of three contemporary prognostic criteria in 171 tumors and a proposal for a modified Armed Forces Institute of Pathology risk criteria. Ann Surg Oncol. 2008;15:2153-2163. 9. Gold JS, Gonen M, Gutierrez A, et al. Development and validation of a prognostic nomogram for recurrence-free survival after complete surgical resection of localised primary gastrointestinal stromal tumour: a retrospective analysis. Lancet Oncol. 2009;10:1045-1052. 10. Verweij J, Casali P, Zalcberg J, et al. Progression-free survival in gastrointestinal stromal tumours with high-dose imatinib: randomised trial. Lancet. 2004;364:1127-1134. 11. Blanke CD, Rankin C, Demetri GD, et al. Phase III randomized, intergroup trial assessing imatinib mesylate at two dose levels in patients 662 apy every 3 months, for a 2-year period, every 6 months for the 3 years thereafter, and annually subsequently up to year 10. Recurrence thereafter is rare 4 and thus the benefits of imaging no longer outweigh the risks. Stock Ownership Honoraria Abbott Laboratories; Boehringer Ingelheim; Eisai; Enzon; GlaxoSmithKline; InteRNA; Johnson & Johnson; Merck Serono; MSD Oncology; Novartis; Otsuka; Pfizer; Sanofi; Sun Pharma; Synthon; Teva REFERENCES Research Funding Expert Testimony JAAP VERWEIJ Other Remuneration with unresectable or metastatic gastrointestinal stromal tumors expressing the kit receptor tyrosine kinase: S0033. J Clin Oncol. 2008;26:626-632. 12. Blanke CD, Demetri GD, von Mehren M, et al. Long-term results from a randomized phase II trial of standard- versus higher-dose imatinib mesylate for patients with unresectable or metastatic gastrointestinal stromal tumors expressing KIT. J Clin Oncol. 2008;26:620-625. 13. Bilimoria KY, Wayne JD, Merkow RP, et al. Incorporation of adjuvant therapy into the multimodality management of gastrointestinal stromal tumors of the stomach in the United States. Ann Surg Oncol. 2012;19:184- 191. 14. Li J, Gong JF, Wu AW, Shen L. Post-operative imatinib in patients with intermediate or high risk gastrointestinal stromal tumor. Eur J Surg Oncol. 2011;37:319-324. 15. Dematteo RP, Ballman KV, Antonescu CR, et al. Adjuvant imatinib mesylate after resection of localised, primary gastrointestinal stromal tumour: a randomised, double-blind, placebo-controlled trial. Lancet. 2009;373: 1097-1104. 16. Joensuu H, Eriksson M, Hartmann J, et al. Twelve versus 36 months of adjuvant imatinib (IM) as treatment of operable GIST with a high risk of recurrence: final results of a randomized trial (SSGXVIII/AIO). J Clin Oncol. 2011;29 (suppl, abstr LBA1). 17. Corless CL, Ballman KV, Antonescu C, et al. Relation of tumor pathologic and molecular features to outcome after surgical resection of localized primary gastrointestinal stromal tumor (GIST): Results of the intergroup phase III trial ACOSOG Z9001. J Clin Oncol. 2010;28 (suppl, abstr 10006). 18. Hohenberger P. Adjuvant imatinib in GIST: a self-fulfilling prophecy, or more? Lancet. 2009;373:1058-1060. 19. Le Cesne A, Ray-Coquard I, Bui B, et al. Continuous versus interruption of imatinib (IM) in responding patients with advanced GIST after three years of treatment: a prospective randomized phase III trial of the French Sarcoma Group. J Clin Oncol. 2007;25 (suppl, abstr 10005). 20. Biron P, Cassier Ph.A, Fumagalli E, et al. Outcome of patients with PDGFRA D842V mutant gastrointestinal stromal tumor treated with imatinib for advanced disease. J Clin Oncol. 2010;28:710s (suppl, abstr 10051).
Management of Tyrosine Kinase Inhibitor–Resistant Gastrointestinal Stromal Tumors By Christine M. Barnett, MD, and Michael C. Heinrich, MD Overview: The treatment of gastrointestinal stromal tumors (GISTs) has been a model for targeted cancer therapy. The discovery of driver somatic mutations in the KIT and PDGFRA receptor tyrosine kinases led to a shift of therapy from conventional cytotoxic chemotherapy to inhibitors of these receptors. Targeted molecular therapy of GIST has markedly increased the overall survival of patients with advanced dis- GISTS ARE the most common sarcoma arising in the abdominal cavity. The annual incidence in the United States is approximately 4,000 to 6,000 new cases per year. The stomach is the most common site of origin, but GISTs can arise anywhere in the gastrointestinal tract. 1 Localized GIST is primarily managed with surgical resection, but these tumors can recur locally or metastasize, typically to the liver or peritoneum. Increasingly, GIST is managed with systemic therapy utilizing tyrosine kinase inhibitor (TKI) therapy, even in the case of localized disease. GIST Biology Only in the last 15 years has GIST been recognized as a distinct pathologic entity. Histologically, there is an overlap of smooth muscle and neural elements, which historically made classification of GIST difficult. GISTs are now recognized as a malignancy of the interstitial cells of Cajal (ICC) which serve as “pacemaker” cells of the gastrointestinal tract. KIT activity is required for development of certain types of ICCs, 1 and in addition, 95% of GISTs are positive for KIT expression by immunohistochemistry. 2 Notably, the types of ICCs that are developmentally dependent on KIT are also the types that can give rise to GIST. KIT (CD117) is a type III receptor tyrosine kinase. This family also includes platelet-derived growth factor receptors A and B (PDGFRA/B), CSF-1R, and FLT3. Binding of stem cell factor results in homodimerization of the KIT receptor with subsequent activation of the intracellular tyrosine kinase domain. 3 Tyrosine phosphorylation of KITinteracting proteins leads to activation of multiple signal transduction pathways that stimulate cell proliferation and resistance to apoptosis. Under normal circumstances, the KIT receptor is autoinhibited by the juxtamembrane domain, which prevents the protein activation loop from assuming the necessary conformation for kinase activity. Oncogenic Mutations in GIST Mutations in KIT and PDGFRA result in ligandindependent kinase activation. 70% to 80% of GISTs have mutations in KIT, 1 making this the single most important therapeutic target for this tumor. The majority of KIT mutations affect the juxtamembrane domain encoded by exon 11, and up to two-thirds of GISTs harbor a mutation of this exon. Exon 11 mutations disrupt the autoinhibitory properties of the juxtamembrane domain, thus allowing kinase activation. 3 ease. However, the ability of kinase therapy to control metastatic disease is ultimately limited by the ability of these agents to overcome intrinsic or acquired resistance mechanisms. Ongoing basic and clinical research is focusing on identifying new agents to inhibit KIT/PDGFRA kinase activity and/or other novel molecular targets in GIST. 7% to 10% of GISTs have mutations of exon 9, which encodes the membrane-proximal most portion of the extracellular domain. These mutations lead to an extracellular conformational change that is similar to that created by ligand binding, resulting in kinase activation. 3 Exon 9 mutations are more commonly seen in GISTs of the small and large bowel origin and are rarely seen in gastric GISTs. There are also less common primary mutations in the activation loop (exon 17), which stabilize the active conformation of the receptor, and the ATP binding region (exon 13), which may affect the inhibitory function of the juxtamembrane domain. 3 Approximately 10% of patients with GIST have tumors with activating mutations of PDGFRA, 1 which is closely related to KIT. KIT and PDGFRA mutations are mutually exclusive. The downstream pathways that are activated by PDGFRA are very similar to those activate by KIT. Most PDGFRA mutations occur in exon 18, which encodes the activation loop of the kinase. In addition, approximately 1% of GISTs have mutations of the PDGFRA juxtamembrane or ATP-binding domains. The remaining 10% to 15% of GISTs lack mutations in PDGFRA or KIT and have been traditionally designated “wild type” because of a lack of mutated kinase targets for therapy. Interestingly, KIT is still strongly phosphorylated in these tumors, indicating the presence of activated KIT. 4 The mechanism responsible for this activation remains undefined. Increasingly, alternative oncogenic drivers have been identified in tumors lacking KIT or PDGFRA mutations. These include BRAF V600E mutations or, less commonly, mutations of RAS family members. 3 These make up an estimated 10% of wild-type GISTs, or 1% to 2% of GISTs overall. Rare loss-of-function mutations of the succinate dehydrogenase (SDH) complex have been identified in some familial syndromes associated with GIST (e.g., Carney- Stratakis). 3 SDH is important in the regulation of HIF1alpha, and loss of SDH complex function has similar biologic consequences as loss of VHL protein (the primary molecular From the Division of Hematology and Medical Oncology, Portland VA Medical Center and the Knight Cancer Institute, Oregon Health & Science University, Portland, OR. Authors’ disclosures of potential conflicts of interest are found at the end of this article. Address reprint requests to Michael C. Heinrich, MD, Division of Hematology/Oncology, Departments of Medicine and Cell and Developmental Biology, Portland VA Medical Center and OHSU Knight Cancer Institute, Oregon Health & Science University, R&D-19 3710 U.S. Veterans Hospital Road, Portland, OR 97239; email: heinrich@ohsu.edu. © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10 663
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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
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LUNG CANCER SCREENING 19. Montes RP
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Molecular Testing of Non-Small Cell
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MOLECULAR TESTING AND NSCLC Fig 1.
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MOLECULAR TESTING AND NSCLC logic d
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THYMOMA AND THYMIC CARCINOMA: UPDAT
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MANAGEMENT OF THYMIC CARCINOMA recu
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MANAGEMENT OF THYMIC CARCINOMA Refe
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The Creation of the International T
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ITMIG AS A MODEL FOR RARE DISEASES
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Thymoma: From Chemotherapy to Targe
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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 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 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: ADJUVANT THERAPY IN HIGH-RISK GASTR
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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