2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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would otherwise have been included with more traditional open approaches because of potential tumor seeding. 7 Treatment De-Intensification in Favorable-Risk Patient Groups De-intensified adjuvant treatment has the potential benefit of lessening the reported long-term adverse effects of primary CRT. The demographic shift of patients with human papillomavirus (HPV)-positive oropharyngeal cancers may present a population that may benefit from the avoidance of the long-term sequelae inherent to RT and CRT. These are important considerations, particularly with respect to ongoing efforts to decrease long-term adverse effects in potentially more favorable groups such as in HPV-positive patients who are diagnosed younger and who will live longer. TORS is one of several potential de-intensification strategies that needs to be studied. The ideal indications and applications of its use have not yet been completely elucidated. Patient selection and adequate preoperative assessment are essential. This would ideally exclude those patients who would clearly benefit from adjuvant CRT, such as those in whom margin clearance would be difficult or whose disease shows evidence of extracapsular nodal extension and invasion on preoperative imaging. Long-term results of randomized trials comparing primary surgery with RT are needed to clarify oncologic outcomes and quality-oflife issues in early-stage orophayrngeal cancer. This would help support the belief that dose de-escalation or avoidance of CRT results in reduced late toxicity and improved quality of life. KEY POINTS ● Examples of early advances in surgical, radiation, and medical oncology have emerged in the treatment of squamous cell carcinomas of the head and neck (SCCHN), including transoral robotic surgery, particle therapy, and molecular strategies to overcome epidermal growth factor receptor (EGFR) resistance. ● Transoral robotic surgery provides better access to challenging anatomic sites while avoiding morbidity associated with open surgery. Its role alone or in combination with other treatments, especially to enable de-intensification of favorable risk oropharyngeal cancers, warrants clinical evaluation. ● Particle therapy such as the use of protons or carbon ions offers dose distribution that may be intensified or escalated for tumor tissues while scatter to adjacent critical healthy structures is minimized; definitive evaluations of comparative effectiveness of particle therapy compared with photon-based radiation therapy are awaited. ● Multiple molecular strategies to overcome EGFR resistance are under clinical development, including targeting other members of the erbB/HER family besides EGFR, other nodes along the EGFR–mitogenactivated protein kinase (MAPK) pathway, or oncogenic pathways other than EGFR, such as the phosphoinositide 3-kinase (PI3K), insulin-like growth factor 1 receptor (IGF-1R) and MET pathways. 374 Novel Advances in Radiotherapy in SCCHN BISSADA, BRANA, AND SIU The ability to optimize the therapeutic ratio by delivering sufficient radiation dose to tumor tissues while sparing adjacent critical organs is highly relevant in the treatment of SCCHN, and it relies on the dose distribution of the radiation energy. Particle therapy using protons or carbon ion has gained increasing interest in the treatment of SCCHN, largely as a result of their physical characteristics to travel only finite distances through tissues and release most of their energy immediately before they come to rest, in the so-called Bragg Peak. The prospect of delivering less radiation to nontargeted healthy tissues is appealing, as is the feasibility to intensify or escalate doses to tumor areas. In a recent systematic review and meta-analysis of RT in various head and neck cancers comparing photons, protons and carbon ions, which included 86 observational studies and eight comparative in silico studies, 5-year survival was markedly higher after carbon ion therapy compared with conventional photon therapy for mucosal malignant melanomas. Additionally, 5-year local control after proton therapy was markedly higher for paranasal and sinonasal cancer compared with intensity-modulated photon therapy. No other substantial differences were observed. However, the overall quality and quantity of data are limited, precluding definitive comparisons of these modalities. 8 Randomized clinical trials in SCCHN evaluating the comparative effectiveness of different RT techniques and particle therapy are awaited. Novel Advances in Systemic Management of SCCHN The systemic management of SCCHN continues to represent an unmet medical need because cetuximab, the monoclonal antibody against the epidermal growth factor receptor (EGFR), remains the only molecularly targeted agents approved by the U.S. Food and Drug Administration (FDA) for the treatment of SCCHN. Targeting EGFR Resistance in SCCHN Multiple mechanisms of resistance to EGFR inhibition have been proposed in SCCHN, including: 1) presence of the mutant type III variant of EGFR (EGFRvIII) as the result of an in-frame deletion mutation of exons 2 to 7 spanning the extracellular ligand-binding domain and 2) extensive crosstalk among the ErbB/HER family receptors and with other signaling pathways. EGFRvIII prevents the binding of EGF and other ligands to the receptor and leads to constitutive activation of the EGFR tyrosine kinase domain and its downstream effectors. 9 With crosstalk, blockade of a single receptor such as EGFR can lead to compensatory upregulation of escape mechanisms along the same EGFR receptor axis or its downstream effectors, or alternatively, via rescue from another pathway. Figure 1 depicts several strategies that are currently being evaluated in clinical trials to overcome EGFR resistance in cancer, including SCCHN. Targeting Members of the ErbB/HER Family Other Than EGFR Currently, agents that target multiple members of the ErbB/HER family other than EGFR are actively being developed in the clinic, with the rationale to overcome de novo and/or acquired resistance to EGFR inhibition. Pan-HER inhibitors. Afatinib and dacomitinib are both orally available, small-molecule, irreversible Pan-HER in-
EARLY ADVANCES IN SCCHN Fig 1. Targeting epidermal growth factor resistance in squamous cell carcinoma of the head and neck. Abbreviations: ERK, extracellular signalregulated kinase; mTOR, mammalian target of rapamycin; PI3K, phosphoinositide 3-kinase; PTEN, phosphatase and tensin homolog. Targeting other receptor tyrosine kinases hibitors with specificities against EGFR, HER2, and HER4 tyrosine kinases. In addition to targeting ErbB/HER family receptor crosstalk, both of these agents have reported activity against EGFRvIII in preclinical models. In a randomized, open-label phase II study of afatinib compared with cetxuimab in 124 platinum-refractory patients with recurrent or metastatic SCCHN, the objective response rate (ORR) favored afatinib compared with cetuximab (22% vs. 13%, respectively), as did the median progression-free survival (PFS; 16 weeks compared with 10 weeks, respectively). The most common adverse events related to afatinib included diarrhea and skin toxicity. 10 Afatinib is currently being evaluated in two phase III trials, including one in the recurrent or metastatic setting against methotrexate after progression with platinum-based chemotherapy (NCT- 01345682), and the other in the locally advanced setting against placebo as maintenance therapy after completion of definitive CRT; this latter trial (NCT01345669) is limited to only those patients whose tumors are HPV negative. Dacomitinib has undergone single-arm, open-label phase II evaluation as a first-line therapy in 69 patients with recurrent or metastatic SCCHN and reported an ORR of 11%, median PFS of 2.8 months, and median overall survival (OS) of 7.6 months. Similar to afatinib, diarrhea and skin toxicity were the most frequent treatment-related adverse events. 11 HER3-targeting agents. HER3 has emerged to become a key target in the therapeutic strategy to overcome EGFR resistance. Despite its catalytically inactive tyrosine kinase domain, HER3 is capable of allosterically activating the kinase domain of its heterodimerized partners, preferably HER2. 12 In addition, phosphorylation of the C-terminal tail of HER3 leads to direct recruitment of the p85 subunit of phosphoinositide 3-kinase (PI3K), rendering it a potent activator of the PI3K-AKT survival pathway. 13,14 Several HER3 targeting agents are undergoing or completing phase I development, including MEHD7945A (Genentech, Inc., South San Francisco, CA), a humanized, dual-specific, immunoglobulin (Ig) G1 antibody capable of binding to both PI3K IRS Shc Grb2 Sos Targeting receptor tyrosine kinases e.g. HER family receptors TSC2 AKT PTEN Ras Targeting TSC1 multiple nodes of the Targeting Raf same RHEB mTOR multiple oncogenic pathways (horizontal blockade) MEK 1/2 ERK 1/2 oncogenic pathway (vertical blockade) S6K 4E-BP Transcription Translation Growth, Proliferation, Metastasis, Survival EGFR and HER3 (NCT01207323) 15 ; MM-121/SAR256212 (NCT00734305; Merrimack Pharmaceuticals Inc., Cambridge, MA and Sanofi Oncology, Paris, France) and U3- 1287/AMG 888 (NCT00730470; U3 Pharma, Munich, Germany and Amgen, Inc., Thousand Oaks, CA), both fully human monoclonal antibodies directed against HER3; among others. In a recent report using a mouse monoclonal antibody (RTJ.2, Santa Cruz Biotechnology, Santa Cruz, CA; dilution 1:750) against HER3, immunohistochemical evaluation of 387 primary SCCHN specimens showed positive membranous and cytoplasmic HER3 expression in 34 (8.8%) and 300 (77.5%) cases, respectively. Membranous HER3 overexpression was significantly associated with worse OS (p � 0.027) and was an independent prognostic factor in multivariate analysis. 16 In addition, Wilson and colleagues demonstrated that a substantial proportion of primary SCCHN samples and cell lines have increased mRNA expression of the ligand heregulin, which in turn can lead to autocrine activation of HER3. 17 As such, heregulindriven tumors with coexpression and activation of HER3 may represent a target SCCHN patient population for HER3-directed therapies. Targeting EGFR–Mitogen-Activated Protein Kinase and Other Oncogenic Pathways Concurrently In many advanced solid tumors, even among molecularly profiled patients whose tumors harbor activating mutations, the activity of selective pathway inhibitors administered as monotherapy appears limited, or in cases of initial response, the duration of response is typically short lived. Therapeutic resistance may occur as a result of incomplete pathway blockade with a single inhibitor, crosstalk and/or upregulation of compensatory escape signaling pathways. A logical approach to evade such mechanisms of resistance is by using targeted combinations with two agents either interrogating the same oncogenic signaling pathway (vertical blockade) or via concurrent modulation of two separate signaling pathways (horizontal blockade). Targeting other receptor ty- 375
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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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Page 399 and 400: RECENT CLINICAL HIGHLIGHTS IN GYNEC
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Page 407 and 408: ESGO EDUCATIONAL AND RESEARCH ACTIV
Page 409 and 410: UPFRONT TREATMENT OF OVARIAN CANCER
Page 411 and 412: ANTIANGIOGENICS AND PARP INHIBITORS
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Page 415 and 416: Intraperitoneal Treatment in Ovaria
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Page 419 and 420: Dose-Dense Chemotherapy and Neoadju
Page 421 and 422: CHEMOTHERAPY FOR OVARIAN CANCER Fig
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Page 425 and 426: UTERINE SARCOMA: CHALLENGING CASES
Page 427 and 428: HISTOLOGIC FEATURES AND MANAGEMENT
Page 433 and 434: SURGICAL OPTIONS FOR UTERINE SARCOM
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Page 437 and 438: PATIENTS WITH HPV-POSITIVE OROPHARY
Page 439 and 440: HPV-INDUCED OROPHARYNX CANCER analy
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Page 443: Important Early Advances in Squamou
Page 447 and 448: Application of Genomic and Proteomi
Page 449 and 450: GENOMIC AND PROTEOMIC TECHNOLOGIES
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Page 453 and 454: TREATMENT OF THYROID CANCERS: NEW I
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Page 459 and 460: Systemic Therapeutic Approaches to
Page 461 and 462: APPROACHES TO ADVANCED THYROID CANC
Page 463 and 464: AVOIDING OVERDIAGNOSIS AND OVERTREA
Page 465 and 466: Table 1. Prevalence of Prostate Can
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Page 469 and 470: Overdiagnosis and Overtreatment of
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Page 475 and 476: COSTS OF CANCER CARE: AFFORDABILITY
Page 477 and 478: REDUCING THE COST OF CANCER CARE Fi
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Page 483 and 484: Why Hasn’t Genomic Testing Change
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Page 487 and 488: MANAGEMENT OF CHRONIC LYMPHOCYTIC L
Page 489 and 490: PREDICTIVE PARAMETERS IN CLL Table
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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
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SYSTEMIC TREATMENT OF THYMOMA cance
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What Is the Best Strategy for Incor
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TREATMENT OF FOLLICULAR LYMPHOMA Fi
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TREATMENT OF FOLLICULAR LYMPHOMA me
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TREATMENT OF FOLLICULAR LYMPHOMA ou
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TREATMENT OPTIONS IN INDOLENT LYMPH
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ROLE OF HCT FOR INDOLENT LYMPHOMA T
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ROLE OF HCT FOR INDOLENT LYMPHOMA T
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ROLE OF HCT FOR INDOLENT LYMPHOMA e
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CONTROVERSIES IN MYELOMA: INDUCTION
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TRANSPLANTATION FOR MYELOMA Alterna
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TRANSPLANTATION FOR MYELOMA compare
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TRANSPLANTATION FOR MYELOMA autolog
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CURRENT STATUS OF MYELOMA THERAPY K
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CURRENT STATUS OF MYELOMA THERAPY F
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CURRENT STATUS OF MYELOMA THERAPY T
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Maintenance Therapy for Myeloma: Ho
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MAINTENANCE THERAPY FOR MULTIPLE MY
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NEW OPTIONS, NEW QUESTIONS: HOW TO
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THERAPIES FOR PATIENTS WITH METASTA
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ANTIEMETICS: CURRENT STANDARDS, EME
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ANTIEMETICS: ASCO GUIDELINE UPDATE
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Chemotherapy-Induced Nausea and Vom
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INCIDENCE AND PREVALENCE OF CHEMOTH
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New Frontiers in Mucositis By Dougl
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MUCOSAL INJURY CAUSED BY CANCER THE
Page 643 and 644:
Page 645 and 646:
Page 647 and 648:
Short- and Long-term Cardiovascular
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Recent Advances in Cardiotoxicity o
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CARDIOTOXICITY OF ANTICANCER THERAP
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CARDIOTOXICITY OF ANTICANCER THERAP
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The Oncologist as the Patient with
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THE ONCOLOGIST AS THE PATIENT OR RE
Page 659 and 660:
Prolonged Febrile Neutropenia in th
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FEBRILE NEUTROPENIA IN PEDIATRIC CA
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FEBRILE NEUTROPENIA IN PEDIATRIC CA
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TREATMENT APPROACHES IN CHILDREN wh
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TREATMENT APPROACHES IN CHILDREN th
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GENETIC COUNSELING OF THE PATIENT W
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CANCER PREDISPOSITION IN CHILDHOOD
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Page 675 and 676:
Page 677 and 678:
Page 679 and 680:
HOW TO MANAGE VERY RARE PEDIATRIC C
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RARE CANCER IN CHILDREN Registries
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Genetic Alterations in Childhood Me
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GENETIC ALTERATIONS IN CHILDHOOD ME
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Desmoid-Type Fibromatosis in Childr
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CHEMOTHERAPY FOR DESMOID TUMOR Tabl
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CHEMOTHERAPY FOR DESMOID TUMOR 14.
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Targeting the Insulin-Like Growth F
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TARGETING THE IGF SYSTEM Fig. 1. Th
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TARGETING THE IGF SYSTEM malignanci
Page 699 and 700:
Hedgehog Pathway in Pediatric Cance
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HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 703 and 704:
HEDGEHOG PATHWAY IN PEDIATRIC CANCE
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Development and Refinement of Augme
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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
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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
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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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