2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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THERAPEUTIC OPTIONS FOR PROSTATE CANCER therapy at each juncture, but today we are often humbled by how poorly we predict patient outcomes. What about combination therapy? Is the metastatic CRPC state to be restricted to a sequencing therapeutic paradigm? Though combination therapy has a certain attraction in CRPC, other than the agents designed to inhibit skeletalrelated events (zoledronic acid and denosumab), there are minimal data on combination therapies using the survivalprolonging agents. Until new data exist, the current sequencing paradigm may be optimal for patients in nonclinical trial settings. It is clear from phase I/II studies that patients with nondocetaxel-pretreated metastatic CRPC are quite responsive to the newer hormonal agents, such as abiraterone and MDV-3100. 9,10 This emphasizes that our division of metastatic CRPC into pre- and postdocetaxel spaces Author’s Disclosures of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role Oliver Sartor Algeta; Amgen; Bayer; Bellicum; Bristol-Myers Squibb; Celgene; Dendreon; Exelixis; GlaxoSmithKline; Johnson & Johnson; Medivation; Oncogenex; Pfizer; Sanofi; Takeda Authors’ Disclosures of Potential Conflicts of Interest 1. Tannock IF, de Wit R, Berry WR, et al. Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. N Engl J Med. 2004;351:1502-1512. 2. Petrylak DP, Tangen CM, Hussain MH, et al. Docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer. N Engl J Med. 2004;351:1513-1520. 3. Kantoff PW, Higano CS, Shore ND, et al. Sipuleucel-T immunotherapy for castration-resistant prostate cancer. N Engl J Med. 2010;363:411-422. 4. de Bono JS, Oudard S, Ozguroglu M, et al. Prednisone plus cabazitaxel or mitoxantrone for metastatic castration-resistant prostate cancer progressing after docetaxel treatment: A randomised open-label trial. Lancet. 2010; 376:1147-1154. 5. de Bono JS, Logothetis CJ, Molina A, et al. Abiraterone and increased survival in metastatic prostate cancer. N Engl J Med. 2011;364:1995-2005. 6. Parker C, Heinrich D, O’Sullivan JM, et al. Overall survival benefit of radium-223 chloride (Alpharadin) in the treatment of patients with symptom- is one based on regulatory and not biologic concerns. Trials are ongoing to further assess both abiraterone and MDV- 3100 in the predoctaxel space and perhaps there will be results from one of these trials by the 2012 ASCO Annual Meeting. All of the FDA-approved agents to date have been approved in a metastatic CRPC setting, yet many patients present to a physician with a rising prostate-specific antigen, a castrate level of testosterone, and no radiographic evidence of metastatic disease. What do you do in this case? The answer is not yet clear and there are no FDA-approved treatments. In my practice, a variety of secondary hormonal agents, such as nilutamide, bicalutamide, low-dose diethylstilbestrol, and ketoconazole are used despite no phase III evidence to support their use. Good clinical trials are always an important consideration as well. Stock Ownership Honoraria REFERENCES Research Funding Sanofi Algeta; AstraZeneca; Cougar Biotechnology; Exelixis; GlaxoSmithKline; Johnson & Johnson; Sanofi Expert Testimony Other Remuneration atic bone metastases in castration-resistant prostate cancer (CRPC): a phase III randomized trial (ALSYMPCA). Eur J Cancer. 2011;47 (suppl 2). 7. Scher HI, Fizazi K, Saad F, et al. Effect of MDV3100, an androgen receptor signaling inhibitor (ARSI), on overall survival in patients with prostate cancer postdocetaxel: Results from the phase III AFFIRM study. J Clin Oncol. 2012;30 (suppl 5; abstr LBA1). 8. Perlroth DJ, Thompson SF, Luna Y, et al. Time to ADT and chemotherapy initiation for treatment of metastatic prostate cancer (mPC). J Clin Oncol. 2012;30 (suppl 5; abstr 41). 9. Attard G, Reid AH, Yap TA, et al. Phase I clinical trial of a selective inhibitor of CYP17, abiraterone acetate, confirms that castration-resistant prostate cancer commonly remains hormone driven. J Clin Oncol. 2008;26: 4563-4571. 10. Scher HI, Beer TM, Higano CS, et al. Antitumour activity of MDV3100 in castration-resistant prostate cancer: A phase 1-2 study. Lancet. 2010;375: 1437-1446. 291
Prognostic, Predictive, and Surrogate Factors for Individualizing Treatment for Men with Castration-Resistant Prostate Cancer By Rhonda L. Bitting, MD, and Andrew J. Armstrong, MD, MSc Overview: With thesurge in therapeutic options for castrationresistant prostate cancer (CRPC) comes increasingly complicated treatment decision making, highlighting the need for biomarkers that can identify appropriate patients for specific WITH THE increasing number of U.S. Food and Drug Administration (FDA) approvals of new systemic agents for men with metastatic CRPC over the past 2 years, the optimal treatment strategy and sequence of therapies are evolving quickly. With novel immunotherapies, hormonal therapies, bone-targeted radioisotopes, bone microenvironment–targeted agents, and chemotherapies emerging in both the predocetaxel and postdocetaxel space, it becomes imperative to develop rational combinations and sequences of these agents, as well as to identify groups of men that are most likely to benefit from a particular treatment. Thus, there is an increasing need for biomarkers to help guide clinical decision making, especially considering the number of emerging agents currently in development and the high cost of these therapies. Here we discuss the role, context of use, and the limitations of existing biomarkers in CRPC. We also examine approaches for the evaluation of novel biomarkers in clinical trials depending on the clinical or research context of use. A biomarker is defined as a “characteristic that is objectively measured and evaluated as an indicator of normal biologic processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.” 1 Biomarkers are intended to guide the treatment of patients, and they can be prognostic, predictive, pharmacodynamic, correlative, and/or surrogate in nature. A prognostic biomarker reflects a patient’s disease outcome independent of therapy (natural history), whereas a predictive biomarker identifies the likelihood of benefit from a specific therapy. 2 A number of prognostic biomarkers have been reported in CRPC (Table 1); however, there are no validated predictive biomarkers in this disease. Although predictive biomarkers exist in oncology (e.g., HER2 overexpression in breast cancer predicts for benefit with anti-HER2 agents, BRAF mutations predict for improved outcomes with BRAF inhibitors in melanoma, anaplastic lymphoma kinase [ALK] fusions predict for benefit to ALK tyrosine kinase inhibitors in lung adenocarcinoma), prostate cancer has lagged behind in the clinical application of predictive biomarkers in drug development. These predictive biomarkers offer the hope of individualized approaches to therapy, breaking down a generally heterogeneous disease into more homogeneous molecularly defined subsets of patients in order to maximize benefit and minimize harm. In addition, surrogate biomarkers of overall survival (OS) remain uncertain in CRPC, in which measures such as progression-free survival (PFS), radiographic or pain responses, and prostate-specific antigen (PSA) declines have generally fallen short of a generalizable surrogate. A surrogate biomarker is a biomarker that can substitute for a 292 treatments and accurately assess disease response. Here we discuss existing and potential prognostic, predictive, and surrogate biomarkers in CRPC. clinically important endpoint such as OS but must meet several statistical criteria (such as Prentice’s criteria) and be validated across multiple trials examining agents with a range of mechanisms and clinical contexts. 3 Ongoing work in CRPC to identify optimal surrogate biomarkers, particularly in the fields of circulating tumor cell (CTC) characterization and optimal classifications of radiographic progression in CRPC, holds some promise in providing early evidence of activity for novel therapies and thus accelerated drug approvals and delivery of active agents into the clinic. However, much work is to be done on this front. Certain biomarkers are entirely used for determining drug mechanism or metabolism (pharmacogenomic or pharmacogenetic) and will not be further discussed in this review. These biomarkers are essential, however, in identifying pathophysiology and drug mechanism and in suggesting predictive and surrogate measures of clinical efficacy, and they are typically explored in the initial characterization, validation, and qualification of a biomarker. As biomarkers emerge in clinical settings, these predictive or surrogate factors can potentially guide treatment decision making (e.g., when to start a therapy, who to offer a therapy to, when to stop a treatment and declare failure or response), underscoring the need for a rigorous approach to the development of predictive and surrogate biomarkers in parallel with drug development in CRPC. Prognostic Biomarkers in CRPC The sections below provide advantages, limitations, and evidence for use of common serologic and urinary biomarkers in CRPC. Imaging response, pain, and quality-of-life changes are not addressed here, though Table 1 provides a comprehensive list of prognostic biomarkers in CRPC. PSA Serum PSA often reflects the disease burden in men with CRPC and has been included in prognostic models as an independent risk factor for disease-related mortality. 4 Changes in PSA over time during treatment may be informative regarding a patient’s response to therapy; however, this response is variable depending on the mechanism of action of the therapy. For example, treatment with the immunotherapy sipuleucel-T improves survival without From the Duke Cancer Institute and the Duke Prostate Center, Durham, NC. Authors’ disclosures of potential conflicts of interest are found at the end of this article. Address reprint requests to Andrew Armstrong, MD, MSc, Duke University Medical Center 102002, Durham, NC 27710; email: andrew.armstrong@duke.edu.. © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10
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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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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
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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
Page 661 and 662:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 663 and 664:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
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TREATMENT APPROACHES IN CHILDREN wh
Page 667 and 668:
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.
Page 693 and 694:
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
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
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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
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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