2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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52. American Cancer Society. Cancer facts and figures for African Americans 2005-2006. Atlanta, 2005. 53. Mead H, Cartwright-Smith L, Jones K, et al. Racial and ethnic disparities in U.S. health care: A chartbook. New York: The Commonwealth Fund, 2008. 54. Ries LAG, Eisner MP, Kossary CL, et al. SEER cancer statistics review 1973-1997. National Cancer Institute. Bethesda, MD, 2000. 55. Hickok JT, Roscoe JA, Morrow GR, et al. Nausea and emesis remain 540 BASCH ET AL significant problems of chemotherapy despite prophylaxis with 5-hydroxytryptamine-3 antiemetics: A University of Rochester James P. Wilmot Cancer Center Community Clinical Oncology Program Study of 360 cancer patients treated in the community. Cancer. 2003;97:2880-2886. 56. Guidance for Industry. Patient-Reported Outcome Measures: Use in Medical Product Development to Support Labeling Claims. http://www.fda. gov/downloads/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/ UCM193282.pdf. Accessed September 1, 2011.
Chemotherapy-Induced Nausea and Vomiting Incidence and Prevalence Overview: Although chemotherapy-induced nausea and vomiting is recognized as having been an important problem during the initial introduction of chemotherapy into the antineoplastic armamentarium, the assumption that this problem has already been solved can restrict optimal management and further advances. Underestimation of nausea and vomiting may have many causes. If these toxicities are assumed to be necessary properties of chemotherapy, then their incidence may be taken for granted. If nausea and vomiting appear after discharge from the clinic several days after chemotherapy, these toxicities may not be reported because of poor recall or THE JEWISH Passover service 1 contains the story of the four sons—one wise, one evil, one simple, and one who does not know how to ask a question. In the explanation of the story, we learn that the most dangerous son is not the evil one, but rather the one who does not know how to ask a question. If we do not know where a lack of knowledge lies, then we cannot begin to address that ignorance or to answer that question. This is also true in medical science and has become pertinent in recent years in several areas of oncology. Approximately 80% of patients with lung cancer have a significant smoking exposure, and we have long assumed that the remainder had a smoking exposure that had not yet been identified. Now that we realize that there is a different unanswered and unaddressed question concerning the role of epidermal growth factor receptor mutations 2 and EML4- ALK translocations, 3 we can begin to address this problem with appropriate targeted agents. We have also always known that smoking and drinking are important risk factors for head and neck cancer, and we assumed that patients without those risk factors simply had bad luck. Now that we appreciate the role of human papillomavirus infection in oropharyngeal cancers, 4 we can begin to address the unique natural history of this illness and the possibility of identifying specific remedies. Although significant progress has been made in the prevention and control of chemotherapy-induced nausea and vomiting, underappreciation of the incidence and prevalence of this problem still limits our effectiveness in addressing its true magnitude. This misunderstanding begins with the systems used to grade intrinsic emetogenicity, which generally divide agents into those that are highly emetogenic, moderately emetogenic, low emetogenic, or minimally emetogenic. 5 The wide range of frequencies of emesis within a given category, particularly moderately emetogenic chemotherapy (30% to 90% vomiting), can lead to significant variability in interpreting the emetogenic risk of any chemotherapeutic agent. It must also be remembered that these grading systems were specifically designed to describe the acute emetogenicity of chemotherapy during the 24 hours after administration of a single intravenous bolus dose without concurrent administration of other chemotherapies and without the administration of antiemetic agents. Numerous modifying factors are therefore not considered, including the presence of delayed nausea and vomiting (24 to 120 hours after chemotherapy) or anticipatory nausea and By Steven M. Grunberg, MD because of efforts by patients to avoid unnecessary complaints. Physician education may be compromised if physicians see nausea and vomiting as population problems but not problems for their own patients. Failure to recognize nausea and vomiting as two distinct entities that may appear independently of each other can also limit understanding of the prevalence of these problems and efforts at effective management. Continued attention to the impact of nausea and vomiting on the patient experience will be necessary to insure optimal maintenance of quality of life. vomiting (before chemotherapy), the possibility of extended infusion or divided doses of chemotherapy, or the route of administration. A single dose of an oral chemotherapy may be less emetogenic than a single dose of an intravenous formulation, but oral chemotherapy regimens are often multiple day–multiple dose regimens and emetogenicity may gradually increase as the latter days of administration are reached. 5 The emetogenicity of combination regimens is also only rarely considered in such tables. Of greater importance is the source of emetogenicity data itself. Phase I studies of new agents are designed to identify dose-limiting toxicities (grade 3 and grade 4 toxicities), and lesser toxicities (such as grade 1 nausea/vomiting) may go unreported, thereby underestimating the true incidence of the problem. Prophylactic use of antiemetics may not be restricted in a phase I study of a new cytotoxic chemotherapy, even if it is not known whether the agent is emetogenic. This can lead to overestimation of the emetogenicity of a new chemotherapy, where administration of a prophylactic antiemetic never was required, or to underestimation of the emetogenicity of a new chemotherapy, where prophylactic administration of antiemetic really was partially effective. Even when the existence of the problem is recognized, the magnitude of the problem may not be appreciated, particularly if pertinent events occur away from direct observation by medical personnel. Advances in clinical practice have moved administration of chemotherapy for most solid tumor patients from the hospital to the clinic setting. Although patients are directly observed on the day of treatment, the following days (delayed period) are often spent at home. In an observational study, 6 we asked 24 physicians and nurses from 14 oncology practices in the United States and Europe to estimate the percentage of patients in their own practices who were having chemotherapy-induced nausea or vomiting after highly or moderately emetogenic chemotherapy. We then surveyed 298 patients from these practices using 5-day antiemetic diaries to determine the actual frequency of From the Division of Hematology/Oncology, University of Vermont, Burlington, VT. Author’s disclosure of potential conflicts of interest are found at the end of this article. Address reprint requests to Steven M. Grunberg, MD, Division of Hematology/Oncology, University of Vermont, 89 Beaumont Avenue - Given Building E214, Burlington, VT 05405; email: steven.grunberg@uvm.edu © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10 541
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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
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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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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 617 and 618: NEW OPTIONS, NEW QUESTIONS: HOW TO
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Page 625 and 626: ANTIEMETICS: CURRENT STANDARDS, EME
Page 627 and 628: ANTIEMETICS: ASCO GUIDELINE UPDATE
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Page 637 and 638: INCIDENCE AND PREVALENCE OF CHEMOTH
Page 639 and 640: New Frontiers in Mucositis By Dougl
Page 641 and 642: MUCOSAL INJURY CAUSED BY CANCER THE
Page 647 and 648: Short- and Long-term Cardiovascular
Page 649 and 650: Recent Advances in Cardiotoxicity o
Page 651 and 652: CARDIOTOXICITY OF ANTICANCER THERAP
Page 653 and 654: CARDIOTOXICITY OF ANTICANCER THERAP
Page 655 and 656: The Oncologist as the Patient with
Page 657 and 658: THE ONCOLOGIST AS THE PATIENT OR RE
Page 659 and 660: Prolonged Febrile Neutropenia in th
Page 661 and 662: FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 663 and 664: FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 665 and 666: TREATMENT APPROACHES IN CHILDREN wh
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Page 669 and 670: GENETIC COUNSELING OF THE PATIENT W
Page 671 and 672: CANCER PREDISPOSITION IN CHILDHOOD
Page 679 and 680: HOW TO MANAGE VERY RARE PEDIATRIC C
Page 681 and 682: RARE CANCER IN CHILDREN Registries
Page 683 and 684: Genetic Alterations in Childhood Me
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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
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Hedgehog Pathway in Pediatric Cance
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HEDGEHOG PATHWAY IN PEDIATRIC CANCE
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HEDGEHOG PATHWAY IN PEDIATRIC CANCE
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Development and Refinement of Augme
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ABFM THERAPY FOR PEDIATRIC ALL than
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ABFM THERAPY FOR PEDIATRIC ALL Auth
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RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 713 and 714:
RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 715 and 716:
Role of Doxorubicin in Rhabdomyosar
Page 717 and 718:
DOXORUBICIN IN RHABDOMYOSARCOMA 8.
Page 719 and 720:
Identification of Novel Biologic Ta
Page 721 and 722:
NOVEL TARGETS IN THE TREATMENT OF D
Page 723 and 724:
Is Biopsy Safe in Children with New
Page 725 and 726:
SAFETY OF DIPG BIOPSY IN CHILDREN F
Page 727 and 728:
SAFETY OF DIPG BIOPSY IN CHILDREN 1
Page 729 and 730:
CHILDREN WITH DIFFUSE INTRINSIC PON
Page 731 and 732:
Communication and Decision Support
Page 733 and 734:
COMMUNICATION AND DECISION SUPPORT
Page 735 and 736:
Page 737 and 738:
Page 739 and 740:
Planning for the Future: The Role o
Page 741 and 742:
present in the office suite but doe
Page 743 and 744:
Summary and Care Plan are provided.
Page 745 and 746:
DOING IT RIGHT, AND FOR LESS: IMPLE
Page 747 and 748:
CLINICAL PATHWAYS STANDARDIZING PER
Page 749 and 750:
CLINICAL PATHWAYS STANDARDIZING PER
Page 751 and 752:
The Future of Oncology Care with Pe
Page 753 and 754:
quantity. Determining the appropria
Page 755 and 756:
THE ASCO QUALITY ONCOLOGY PRACTICE
Page 757 and 758:
IMPROVING VALUE OF CARE IN ONCOLOGY
Page 759 and 760:
Page 761 and 762:
Page 763 and 764:
PHYSICIAN WELLNESS: COPING WITH REP
Page 765 and 766:
also provides insight on how clinic
Page 767 and 768:
good resource for exploring the pri
Page 769 and 770:
of death or following death and inc
Page 771 and 772:
telephone call to the family, sendi
Page 773 and 774:
New Insights in Cross-Cultural Comm
Page 775 and 776:
CROSS-CULTURAL COMMUNICATION Sideba
Page 777 and 778:
THE ONCOLOGIST, THE PATIENT, AND TH
Page 779 and 780:
estimate of the proportion of their
Page 781 and 782:
exactly the same treatment, even th
Page 783 and 784:
How to Decide Whether to Offer and
Page 785 and 786:
NONSTANDARD THERAPIES FOR ADVANCED
Page 787 and 788:
NONSTANDARD THERAPIES FOR ADVANCED
Page 789 and 790:
TARGETED THERAPIES IN TARGETED OR U
Page 791 and 792:
TARGETED THERAPY IN SARCOMA rates a
Page 793 and 794:
TARGETED THERAPY IN SARCOMA seen in
Page 795 and 796:
TARGETED THERAPY IN SARCOMA recepto
Page 797 and 798:
Adjuvant Treatment of Gastrointesti
Page 799 and 800:
ADJUVANT THERAPY IN HIGH-RISK GASTR
Page 801 and 802:
Management of Tyrosine Kinase Inhib
Page 803 and 804:
TKI-RESISTANT GIST Primary Imatinib
Page 805 and 806:
TKI-RESISTANT GIST Table 2. Clinica
Page 807 and 808:
BIOLOGIC PRINCIPLES OF TARGETED COM
Page 809 and 810:
COMBINING TARGETED AGENTS IN CLINIC
Page 811 and 812:
COMBINING TARGETED AGENTS IN CLINIC
Page 813 and 814:
Combination Therapies Building on t
Page 815 and 816:
COMBINATIONS FOR MELANOMA agents th
Page 817 and 818:
MECHANISMS OF RESISTANCE TO TARGETE
Page 819 and 820:
RESISTANCE MECHANISMS TO MAPK INHIB
Page 821 and 822:
RESISTANCE MECHANISMS TO MAPK INHIB
Page 823 and 824:
Mechanisms of Resistance to Targete
Page 825 and 826:
RESISTANCE TO TARGETED THERAPIES IN
Page 827 and 828:
RESISTANCE TO TARGETED THERAPIES IN
Page 829 and 830:
Translating PI3K-Delta Inhibitors t
Page 831 and 832:
THE STORY OF CAL-101 6% of patients
Page 833 and 834:
PI3 Kinase in Cancer: From Biology
Page 835 and 836:
PI3 KINASE IN CANCER Fig. 1. The PI
Page 837 and 838:
PI3 KINASE IN CANCER Fig. 3. In viv
Page 840:
This publication is supported by an
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2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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