2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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ANTIBODY CONJUGATES: TARGETED THERAPY MEETS CHEMOTHERAPY IN ONE DRUG CHAIR Howard A. Burris III, MD The Sarah Cannon Research Institute Nashville, TN SPEAKERS John P. Leonard, MD Weill Cornell Medical College New York, NY James D. Marks, MD, PhD University of California, San Francisco San Francisco, CA
Trastuzumab Emtansine (T-DM1): Hitching a Ride on a Therapeutic Antibody Overview: The treatment of cancers with chemotherapy is frequently limited by side effects. The effectiveness may be improved by the use of monoclonal antibodies to deliver cytotoxic agents to cancer cells while limiting exposure to normal tissues. The use of antibody-drug conjugates (ADCs) is one such strategy: a drug connected by a linker to an antibody specific for a tumor antigen is the basic makeup of an ADC. Overexpression and amplification of HER2 is associated with clinically aggressive breast cancers, and the use of trastuzumab to target HER2 has been highly effective. That said, most patients with HER2-positive metastatic breast cancer will eventually have disease progression during targeted therapy. Trastuzumab emtansine (T–DM1) is a novel ADC that combines the humanized antibody trastuzumab and the potent antimicrotubule agent T-DM1 (derivative of maytansine) using a unique and highly stable linker. The potential of maytansine was found in the 1970s with clinical responses noted against breast cancer; however, substantial toxicity prohibited further development. DM1 possesses in vitro cytotoxicity 10 to 200 times greater than that of taxanes and vinca alkaloids. A phase I trial of T-DM1 for patients with heavily pretreated HER2positive breast cancer determined a recommended dose of 3.6 THE TREATMENT of many cancers is often based on the use of standard chemotherapy agents and regimens. The effectiveness of this approach is frequently limited by substantial systemic toxicities associated with these agents. The therapeutic index can be markedly improved with the use of monoclonal antibodies to deliver potent cytotoxic agents to cancer cells, thus minimizing the exposure of the agents to normal tissues. The use of antibody-drug conjugates (ADCs) is one such strategy; a cytotoxic drug connected by a chemical linker to a monoclonal antibody specific for a tumor antigen is the basic makeup of an ADC. More stable linkers and different cytotoxic agents have enabled a new generation of ADCs to enter the clinic. First and foremost, the design of an ADC centers on the selection of an antigen that is tumor-specific and accessible to antibody binding at the tumor cell. Overexpression and amplification of HER2 is associated with clinically aggressive breast cancers that have historically had an overall poor prognosis and therapeutic resistance to traditional drugs. The use of trastuzumab to target the extracellular domain of HER2 has been highly effective in the treatment of this type of breast cancer. Multiple mechanisms for the efficacy of trastuzumab have been proposed, including inhibition of the PI3K signal transduction pathway, antibody-dependent cell-mediated cytotoxicity (ADCC), and induction of apoptosis. When combined with chemotherapy, trastuzumab improves the time to disease progression and overall survival for patients with HER2positive metastatic breast cancer. Furthermore, mature data from four large phase III trials in which trastuzumab was evaluated in the adjuvant setting, have demonstrated marked improvements in both disease-free and overall survival. That said, most patients with HER2-positive metastatic breast cancer will eventually have disease progression during targeted therapy while the cancer continues to both By Howard A. Burris III, MD mg per kilogram delivered every 3 weeks. Responses were seen in multiple patients. T-DM1 was then studied in phase II trials of patients with HER2-positive metastatic breast cancer. In a studies of 112 and 110 patients in whom disease had progressed during HER2-directed therapy, T-DM1 was associated with objective response rates of 26% and 34%, respectively. The agent was well tolerated in both trials, with most toxicities being grade 1 and 2, and no bleeding episodes or cardiac events occurring. Additional phase II and III trials are now evaluating T-DM1 in the first-line setting. In one such trial, T-DM1 was compared with standard dosing of trastuzumab every 3 weeks plus docetaxel every 3 weeks. Objective response rates were comparable and grade 3 or4 adverse events were substantially reduced in the T-DM1 arm. The anticipated selective activity and reduction in side effects were thus noted. Randomized multicenter phase III trials are ongoing, including the EMILIA trial, an open-label trial of T-DM1 compared with the U.S. Food & Drug Administrationapproved regimen of capecitabine plus lapatinib. The results of studies completed to date suggest T-DM1 is active in patients who have cancer resistant to trastuzumab-based combinations. express HER2 and demonstrate sensitivity to antimicrotubule agents. T-DM1 is a novel ADC that combines the humanized antibody trastuzumab and the potent antimicrotubule agent DM1 (derivative of maytansine) using a unique and highly stable linker. 1 T-DM1, with its ability to bind HER2 with the same affinity as trastuzumab, maintains the activity of trastuzumab in addition to providing intracellular delivery of the antimicrotubule agent DM1. It is hypothesized that when T-DM1 binds to HER2 receptors, a portion of them undergo receptor internalization, followed by lysosomal degradation. Activated DM1 is then released from lysosome into the cellular cytoplasm after antibody degradation, inhibiting microtubule assembly and causing cell death. Potent cytotoxic agents are needed to maximize the role of drug conjugates. In addition, the drug must be inactive and nontoxic in the conjugated form to avoid systemic toxicities. Few agents are able to fulfill these characteristics, including the inhibitors of tubulin polymerization (the maytansinoids and the auristatins). The potential of maytansine as an anticancer agent was originally discovered in the 1970s with clinical responses noted against breast cancer. However, substantial and random toxicities of neuropathy and myelosuppression were prohibitive of further clinical development. Recently, an attempt at improving the therapeutic index through conjugation with trastuzumab was undertaken, leading to the From the Sarah Cannon Research Institute, Nashville, TN. Author’s disclosures of potential conflicts of interest are found at the end of this article. Address reprint requests to Howard A. Burris, MD, Tennessee Oncology/Sarah Cannon Research Institute, 250 25 th Avenue N., Suite 110, Nashville, TN 37203; email: Howard.burris@scresearch.net © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10 159
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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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GLIOBLASTOMA: BIOLOGY, GENETICS AND
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Page 135 and 136: FUTURE DIRECTIONS IN GBM THERAPY pr
Page 137 and 138: FUTURE DIRECTIONS IN GBM THERAPY Ch
Page 139 and 140: ESTABLISHING TREATMENTS FOR GLIOBLA
Page 145 and 146: Current Concepts in Brain Tumor Ima
Page 147 and 148: CONCEPTS IN BRAIN TUMOR IMAGING tum
Page 149 and 150: CONCEPTS IN BRAIN TUMOR IMAGING Aut
Page 151 and 152: PERSPECTIVES ON HEADLINE-MAKING NEW
Page 153 and 154: TTF THERAPY IN GLIOBLASTOMA Fig. 1.
Page 155 and 156: TTF THERAPY IN GLIOBLASTOMA istics.
Page 157 and 158: TTF THERAPY IN GLIOBLASTOMA because
Page 159 and 160: Limitations of Adaptive Clinical Tr
Page 161 and 162: LIMITATIONS OF ADAPTIVE CLINICAL TR
Page 163 and 164: LIMITATIONS OF ADAPTIVE CLINICAL TR
Page 165 and 166: Capturing the Patient Perspective:
Page 167 and 168: PATIENT-REPORTED OUTCOMES AS TRIAL
Page 169 and 170: PATIENT-REPORTED OUTCOMES AS TRIAL
Page 171 and 172: NEW LOOKS AND CHALLENGES FOR COOPER
Page 173 and 174: NCI NATIONAL CLINICAL TRIALS NETWOR
Page 175 and 176: Successful Integration of Cooperati
Page 177 and 178: COG: GIVING NEW MEANING TO COOPERAT
Page 179 and 180: A Critical Review of the Enrollment
Page 181 and 182: BLACK PATIENTS AND CANCER CLINICAL
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Page 187 and 188: T-DM1 AND THERAPEUTIC ANTIBODIES ag
Page 189 and 190: TARGETING CD30 IN HODGKIN LYMPHOMA
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Page 195 and 196: Table 1. Response Rates in Expanded
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Page 199 and 200: that the core pathway is not comple
Page 201 and 202: This situation is not surprising, g
Page 203 and 204: Practical Management of Immune-Rela
Page 205 and 206: the anterior pituitary axis is invo
Page 207 and 208: TARGETING CRITICAL MOLECULAR ABERRA
Page 209 and 210: Abl suppression; and 3) the early e
Page 211 and 212: 50% 50% 100% Change in Tumor Size m
Page 213 and 214: vanced solid tumors, even if they a
Page 215 and 216: Targeting Molecular Aberrations in
Page 217 and 218: date. With the advent of gene expre
Page 219 and 220: consortium to facilitate the testin
Page 221 and 222: ETHICAL CHALLENGES OF HEALTH CARE R
Page 223 and 224: HEALTH CARE REFORM AND ONCOLOGY dev
Page 225 and 226: HEALTH CARE REFORM AND ONCOLOGY aut
Page 227 and 228: INTERNATIONAL VARIATION IN UNDERSTA
Page 229 and 230: midcareer physician; in one cross-s
Page 231 and 232: Table 1. Recommendations for Person
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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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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
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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
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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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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
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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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