2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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with the mTOR pathway. 44 The combined treatment led to an impressive 6.5 month extension of PFS. 43 There are four additional classes of PI3K pathway inhibitors in clinical development: dual PI3K-mTOR inhibitors, PI3K inhibitors that do not inhibit mTOR, AKT inhibitors, and mTOR catalytic inhibitors (also called pan-mTOR inhibitors because they inhibit mTORC2 in addition to mTORC1) (Fig. 1). The future will tell if these newer agents are effective and tolerable pathway inhibitors or are able to overcome feedback inhibition normally observed with mTORC1 inhibitors. Of critical importance will be the identification of populations in which the benefits of these PI3K pathway inhibitors will justify their manageable but real toxicity–the current assumption is that PI3KCA-mutated cancers and PTENdeficient cancers will be at the top of the list. This would suggest that this family of compounds may find a role in all three types of breast cancer. Recently, there has been growing interest in combining PI3K with MEK pathway inhibitors. Many cancers sensitive to PI3K pathway inhibitors show tumor stasis rather than regression. The MEK pathway can represent an escape route in the presence of effective downregulation of the PI3K pathway. Therapeutic inhibition of both pathways is under clinical investigation with the use of MEK and PI3K inhibitors (Table 1). Instability of the genome is inherent to the great majority of human cancer cells and is instrumental for tumor progression. It has been proposed as a fundamental hallmark of cancer. 45 Although PARP inhibitors have clearly demonstrated striking antitumor activity in BRCA mutation carriers with advanced breast cancer, their activity in sporadic triplenegative breast cancer, alone or in combination with chemotherapy, has been less consistent. Myelosuppression has been an obstacle to their development. It remains uncertain whether PARP inhibitors will find an application beyond the treatment of BRCA-mutated tumors. Strategies directed at hallmarks of cancer in early development for MBC. Cyclin-dependent kinase inhibitors target evasion from growth suppressors by directly interfering with the cell cycle, downstream of the receptor tyrosine kinase signaling cascades. Several CDK inhibitors are in phase I or II trials, in combinations with either endocrine therapy in luminal cancers or chemotherapy for basal-like cancers. A randomized trial of letrozole with or without a CDK-4, -6 inhibitor 25 has generated promising results. 46 A similar anticancer strategy is inhibition of Aurora kinases. These serine/threonine kinases play an essential role in cellular proliferation, through control over chromatid segregation. Agents targeting Aurora kinases have entered early clinical trials. Proapoptotic agents aim at antagonizing “resistance to cell death,” and a number of them are in phase I clinical trials (Table 1). Triple-negative breast cancer seems to be a priority given the high prevalence of p53 mutations seen in this subtype. Strategies directed at epigenetic aberrations or at downregulation of key intracellular targets. As our understanding of the deregulation of epigenetic mechanisms evolves, growing interest in targeting these aberrations has emerged. Histone deacetylase inhibitors are progressing from phase I to phase II trials with interesting results seen when these 36 SLEDGE, CARDOSO, WINER, AND PICCART agents are combined with endocrine agents or anti-HER2 drugs. Heat shock protein 90 (HSP90) represents another interesting anticancer target in MBC. 47 A molecular chaperone, HSP90 plays a vital role in the intact function of several oncogenic proteins and, thus, promotes key molecular events in malignant progression. Several agents have been tested with promising results in HER2-positive MBC. Antihormone strategies. The androgen and prolactin receptors are being explored in advanced breast cancer. The androgen receptor (AR) has recently been shown to play a role in HER2-positive/estrogen receptor-negative breast cancers, which can get stimulated by testosterone and also show upregulation of the Wnt signaling pathway. 48 Moreover, AR positivity has been found in approximately 20% of triple-negative breast cancers, 49 and a phase II study with bicalutamide for ER-negative breast cancer expressing AR has recently been performed. Targeting Breast Cancer Stem Cells The identification of a cellular subpopulation in breast cancer with a specific immunophenotype (i.e., CD44 � CD24 - ) 50 bearing a tumor-initiating capacity was the first identification of cancer stem cells (CSCs) in the setting of a solid tumor. Ever since, a detailed exploration of this cellular compartment of breast cancer has been undertaken, and this expanding knowledge provides novel therapeutic targets 51 for this therapy-resistant cellular population. One of the fundamental aspects of CSCs is their capacity for self-renewal, mediated through well-conserved developmental signaling pathways 52 (the Notch, Hedgehog, and Wnt pathways) amenable to therapeutic targeting. The Notch signaling pathway, frequently deregulated in breast cancer, 53 can be targeted by gammasecretase inhibitors (Table 2). These small molecules block the translocation of the intracellular part of the Notch receptor to the nucleus and corresponding signaling pathway activation. The Hedgehog signaling pathway has also been shown to promote the tumor-initiating ability of breast CSCs. 54 A class of compounds called Smo-antagonists has entered clinical trials (Table 2). A second approach targeting breast CSCs is based on high-throughput screening methods. A population of breast cancer cells enriched for CSCs are screened either for druggable targets through shRNA/siRNA technology or through the testing of extended small molecule compound collections. Based on the latter approach, Gupta and colleagues 55 recently discovered that salinomycin is able to eradicate breast CSCs. Targeting the Tumor Microenvironment Tumor cells are integrated into their microenvironment, constantly interacting with it. 56 These components are appealing therapeutic targets, with antiangiogenic factors being the most clinically advanced. The failure of bevacizumab, a humanized monoclonal antibody targeting VEGF-A, to extend OS of MBC patients 23,57 should not be regarded as a proof of failure of the concept of antiangiogenic therapy in breast cancer. The assumption that bevacizumab administration potentiates the delivery of higher intratumor chemotherapy concentrations proved incorrect. 58 Moreover, the redundancy of different angiogenic mechanisms and proangiogenic factors could explain this clinical failure, as
TREATMENT OF ADVANCED BREAST CANCER inhibition of VEGF-A rapidly leads to compensatory activation of alternative pathways. 59,60 Other compounds targeting the tumor microenvironment can be found in Table 3. Conclusion MBC represents a continuing challenge to physicians and patients. An improved understanding of breast cancer biology has improved prognosis, and progress based on biologic Authors’ Disclosures of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role George W. Sledge Jr.* Fatima Cardoso Abraxis BioScience; AstraZeneca; Celgene; Eisai; GlaxoSmithKline; Johnson & Johnson; Novartis; Pfizer; Roche Eric P. Winer Novartis; Roche/ Genentech (U) Martine J. Piccart Amgen; Bayer Schering Pharma; Boehringer Ingelheim; Bristol-Myers Squibb; GlaxoSmithKline; PharmaMar; Roche; Sanofi *No relevant relationships to disclose. 1. Greenberg P, Hortobagyi G, Smith T, et al. Long-term follow-up of patients with complete remission following combination chemotherapy for metastatic breast cancer. J Clin Oncol. 1996;14:2197-2205. 2. Giordano S, Buzdar A, Smith T, et al. Is breast cancer survival improving? Cancer. 2004;100(1):44-52. 3. Tevaarwerk A, Gray R, Schneider B, et al. Survival in Metastatic Breast Cancer (MBC): No Evidence for Improved Survival Following Distant Recurrence after Adjuvant Chemotherapy. Presented at: San Antonio Breast Cancer Symposium. 2011; San Antonio, TX. 4. Slamon D, et al. Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2. N Engl J Med. 2001;344:783-792. 5. Cortes J, O’Shaughnessy J, Loesch D, et al. Eribulin monotherapy versus treatment of physician’s choice in patients with metastatic breast cancer (EMBRACE): a phase 3 open-label randomised study. Lancet. 2011; 377:914-923. 6. A’Hern R, Smith I, Ebbs S. Chemotherapy and survival in advanced breast cancer: The inclusion of doxorubicin in Cooper type regimens. Br J Cancer. 1993;67:801-805. 7. Gibson L, Lawrence D, Dawson C, et al. Aromatase inhibitors for treatment of advanced breast cancer in postmenopausal women. Cochrane Database Syst Rev. 2009; CD003370. 8. Broglio K, Berry D. Detecting an overall survival benefit that is derived from progression-free survival. J Natl Cancer Inst. 2009;101:1642-1649. 9. Pagani O, Senkus E, Wood W, et al. International guidelines for management of metastatic breast cancer (MBC) from the European School of Oncology (ESO)-MBC Task Force: Can metastatic breast cancer be cured? J Natl Cancer Inst. 2010;102(7):456-463. 10. Cardoso F, Di Leo A, Lohrisch C, et al. Second and subsequent lines of chemotherapy for metastatic breast cancer: What did we learn in the last two decades? Ann Oncol. 2002;13:197-207. 11. Burzykowski T, Buyse M, Piccart-Gebhart M, et al. Evaluation of tumor response, disease control, progression-free survival, and time to pro- subtyping continues to advance therapy. The twin revolutions of cancer genomics and computational chemistry should lead to many new treatment options for patients in coming years. Acknowledgments M. Piccart would like to thank Jose Baselga, MD, PhD for useful advice and Dimitrios Zardavas, MD, for great help in preparation of the tables listing newer targets and drugs. Stock Ownership Honoraria REFERENCES Abraxis BioScience; AstraZeneca; Celgene; Eisai; GlaxoSmithKline; Johnson & Johnson; Novartis; Pfizer; Roche Amgen; Bayer Schering Pharma; Boehringer Ingelheim; Bristol-Myers Squibb; GlaxoSmithKline; PharmaMar; Roche; Sanofi Research Funding AstraZeneca; Novartis Roche/Genentech Bristol-Myers Squibb; Pfizer; Roche Expert Testimony Other Remuneration gression as potential surrogate end points in metastatic breast cancer. J Clin Oncol. 2008;26:1987-1992. 12. Mauri D, Pavlidis N, Polyzos N, et al. Survival with aromatase inhibitors and inactivators versus standard hormonal therapy in advanced breast cancer: Meta-analysis. J Natl Cancer Inst. 2006;98:1285-1291. 13. Piccart-Gebhart M, Burzykowski T, Buyse M, et al. Taxanes alone or in combination with anthracyclines as first-line therapy of patients with metastatic breast cancer. J Clin Oncol. 2008;26:1980-1986. 14. Cardoso F, Bedard P, Winer E, et al. International guidelines for management of metastatic breast cancer: Combination vs. sequential singleagent chemotherapy. J Natl Cancer Inst. 2009;101:1174-1181. 15. Gennari A, Stockler M, Puntoni M, et al. Duration of chemotherapy for metastatic breast cancer: A systematic review and meta-analysis of randomized clinical trials. J Clin Oncol. 2011;29:2144-2149. 16. Riemsma R, Forbes C, Kessels A, et al. Systematic review of aromatase inhibitors in the first-line treatment for hormone sensitive advanced or metastatic breast cancer. Breast Cancer Res Treat. 2010;123:9-24. 17. Chia S, Gradishar W, Mauriac L, et al. Double-blind, randomized placebo controlled trial of fulvestrant compared with exemestane after prior nonsteroidal aromatase inhibitor therapy in postmenopausal women with hormone receptor-positive, advanced breast cancer: Results from EFECT. J Clin Oncol. 2008;26:1664-1670. 18. Mehta R, Barlow W, Albain K, et al. A Phase III Randomized Trial of Anastrozole Versus Anastrozole and Fulvestrant as First-Line Therapy for Postmenopausal Women with Metastatic Breast Cancer: SWOG S0226. Presented at: San Antonio Breast Cancer Symposium; 2011; San Antonio, TX. 19. Klijn J, Blarney R, Boccardo F, et al. Combination LHRH-agonist plus tamoxifen treatment is superior to medical castration alone in premenopausal metastatic breast cancer. Breast Cancer Res Treat. 1998;50:227. 20. Talbot D, Moiseyenko V, Van Belle S, et al. Randomised, phase II trial comparing oral capecitabine (Xeloda) with paclitaxel in patients with metastatic/advanced breast cancer pretreated with anthracyclines. Br J Cancer. 2002;86:1367-1372. 21. Lin N, Claus E, Sohl J, et al. Sites of distant recurrence and clinical 37
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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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Page 17 and 18: Matti S. Aapro, MD Clinique De Geno
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Page 27 and 28: Letter from the Editor The theme of
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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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TREATMENT OPTIONS IN INDOLENT LYMPH
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Page 587 and 588:
Page 589 and 590:
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
Page 605 and 606:
CURRENT STATUS OF MYELOMA THERAPY F
Page 607 and 608:
CURRENT STATUS OF MYELOMA THERAPY T
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Maintenance Therapy for Myeloma: Ho
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MAINTENANCE THERAPY FOR MULTIPLE MY
Page 613 and 614:
Page 615 and 616:
Page 617 and 618:
NEW OPTIONS, NEW QUESTIONS: HOW TO
Page 619 and 620:
THERAPIES FOR PATIENTS WITH METASTA
Page 621 and 622:
Page 623 and 624:
Page 625 and 626:
ANTIEMETICS: CURRENT STANDARDS, EME
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ANTIEMETICS: ASCO GUIDELINE UPDATE
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Page 631 and 632:
Page 633 and 634:
Page 635 and 636:
Chemotherapy-Induced Nausea and Vom
Page 637 and 638:
INCIDENCE AND PREVALENCE OF CHEMOTH
Page 639 and 640:
New Frontiers in Mucositis By Dougl
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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
Page 657 and 658:
THE ONCOLOGIST AS THE PATIENT OR RE
Page 659 and 660:
Prolonged Febrile Neutropenia in th
Page 661 and 662:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 663 and 664:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 665 and 666:
TREATMENT APPROACHES IN CHILDREN wh
Page 667 and 668:
TREATMENT APPROACHES IN CHILDREN th
Page 669 and 670:
GENETIC COUNSELING OF THE PATIENT W
Page 671 and 672:
CANCER PREDISPOSITION IN CHILDHOOD
Page 673 and 674:
Page 675 and 676:
Page 677 and 678:
Page 679 and 680:
HOW TO MANAGE VERY RARE PEDIATRIC C
Page 681 and 682:
RARE CANCER IN CHILDREN Registries
Page 683 and 684:
Genetic Alterations in Childhood Me
Page 685 and 686:
GENETIC ALTERATIONS IN CHILDHOOD ME
Page 687 and 688:
Desmoid-Type Fibromatosis in Childr
Page 689 and 690:
CHEMOTHERAPY FOR DESMOID TUMOR Tabl
Page 691 and 692:
CHEMOTHERAPY FOR DESMOID TUMOR 14.
Page 693 and 694:
Targeting the Insulin-Like Growth F
Page 695 and 696:
TARGETING THE IGF SYSTEM Fig. 1. Th
Page 697 and 698:
TARGETING THE IGF SYSTEM malignanci
Page 699 and 700:
Hedgehog Pathway in Pediatric Cance
Page 701 and 702:
HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 703 and 704:
HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 705 and 706:
Development and Refinement of Augme
Page 707 and 708:
ABFM THERAPY FOR PEDIATRIC ALL than
Page 709 and 710:
ABFM THERAPY FOR PEDIATRIC ALL Auth
Page 711 and 712:
RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 713 and 714:
RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 715 and 716:
Role of Doxorubicin in Rhabdomyosar
Page 717 and 718:
DOXORUBICIN IN RHABDOMYOSARCOMA 8.
Page 719 and 720:
Identification of Novel Biologic Ta
Page 721 and 722:
NOVEL TARGETS IN THE TREATMENT OF D
Page 723 and 724:
Is Biopsy Safe in Children with New
Page 725 and 726:
SAFETY OF DIPG BIOPSY IN CHILDREN F
Page 727 and 728:
SAFETY OF DIPG BIOPSY IN CHILDREN 1
Page 729 and 730:
CHILDREN WITH DIFFUSE INTRINSIC PON
Page 731 and 732:
Communication and Decision Support
Page 733 and 734:
COMMUNICATION AND DECISION SUPPORT
Page 735 and 736:
Page 737 and 738:
Page 739 and 740:
Planning for the Future: The Role o
Page 741 and 742:
present in the office suite but doe
Page 743 and 744:
Summary and Care Plan are provided.
Page 745 and 746:
DOING IT RIGHT, AND FOR LESS: IMPLE
Page 747 and 748:
CLINICAL PATHWAYS STANDARDIZING PER
Page 749 and 750:
CLINICAL PATHWAYS STANDARDIZING PER
Page 751 and 752:
The Future of Oncology Care with Pe
Page 753 and 754:
quantity. Determining the appropria
Page 755 and 756:
THE ASCO QUALITY ONCOLOGY PRACTICE
Page 757 and 758:
IMPROVING VALUE OF CARE IN ONCOLOGY
Page 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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