2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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that the HH pathway may contribute to the more unfavorable biologic behaviors of these renal tumors. 18 Hepatic Tumors Eichenmuller and colleagues reported that HH signaling is active in pediatric hepatoblastoma and showed that blocking HH signaling with cyclopamine in hepatoblastoma cells leads to a significant decrease in cell viability and increased apoptosis. 29 In another study, IHC of 11 hepatoblastoma cases demonstrated that 100% of tumors stained positive for SHH and PTCH1, while eight (73%) were positive for GLI1. 18 One case of embryonal carcinoma and two hepatic tumor cell lines (Heh6 and Heh7) showed strong expression of all three HH pathway markers. No relationship was observed between GLI1 expression and histologic subtype, clinical stage, or prognosis. Osteosarcoma Recently published data also suggest HH signaling may play a role in the pathogenesis of osteosarcoma. A study of osteosarcoma cell lines and biopsy specimens showed overexpression of HH target genes via real-time PCR. 30 Inhibition of the HH pathway with cyclopamine in vitro promoted G1 arrest and reduced the expression of positive cell-cycle regulators, including cyclins D1 and E1. In addition, SMO knockdown with SMO shRNA prevented the growth of osteosarcoma, both in vitro and in vivo. 30 HH Pathway Inhibitors in Pediatric Clinical Trials Inhibitors of HH signaling have recently been the focus of intense research. It is noteworthy that many tumors that appear to lack specific HH pathway mutations have been reported to be sensitive to SMO inhibitors in vitro and in vivo. 3 This has led to estimates that as many as 25% of human tumors may depend on HH pathway activity for growth. As a consequence, a wide range of tumors have been included in the early-adult clinical trials investigating SMO inhibitors. 3 Xenograft tumor models have shown that hu- Author’s Disclosure of Potential Conflicts of Interest Employment or Leadership Consultant or Author Positions Advisory Role Tobey J. MacDonald Novartis 1. Nusslein-Volhard C, Wieschaus E. Mutations affecting segment number and polarity in Drosophila. Nature. 1980;287:795-801. 2. Ingham PW, Nakano Y, Seger C. Mechanisms and functions of Hedgehog signalling across the metazoa. Nat Rev Genet. 2011;12:393-406. 3. Ng JM, Curran T. The Hedgehog’s tale: Developing strategies for targeting cancer. Nat Rev Cancer. 2011;11:493-501. 4. McMahon AP, Ingham PW, Tabin CJ. Developmental roles and clinical significance of hedgehog signaling. Curr Top Dev Biol. 2003;53:1-114. 5. Lee J, Platt KA, Censullo P, et al. Gli1 is a target of Sonic hedgehog that induces ventral neural tube development. Development. 1997;124:2537-2552. 6. Johnson RL, Rothman AL, Xie J, et al. Human homolog of patched, a candidate gene for the basal cell nevus syndrome. Science. 1996;272:1668-1671. 7. Epstein EH. Basal cell carcinomas: Attack of the hedgehog. Nat Rev Cancer. 2008;8:743-754. 8. Raffel C, Jenkins RB, Frederick L, et al. Sporadic medulloblastomas contain PTCH mutations. Cancer Res. 1997;57:842-845. 9. Thompson MC, Fuller C, Hogg TL, et al. Genomics identifies medullo- 608 man tumors without HH pathway mutations that express HH ligands actually induce upregulation of HH pathway target genes in the stromal cells of mouse origin, rather than in the tumor cells. 3 Under these conditions, treatment with SMO inhibitors inhibited tumor growth to some degree, but did not eliminate the tumors. Some leukemias have also been reported to depend on SMO signaling for growth, but more recent studies indicate that survival was not dependent on HH ligands or SMO activity. 3 The proof of concept for the clinical utility of SMO inhibitors has been established in patients with metastatic or locally advanced BCC or MB. 15-17 The more recent data suggest that this class of agents may have broader utility in other adult and pediatric cancers. The dilemma is to identify tumors that would benefit most from HH inhibitor treatment, as the mere presence of HH ligands or a pathway signature does not guarantee a response. Because of the importance of the HH signaling pathway in the normal growth and development, the use of SMO inhibitors in children is a specific concern that will need to be carefully assessed in order to manage the potential adverse effects on bone growth plates, developing teeth, and the immature reproductive system. 3 At present, early phase I and II clinical trials with the SMO inhibitors LDE225 (Novartis) and GDC-0449 (Genentech) are being evaluated in pediatric medulloblastoma and other pediatric tumors that are potentially dependent on HH pathway signaling (Table 1). Stock Ownership Honoraria REFERENCES Table 1. Hedgehog Pathway Inhibitors in Current Clinical Trials Agent Target Research Funding Expert Testimony TOBEY J. MACDONALD Mechanism of Action Manufacturer GDC-0449* SMO Antagonist GDC-0449 (Genentech) LDE225* SMO Antagonist LDE225 (Novartis) LEQ506 SMO Antagonist LEQ506 (Novartis) PF-04449913 SMO Antagonist PF-04449913 (Pfizer) IPI-926 SMO Antagonist IPI-926 (Ifinity) BMS-833923 SMO Antagonist BMS-833923 (Bristol-Myers Squibb) * Currently being investigated in pediatric cancer. As of February 8, 2012 (Clinicaltrials.gov). Other Remuneration blastoma subgroups that are enriched for specific genetic alterations. J Clin Oncol. 2006;24:1924-1931. 10. Taylor MD, Liu L, Raffel C, et al. Mutations in SUFU predispose to medulloblastoma. Nature Genet. 2002;31:306-310. 11. Pastorino, L. Ghiorzo P, Nasti S, et al. Identification of a SUFU germline mutation in a family with Gorlin syndrome. Am J Med Genet A. 2009;149A:1539-1443. 12. Wetmore C, Eberhart DE, Curran T. Loss of p53 but not ARF accelerates medulloblastoma in mice heterozygous for patched. Cancer Res. 2001;61: 513-516. 13. Yang ZJ, Ellis T, Markant SL, et al. Medulloblastoma can be initiated by deletion of Patched in lineage-restricted progenitors or stem cells. Cancer Cell. 2008;14:135-145. 14. Hatton BA, Knoepfler PS, Kenney AM, et al. N-myc is an essential downstream effector of Shh signaling during both normal and neoplastic cerebellar growth. Cancer Res. 2006;66:8655-8661. 15. Von Hoff DD, LoRusso PM, Rudin CM, et al. Inhibition of the hedgehog
HEDGEHOG PATHWAY IN PEDIATRIC CANCER pathway in advanced basal-cell carcinoma. N Engl J Med. 2009;361:1164- 1172. 16. Romer JT, Kimura H, Magdaleno S, et al. Suppression of the Shh pathway using a small molecule inhibitor eliminates medulloblastoma in Ptc1(�/�)p53(�/�) mice. Cancer Cell. 2004;6:229-240. 17. Rudin CM, Hann CL, Laterra J, et al. Treatment of medulloblastoma with hedgehog pathway inhibitor GDC-0449. N Engl J Med. 2009;361:1173- 1178. 18. Oue T, Yoneda A, Uehara S, et al. Increased expression of the hedgehog signaling pathway in pediatric solid malignancies. J Pediatr Surg. 2010;45: 387-392. 19. Monje M, Mitra SS, Freret ME, et al. Hedgehog-responsive candidate cell of origin for diffuse intrinsic pontine glioma. Proc Natl Acad Sci USA. 2011;108:4453-4458. 20. Rush SZ, Abel TW, Valadez, et al. Activation of the Hedgehog pathway in pilocytic astrocytomas. Neuro Oncol. 2010;12:790-798. 21. Tostar U, Malm CJ, Meis-Kindblom JM, et al. Deregulation of the hedgehog signalling pathway: a possible role for the PTCH and SUFU genes in human rhabdomyoma and rhabdomyosarcoma development. J Pathol. 2006;208:17-25. 22. Paulson V, Chandler G, Rakheja D, et al. High-resolution array CGH identifies common mechanisms that drive embryonal rhabdomyosarcoma pathogenesis. Genes Chromosomes Cancer. 2011;50:397-408. 23. Zibat A, Missiaglia E, Rosenberger A, et al. Activation of the hedgehog pathway confers a poor prognosis in embryonal and fusion gene-negative alveolar rhabdomyosarcoma. Oncogene. 2010;29:6323-6330. 24. Pressey JG, Anderson JR, Crossman DK, et al. Hedgehog pathway activity in pediatric embryonal rhabdomyosarcoma and undifferentiated sarcoma: A report from the Children’s Oncology Group. Pediatr Blood Cancer. 2011;57:930-938. 25. Rubin BP, Nishijo K, Chen HI, et al. Evidence for an unanticipated relationship between undifferentiated pleomorphic sarcoma and embryonal rhabdomyosarcoma. Cancer Cell. 2011;19:177-191. 26. Ecke I, Rosenberger A, Obenauer S, et al. Cyclopamine treatment of full-blown Hh/Ptch-associated RMS partially inhibits Hh/Ptch signaling, but not tumor growth. Mol Carcinog. 2008;47:361-372. 27. Souzaki R, Tajiri T, Souzaki M, et al. Hedgehog signaling pathway in neuroblastoma differentiation. J Pediatr Surg. 2010;45:2299-2304. 28. Gershon TR, Shirazi A, Qin LX, et al. Enteric neural crest differentiation in ganglioneuromas implicates Hedgehog signaling in peripheral neuroblastic tumor pathogenesis. PLoS One. 2009;4(10):e7491. 29. Eichenmüller M, Gruner I, Hagl B, et al. Blocking the hedgehog pathway inhibits hepatoblastoma growth. Hepatology. 2009;49:482-490. 30. Hirotsu M, Setoguchi T, Sasaki H, et al. Smoothened as a new therapeutic target for human osteosarcoma. Molecular Cancer. 2010;9:5. 609
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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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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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Page 615 and 616:
Page 617 and 618:
NEW OPTIONS, NEW QUESTIONS: HOW TO
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THERAPIES FOR PATIENTS WITH METASTA
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Page 623 and 624:
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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
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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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Page 645 and 646:
Page 647 and 648:
Short- and Long-term Cardiovascular
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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
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 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: 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 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
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quantity. Determining the appropria
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THE ASCO QUALITY ONCOLOGY PRACTICE
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IMPROVING VALUE OF CARE IN ONCOLOGY
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Page 761 and 762:
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PHYSICIAN WELLNESS: COPING WITH REP
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also provides insight on how clinic
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good resource for exploring the pri
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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
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CROSS-CULTURAL COMMUNICATION Sideba
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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
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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
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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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