2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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Authors’ Disclosures of Potential Conflicts of Interest Employment or Leadership Positions Consultant or Advisory Role Author Nathan J. Robison* Mark W. Kieran AstraZeneca; Celgene; Infinity; Merck; Novartis *No relevant relationships to disclose. 1. Hargrave D, Bartels U, Bouffet E. Diffuse brainstem glioma in children: critical review of clinical trials. Lancet Oncol. 2006;7:241-248. 2. Fangusaro J. Pediatric high-grade gliomas and diffuse intrinsic pontine gliomas. J Child Neurol. 2009;24:1409-1417. 3. Khatua S, Moore KR, Vats TS, et al. Diffuse intrinsic pontine gliomacurrent status and future strategies. Childs Nerv Syst. 2011;27:1391-1397. 4. Cohen KJ, Heideman RL, Zhou T, et al. Temozolomide in the treatment of children with newly diagnosed diffuse intrinsic pontine gliomas: a report from the Children’s Oncology Group. Neuro-oncology. 2011;13:410-416. 5. Haas-Kogan DA, Banerjee A, Poussaint TY, et al. Phase II trial of tipifarnib and radiation in children with newly diagnosed diffuse intrinsic pontine gliomas. Neuro-oncology. 2011;13:298-306. 6. Pollack IF, Stewart CF, Kocak M, et al. A phase II study of gefitinib and irradiation in children with newly diagnosed brainstem gliomas: a report from the Pediatric Brain Tumor Consortium. Neuro-oncology. 2011;13:290-297. 7. Pollack IF, Jakacki RI, Blaney SM, et al. Phase I trial of imatinib in children with newly diagnosed brainstem and recurrent malignant gliomas: a Pediatric Brain Tumor Consortium report. Neuro-oncology. 2007;9:145-160. 8. Louis DN, Rubio MP, Correa KM, et al. Molecular genetics of pediatric brain stem gliomas. Application of PCR techniques to small and archival brain tumor specimens. J Neuropathol Exp Neurol. 1993;52:507-515. 9. Zhang S, Feng X, Koga H, et al. p53 gene mutations in pontine gliomas of juvenile onset. Biochem Biophys Res Commun. 1993;196:851-857. 10. Gilbertson RJ, Hill DA, Hernan R, et al. ERBB1 is amplified and overexpressed in high-grade diffusely infiltrative pediatric brain stem glioma. Clin Cancer Res. 2003;9:3620-3624. 11. Zarghooni M, Bartels U, Lee E, et al. Whole-genome profiling of pediatric diffuse intrinsic pontine gliomas highlights platelet-derived growth factor receptor alpha and poly (ADP-ribose) polymerase as potential therapeutic targets. J Clin Oncol. 2010;28:1337-1344. 12. Warren KE, Killian K, Suuriniemi M, et al. Genomic aberrations in pediatric diffuse intrinsic pontine gliomas. Neuro-oncology. 2011. doi:10.1093/ neuonc/nor190. 13. Paugh BS, Broniscer A, Qu C, et al. Genome-wide analyses identify recurrent amplifications of receptor tyrosine kinases and cell-cycle regulatory genes in diffuse intrinsic pontine glioma. J Clin Oncol. 2011;29:3999-4006. 14. Wu G, Broniscer A, McEachron TA, et al. Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas. Nat Genet. 2012. doi:10.1038/ng. 1102. 15. Joshi BH, Puri RA, Leland P, et al. Identification of interleukin-13 628 Stock Ownership Honoraria REFERENCES Research Funding Advantagene; Amersham; AstraZeneca; Celgene; Merck KGaA; Novartis; Schering-Plough; Transmolecular Expert Testimony ROBISON AND KIERAN Other Remuneration receptor alpha2 chain overexpression in situ in high-grade diffusely infiltrative pediatric brainstem glioma. Neuro-oncology. 2008;10:265-274. 16. Broniscer A, Baker JN, Baker SJ, et al. Prospective collection of tissue samples at autopsy in children with diffuse intrinsic pontine glioma. Cancer. 2010;116:4632-4637. 17. Barrow J, Adamowicz-Brice M, Cartmill M, et al. Homozygous loss of ADAM3A revealed by genome-wide analysis of pediatric high-grade glioma and diffuse intrinsic pontine gliomas. Neuro-oncology. 2011;13:212-222. 18. Roujeau T, Machado G, Garnett MR, et al. Stereotactic biopsy of diffuse pontine lesions in children. J Neurosurg. 2007;107:1-4. 19. Paugh BS, Qu C, Jones C, et al. Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease. J Clin Oncol. 2010;28:3061-3068. 20. Grill J, Puget S, Andreiuolo F, et al. Critical oncogenic mutations in newly diagnosed pediatric diffuse intrinsic pontine glioma. Pediatr Blood Cancer. 2011. doi:10.1002/pbc. 24060. 21. Geoerger B, Hargrave D, Thomas F, et al. Innovative therapies for children with cancer pediatric phase I study of erlotinib in brainstem glioma and relapsing/refractory brain tumors. Neuro-oncology. 2011;13:109-118. 22. Faury D, Nantel A, Dunn SE, et al. Molecular profiling identifies prognostic subgroups of pediatric glioblastoma and shows increased YB-1 expression in tumors. J Clin Oncol. 2007;25:1196-1208. 23. Bax DA, Mackay A, Little SE, et al. A distinct spectrum of copy number aberrations in pediatric high-grade gliomas. Clin Cancer Res. 2010;16:3368- 3377. 24. Becher OJ, Hambardzumyan D, Walker TR, et al. Preclinical evaluation of radiation and perifosine in a genetically and histologically accurate model of brainstem glioma. Cancer Res. 2010;70:2548-2557. 25. Masui K, Suzuki SO, Torisu R, et al. Glial progenitors in the brainstem give rise to malignant gliomas by platelet-derived growth factor stimulation. Glia. 2010;58:1050-1065. 26. 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. 27. Geoerger B, Kieran MW, Grupp S, et al. Phase II trial of temsirolimus in children with high-grade glioma, neuroblastoma and rhabdomyosarcoma. Eur J Cancer. 2012;48:253-262. 28. Gururangan S, Chi SN, Young Poussaint T, et al. Lack of efficacy of bevacizumab plus irinotecan in children with recurrent malignant glioma and diffuse brainstem glioma: a Pediatric Brain Tumor Consortium study. J Clin Oncol. 2010;28:3069-3075.
Is Biopsy Safe in Children with Newly Diagnosed Diffuse Intrinsic Pontine Glioma? By Stephanie Puget, MD, PhD, Thomas Blauwblomme, MD, and Jacques Grill, MD, PhD Overview: Diffuse intrinsic pontine gliomas (DIPGs), with a median survival of 9 months, represent the biggest therapeutic challenge in pediatric neuro-oncology. Despite many clinical trials, no major improvements in treatment have been made over the past 30 years. In most cases, biopsy is not needed for diagnosis because DIPG diagnosis is based on a typical clinical picture with radiologic evidence on magnetic resonance imaging. Therefore, little data on newly diagnosed DIPG have been published and are confounded by including autopsy (i.e., postradiation therapy) cases. In most cancers, advancing to cure has been linked to the discovery of relevant biomarkers, only found by access to tissue. Therefore, to further understand the biology of DIPG, fresh tissue samples must be DIFFUSE INTRINSIC pontine gliomas (DIPGs), which represent 15% of all childhood brain tumors, are inoperable neoplasms. Response to radiation therapy is only transient and chemotherapy has not improved long-term survival. The development of targeted therapies for these tumors has been hampered by the lack of knowledge of their biology and many trials to date have been carried out based on the misconception that DIPG biology is similar either to its adult counterparts 1-3 or to other pediatric supratentorial malignant gliomas. 1,4 Diagnosis is usually based on the association of a short history of less than 2 months, cranial nerves palsies, long-tract signs, and ataxia with typical imaging findings. DIPG is usually described as an infiltrating tumor mass of the pons, hypointense on T1 and hyperintense on T2 and fluid-attenuated inversion recovery; by definition, at least 50% of the pons should be involved. Contrast enhancement, if any, is usually limited and annular. Grading of these lesions has been difficult based on small biopsies and could therefore not be linked to outcome. Biopsy of these tumors has been controversial, and most neurosurgical teams limit the use biopsy to patients with lesions that have unusual presentation. However, the urgent need to improve the prognosis for patients with these devastating tumors has led to the reconsideration of the role of stereotactic biopsy for patients with DIPG. This article will address the feasibility and safety of stereotactic biopsy for patients with DIPG, its diagnostic yield, and its role in redefining this tumor by its molecular signature and profiling targeted therapy. Is It Safe to Perform a Biopsy for Patients Newly Diagnosed with DIPG? Stereotactic biopsies are now completely integrated in the diagnosis and management of several intracranial lesions. The role of stereotactic biopsy for patients with newly diagnosed DIPG remains controversial, and currently the general attitude is not to biopsy the tumors of these patients. Stereotactic biopsy of brainstem tumors is an old procedure; it became popular after the first report of this procedure in 1978. 5 Ten years later, arguments against brainstem biopsy were strong because it was believed to have no use, to be dangerous, and to offer poor yield. 6-8 The 1993 manuscript published by Albright and colleagues changed the course of pediatric DIPG management by claiming that obtained at diagnosis. However, most neurosurgical teams are reluctant to perform biopsy in pediatric patients, citing potential risks and lack of direct benefit. Yet, in reviewing 90 patients with and the published data on brainstem biopsy, these procedures have a diagnostic yield and morbidity and mortality rates similar to those reported for other brain locations. In addition, the quality and quantity of the material obtained confirm the diagnosis and inform an extended molecular screen, including biomarker study—information important to designing next-generation trials with targeted agents. Stereotactic biopsies can be considered a safe procedure in well-trained neurosurgical teams and could be incorporated in well-defined protocols for patients with DIPG. magnetic resonance imaging (MRI) “. . . scans provide images that are virtually diagnostic of brainstem gliomas and yield prognostic information equivalent to that obtainable from biopsies ...”. 8 Since then, the neurosurgical world was divided into “for” and “against” the brainstem biopsy. Despite the reluctance of some neurosurgical teams, others chose to perform biopsies of brainstem lesions in children and adults for both unusual lesions and typical ones as part of a clinical trial. 9-16 Papers on stereotactic biopsies in the brainstem published in the last 20 years represent a substantial amount of knowledge, yet unfortunately often report mixed series of adults and children with a wide range of diagnoses. These mixed series cite morbidity rates between 0% and 10% and mortality rates between 0% to 3% (Table 1). However, when biopsy data on pediatric patients with DIPG are extracted, the diagnostic yield ranges from 96% to 100%, with no mortality and morbidity less than 5% for the largest series. Samadani and Judy performed a meta-analysis of 13 studies of stereotactic biopsy of brainstem lesions in 381 children and adults. 17 With a diagnostic yield of 96%, this study reported one death attributable to a biopsy of a vascular lesion in an adult, with rates of permanent and transient neurologic deficits of 4% and 1%, respectively. A few years later, a second meta-analysis on brainstem lesions in pediatric patients was published by Pincus and colleagues. 13 This review of 192 children revealed a diagnostic yield of 94.9%, and mortality and morbidity rates of 0.7% and 4.9%, respectively. Recently, Rajshekhar and Moorthy reported a series of stereotactic biopsies in 106 children with brainstem masses. With no mortality or permanent morbidity reported, the authors highlighted that “. . . this procedure is safe in children and the benefits outweigh the risks in patients who are appropriately selected to undergo this procedure. . . ” 11 A few years ago, our group started to use From the Necker Enfants Malades Hospital, Université Paris Descartes, Sorbonne Paris Cité, France; Gustave Roussy Cancer Institute, Universite Paris Sud, Villejuif, France. Authors’ disclosures of potential conflicts of interest are found at the end of this article. Address reprint requests to Stephanie Puget, MD, PhD, Department of Pediatric Neurosurgery, Necker Enfants Malades Hospital, 149 rue de Sèvres, 75015 Paris, Université Paris Descartes, Sorbonne Paris Cité, France; email: stephanie.puget@gmail.com © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10 629
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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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FUTURE DIRECTIONS IN GBM THERAPY pr
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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
Page 545 and 546:
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
Page 553 and 554:
Molecular Testing of Non-Small Cell
Page 555 and 556:
MOLECULAR TESTING AND NSCLC Fig 1.
Page 557 and 558:
MOLECULAR TESTING AND NSCLC logic d
Page 559 and 560:
THYMOMA AND THYMIC CARCINOMA: UPDAT
Page 561 and 562:
MANAGEMENT OF THYMIC CARCINOMA recu
Page 563 and 564:
MANAGEMENT OF THYMIC CARCINOMA Refe
Page 565 and 566:
The Creation of the International T
Page 567 and 568:
ITMIG AS A MODEL FOR RARE DISEASES
Page 569 and 570:
Thymoma: From Chemotherapy to Targe
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SYSTEMIC TREATMENT OF THYMOMA Study
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SYSTEMIC TREATMENT OF THYMOMA cance
Page 575 and 576:
What Is the Best Strategy for Incor
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TREATMENT OF FOLLICULAR LYMPHOMA Fi
Page 579 and 580:
TREATMENT OF FOLLICULAR LYMPHOMA me
Page 581 and 582:
TREATMENT OF FOLLICULAR LYMPHOMA ou
Page 583 and 584:
TREATMENT OPTIONS IN INDOLENT LYMPH
Page 585 and 586:
Page 587 and 588:
Page 589 and 590:
ROLE OF HCT FOR INDOLENT LYMPHOMA T
Page 591 and 592:
ROLE OF HCT FOR INDOLENT LYMPHOMA T
Page 593 and 594:
ROLE OF HCT FOR INDOLENT LYMPHOMA e
Page 595 and 596:
CONTROVERSIES IN MYELOMA: INDUCTION
Page 597 and 598:
TRANSPLANTATION FOR MYELOMA Alterna
Page 599 and 600:
TRANSPLANTATION FOR MYELOMA compare
Page 601 and 602:
TRANSPLANTATION FOR MYELOMA autolog
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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
Page 609 and 610:
Maintenance Therapy for Myeloma: Ho
Page 611 and 612:
MAINTENANCE THERAPY FOR MULTIPLE MY
Page 613 and 614:
Page 615 and 616:
Page 617 and 618:
NEW OPTIONS, NEW QUESTIONS: HOW TO
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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
Page 641 and 642:
MUCOSAL INJURY CAUSED BY CANCER THE
Page 643 and 644:
Page 645 and 646:
Page 647 and 648:
Short- and Long-term Cardiovascular
Page 649 and 650:
Recent Advances in Cardiotoxicity o
Page 651 and 652:
CARDIOTOXICITY OF ANTICANCER THERAP
Page 653 and 654:
CARDIOTOXICITY OF ANTICANCER THERAP
Page 655 and 656:
The Oncologist as the Patient with
Page 657 and 658:
THE ONCOLOGIST AS THE PATIENT OR RE
Page 659 and 660:
Prolonged Febrile Neutropenia in th
Page 661 and 662:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 663 and 664:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 665 and 666:
TREATMENT APPROACHES IN CHILDREN wh
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 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: NOVEL TARGETS IN THE TREATMENT OF D
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
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 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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