2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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Evaluation of Patients with Disseminated or Locoregionally Advanced Thyroid Cancer: A Primer for Medical Oncologists By A. Dimitrios Colevas, MD, and Manisha H. Shah, MD Overview: Historically, patients with thyroid cancers are managed by endocrinologists, surgeons and radiation oncologists. Due to recent progress in this field with advances in treatment of thyroid cancer, medical oncologists are now commonly involved in care of patients with advanced thyroid TRADITIONALLY, TREATMENT of patients with differentiated thyroid carcinomas (DTC), which includes papillary, follicular, and Hurthle cell carcinomas, has been highly constrained by the lack of effective treatment of patients with metastatic or recurrent locoregional disease after surgical treatments have been exhausted or are not feasible. Treatments in this setting have been mostly limited to external-beam radiation treatment focused on the area of concern or systemic radioactive iodine (RAI) for patients with rising serum thyroglobulin levels or evidence of iodineavid evaluable metastases. Because there are no convincing data on extending survival for patients with disease that is evaluable only by thyroglobulin levels, endocrinologists and nuclear medicine physicians have struggled with the selection of patients for whom RAI is indicated. 1 Although some advocate treatment with RAI for most patients with thyroglobulin levels higher than 10 ng/mL, others support a more focused approach of treatment for patients who are thought to be at high risk for clinically relevant sequellae of progressive disease, as disease volume can be reduced even in patients with thyroglobulin-positive but imaging-negative disease. 2,3 Therefore, patients referred to the medical oncologist for RAI-refractory thyroid cancer have commonly received RAI in the adjuvant setting and often with an additional one or two doses of RAI in the metastatic setting, defined by elevated thyroglobulin levels in the absence of radiographically evaluable metastatic disease. Historically, it was not uncommon to encounter patients with relatively indolent disease who had received cumulative RAI doses exceeding 600 mCi. More recently, because of an increased awareness of long-term adverse events from RAI, such as bone marrow suppression, salivary gland compromise, and gonadal dysfunction, many patients treated with RAI, even those with clinically indolent disease, are referred to the medical oncologist with lower prior cumulative RAI doses, in the range of 200–400 mCi. Traditional cytotoxic chemotherapy has played a minimal role in the treatment of patients with RAI-refractory thyroid cancer. Despite reports or small retrospective experiential reviews suggesting promise, especially in the induction setting for patients with no prior cancer treatment, most well-documented studies demonstrate little to no response to conventional chemotherapy in patients with RAI-refractory disease. 4,5 Doxorubicin is often cited as a standard of care on the basis of a 37% response rate, but that rate was reported in an oldstudy, and neither the time to progression nor the methods used to determine responses were reported. 6 Subsequent studies in patients with RAI-refractory disease have yielded a 5% response rate. 7 Combination chemotherapy has 384 cancers. In this manuscript, we describe general principles in management of patients with various types of thyroid cancers including differentiated, medullary and anaplastic thyroid cancers. been equally disappointing. In a small study in which the combination of cisplatin and doxorubicin was compared with doxorubicin alone, the combination had a numerically lower response rate than single-agent doxorubicin. 8 There are hints that newer combinations of cytotoxic chemotherapy may be achieving better results. In a study of 14 patients treated with gemcitabine plus oxaliplatin, a complete response was achieved in one patient and a partial response was achieved in seven. 9 The medical oncologist caring for patients with advanced thyroid cancer should be familiar with alternatives to systemic cytotoxic chemotherapy for patients who have received RAI (Sidebar 1). Patients with locoregionally recurrent disease following thyroidectomy and RAI should be considered for surgery or external-beam radiation treatment. Occasionally, patients benefit from other locoregional modalities, such as the use of ethanol injection or radiofrequency ablation for lymph nodes involved with clinically apparent recurrent disease. In patients with locoregionally recurrent or metastatic disease, the medical oncologist should also ensure that aggressive suppression of thyroid-stimulating hormone has been achieved. Some data suggest that aggressive thyroid stimulating hormone (TSH) suppression leads to improved outcomes, although one large randomized controlled study of TSH suppression compared with replacement in the adjuvant setting after surgery did not demonstrate superiority of suppression. 10,11 There is consensus among experts that, for patients with known recurrent differentiated thyroid cancer (as opposed to patients being treated in the adjuvant setting), the target TSH level should be less than 0.1 mU/L. For patients who have clinically meaningful progression of disease during submaximal TSH suppression (TSH � 0.1 mU/L), the trade-off of side effects from more aggressive TSH suppression must be weighed against the possibility of antitumor benefit. The levothyroxine dose necessary to achieve suppression is typically higher than 1.6 mcg/kg/day, often cited in the literature as a minimal thyroid suppressive dose for patients with benign thyroid conditions. One study found that 2.56 mcg/kg/d was the average dose neces- From the Stanford Cancer Institute, Stanford University, Palo Alto, CA; The Ohio State University Comprehensive Cancer Center, Columbus, OH. Authors’ disclosures of potential conflicts of interest are found at the end of this article. Address reprint requests to Manisha H. Shah, MD, Ohio State University, 320 W. 10 th Avenue, A438 Starling-Loving Hall, Columbus, OH 43210; email: manisha.shah@osumc.edu. © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10
EVALUATION OF ADVANCED THYROID CANCER Sidebar 1. Treatment Considerations for Recurrent or Metastatic Differentiated Thyroid Carcinoma Consideration Surgery External-beam radiation Thyrotropin suppression Confirmation of optimal preparation for prior radioactive iodine treatments Bone lesions sary to adequately suppress TSH in patients with thyroid cancer. 12 It is essential that the medical oncologist seeing patients with recurrent or metastatic DTC be familiar with issues usually addressed by endocrinologists or nuclear medicine physicians. For example, before considering treatment with either cytotoxic chemotherapy or molecularly targeted systemic agents, the medical oncologist should determine whether RAI is an option for the patient. There is no universally accepted definition of RAI-refractory DTC (Sidebar 2). Some clinicians accept a rise in thyroglobulin level following administration of RAI as evidence of refractory KEY POINTS ● Spectrum of thyroid follicular-cell derived cancers ranges from indolent differentiated thyroid cancers (DTC) to very aggressive undifferentiated thyroid cancer commonly known as anaplastic thyroid cancer (ATC). ● Medullary thyroid cancer (MTC) originates from parafollicular c-cells of thyroid and is one of the best characterized solid tumors. ● Surgery plays critical role in management of all types of thyroid cancers while targeted systemic therapies with levo-thyroxine for thyroid stimulating hormonesuppression and radio-iodine are restricted to management of differentiated thyroid cancer. ● Tyrosine kinase inhibitors are promising novel therapies for patients with DTC and MTC. Vandetanib was approved by the U.S. Food and Drug Administration in 2011 for treatment of progressive or symptomatic advanced MTC. ● Despite multimodality treatment with surgery, radiation and cytotoxic chemotherapy, prognosis remains dismal with median survival of 6 months in patients with advanced ATC. Specific Issues Selected patients may benefit from repeated neck dissections or metastatectomies of limited disease. Often useful to control inoperable relapses in the neck and treatment of foci of metastatic disease, especially central nervous system or bone lesions Target serum thyroid stimulating hormone level �0.1 mU/L. May require 2.5 mcg/kg/d or more of levothyroxine Was a low iodine diet maintained? Was the TSH adequately elevated via thyroid hormone withdrawal or recombinant TSH administration? Did the patient receive iodinated contrast medium in the 3 mos. preceding treatment with radioactive iodine? Was a low-iodine diet maintained prior to treatment with radioactive iodine? Bisphosphonates or RANK-ligand inhibitors reduce the risk of fracture. disease. Others cite lack of detectable radioactivity on a whole-body scan following diagnostic or therapeutic administration of RAI as definition of RAI-refractory disease. Although progression after RAI treatment as documented by conventional imaging with computerized tomography (CT), magnetic resonance imaging, or bone scans is probably the most conservative method of declaring a patient’s tumor to be RAI refractory, conventional imaging comparisons are often not available for patients who have been followed up exclusively by serum thyroglobulin levels and whole-body scans. Because of the inverse relationship between fluorodeoxyglucose-positron emission tomography (FDG- PET) avidity and RAI uptake, some clinicians consider a positive FDG-PET scan itself as a definition of RAIrefractory disease. 13,14 Under certain circumstances, it is important to review how therapeutic RAI was administered to ensure that it was given in a setting in which efficacy was maximized. In order to facilitate maximal RAI uptake by the disease, there must not be a sink for the RAI. In general, normal thyroid tissue is more iodine avid than DTC; because of this, the presence Sidebar 2. Various Definitions of Radioactive Iodine (RAI) Refractory Differentiated Thyroid Carcinoma 1. Lack of uptake seen on a whole-body scan following diagnostic RAI dosing 2. Lack of uptake seen on a whole-body scan following therapeutic RAI dosing. 3. Rising thyroglobulin following therapeutic RAI dosing 4. Progression of lesions as documented by conventional imaging (e.g., computerized tomography, magnetic resonance imaging or bone scan) following therapeutic RAI dosing. 5. Cumulative dose of � 600 mCi of 131-iodine ( 131 I) 6. Fluorodeoxyglucose (FDG)–avid lesions on FDGpositron emission tomography. 385
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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 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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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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Advanced Imaging Techniques for the
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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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PROSTATE CANCER RISK REDUCTION men
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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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CONCEPTS IN BRAIN TUMOR IMAGING Aut
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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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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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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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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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0.001), progression-free survival (
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treatment (tx) for metastatic color
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effect. The most common drug that h
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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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STAGE III COLON CANCER: WHAT WORKS,
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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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Conclusion There are clear differen
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prematurely due to poor accrual. 18
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Adjuvant Treatments for Localized A
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HCC, with encouraging outcomes in e
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a 5-year survival rate of 70% follo
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of therapeutic options, patient sel
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less informative than the GRETCH an
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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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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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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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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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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 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 OPTIONS IN INDOLENT LYMPH
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CONTROVERSIES IN MYELOMA: INDUCTION
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TRANSPLANTATION FOR MYELOMA compare
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Maintenance Therapy for Myeloma: Ho
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NEW OPTIONS, NEW QUESTIONS: HOW TO
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Short- and Long-term Cardiovascular
Page 649 and 650:
Recent Advances in Cardiotoxicity o
Page 651 and 652:
CARDIOTOXICITY OF ANTICANCER THERAP
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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 673 and 674:
Page 675 and 676:
Page 677 and 678:
Page 679 and 680:
HOW TO MANAGE VERY RARE PEDIATRIC C
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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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