2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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aggressive disease for early-stage disease: presence of highrisk iFISH (del(17p13) del(11q22) or complex iFISH (multiple iFISH defects), p53 mutations, unmutated IgVH status, or combinations of these defects. The studies of IgVH status are most useful in showing the relative power of a single prognostic factor related to the biology of the CLL B cell. Thus the pivotal study of IgVH demonstrated that patients with CLL who had mutated immunoglobulin IgVH had a survival of more than 20 years, whereas those with unmutated IgVH had median survival of around 8-years. 11,12 The ability of IgVH mutation status to stratify OS remains when applied exclusively to patients with early-stage disease. 12 For prediction of response to therapy, patients with del(17p13) or del(11q22) defects are less likely to have a vigorous response to even the most aggressive upfront treatments. For patients with unmutated and/or del(17p13), the durability of response to therapy is markedly reduced. Recent work has shown that clinical course in patients with iFISH-detectable del(17p13) is profoundly affected by the presence or absence of TP53 mutations. 23 If TP53 mutations (detected by SNP microarray or by sequencing of the p53 gene) are present along with the del(17p13), OS is adversely affected. 24 Most recently there have been advances in putting together prognostic models for prediction of clinical courses and response to therapy. Overview of Prognostic Models in CLL Most patients in the 21 st century are diagnosed with early-stage disease and within this early-stage group, the vast majority do not require immediate treatment. There is, however, a small subgroup of patients who do present with early-stage disease and with symptoms such as fatigue or night sweats or with advanced-stage disease, requiring treatment. Although the latter cohort is not a clinical dilemma in terms of treatment decisions, the majority of patients with early-stage CLL do need better prognostication and subsequent enhanced counseling with regard to follow-up times and to their individual risk of progression. There have been a limited but important set of published work on the development of prognostic models for important clinical end points such as time to first treatment, clinical levels of responses, and duration of responses. These models are important to develop and validate because they may be very useful for patient clinical trial stratification and for providing patient-comparison platforms across clinical trials (Table 2). Table 2. Prognostic Models Factors in Model Risk Groups Defined Clinical Application Focus Reference * Age Low a) To predict survival (5 and 10 yr) Ref 10 * Beta-2 microglobulin Intermediate b) Useful for all Rai stages * Absolute lymphocyte count High * Sex * Rai stage * Number of involved lymph node groups * Lymphocyte doubling time Multivariable models developed for early stage Useful for predicting TTFT and OS Ref 30 * IGHV Mutation Status *CD38 * Age at Diagnosis * Treatment Regimen Nomograms Developed a) Predict response to initial therapy Ref 29 * Beta-2 Microglobulin b) Useful for prediction of CR, TTFT, and OS * Age Abbreviations: CR, complete response; OS, overall survival, TTFT, time to first therapy. 396 NEIL E. KAY A pivotal and pioneering study of clinical outcome was conducted in an initial large series of patients with CLL patients. This analysis identified six factors including age, stage, sex, ALC, beta-2 microglobulin, and number of lymph node regions involved that were independently associated with patient survival. 10 From this set of data these various factors were then combined in a prognostic index that was able to predict OS more accurately than clinical stage alone. Further work validating the prognostic index was subsequently published by two groups indicating that this is a valuable and practical model. 25,26 In one of these studies it was extended to show that the index remained useful even when applied just to Rai stage 0 for the prediction of time to treatment and of OS. 25 Subsequent prognostic models have been developed that also incorporated the biologic factors shown to reflect the pathobiology of the CLL B cell. The initial work on this included an analysis of four novel markers: ZAP-70, CD38, iFISH, and IgVH mutation status for predicting time to treatment in a study of more than 1,000 patients with CLL. 19 The analysis found three groups: low-, intermediate-, and high-risk groups based on ZAP-70 and IgVH mutation status. In summary ZAP-70–positive patients were high risk irrespective of IgVH mutation status; patients with CLL who are ZAP-70 negative can be classified as low (mutated IgVH) or intermediate (unmutated IgVH) risk based on IgVH status. However widespread application of this model is difficult because of the lack of standardization of ZAP-70 measurements. Further work on the ability of iFISH detectable del(17p13) and IgVH mutation status in a cohort of 99 nontreated early-stage patients found surprisingly better time to treatment and survival in some. 27 However if Rai stage was 1 or greater and/or the patient also had an unmutated IgVH status, the favorable clinical course dropped off sharply. A European study found that Binet A patients could be categorized into low-, intermediate-, and high-risk groups based on the combination of iFISH and IgVH mutation status. 15 Here patients with del(17p13) were high risk regardless of mutation status, whereas patients with del(11q22) and/or unmutated IgVH genes were intermediate risk. Finally patients with mutated IgVH without del(17p13) or del(11q22) were low risk. Another recent study analyzed 930 patients with CLL for time to first treatment where both traditional and new prognostic factors were measured. 28 For this study the
PREDICTIVE PARAMETERS IN CLL patients did not have active CLL requiring initiation of treatment within 3 months of first visit and were observed for time to first treatment. The results from this study showed a mix of both types of prognostic parameters were found to be independently associated with a shorter time to first therapy. These parameters included: three involved lymph node sites, increased size of cervical lymph nodes, presence of del(17p13) or del(11q22) increased serum lactate dehydrogenase, and unmutated IgVH mutation status. From a subset of patients a multivariable model was constructed and a nomogram was developed using the latter prognostics to predict the risk of time to first treatment. The authors make the point that this nomogram model system was constructed from only patients with early-stage CLL and where they had very prolonged clinical follow-up using strict criteria to decide on treatment initiation. The same group of investigators has also attempted to develop prognostic features to better predict response to first therapy and subsequent clinical course. Rationale for this is that responses to upfront therapy can be very heterogeneous. Knowledge of critical patient features that are strongly associated with clinical courses post–therapy will again aid in counseling and even in performing relevant clinical trials. For 595 patients who underwent upfront therapy, researchers looked for predictors of three aspects: complete response, time to treatment failure, and OS. 29 In patients who achieved a complete response there was a more favorable durability and survival, but having received combination chemotherapy with antibody regimen was very significant for all three clinical outcomes. The use of various clinical parameters (i.e., age, serum beta-2 microglobulin) generated two nomograms that could be used to predict 5and 10-year OS. Author’s Disclosure of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role Finally there was a very recent and quite large study of 1,154 patients with Binet stage A CLL recently reported that studied both traditional and novel prognostic factors in association with clinical outcome. 30 This study found that LDT was most significantly associated with time to first therapy but that IgVH was strongest in association with OS. In addition only LDT, mutation status, CD38, and age at diagnosis were independent prognostic variables for time to first therapy and OS. Their recommendation was to assess IgVH mutation status and CD38 expression at initial evaluation as they have independent prognostic value in earlystage CLL. Conclusion The use of both traditional and novel prognostic parameters can be a very valuable ally in determining the relative risk of the individual patient’s clinical course of CLL. There are multiple parameters other than individual prognostic factors that can be used at initial prognostic evaluation and can inform the practitioner about disease progression risk and time to therapy. However, the routine use of these parameters, either in single use or in models, is not absolutely mandated in the care of the patients with CLL. In addition, prognostic parameters should include the recognition of other influences on the course of all patients with CLL, such as advanced age and poor biologic fitness (defined as impaired physical fitness and organ function), which considerably increase the risk for adverse consequences of progressive disease and contribute to the decreased survival for patients with CLL compared with the age-matched population. Stock Ownership Honoraria Research Funding Neil E. Kay Genentech; Hospira 1. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2008. CA Cancer J Clin. 2008;58(2):71-96. Epub 2008 Feb 20. 2. Dighiero G, Maloum K, Desablens B, et al. Chlorambucil in indolent chronic lymphocytic leukemia. French Cooperative Group on Chronic Lymphocytic Leukemia. N Engl J Med. 1998;338(21):1506-1514. 3. Shanafelt TD, Bowen D, Venkat C, et al. Quality of life in chronic lymphocytic leukemia: An international survey of 1482 patients. Br J Haematol. 2007;139(2):255-264. 4. Shanafelt TD, Bowen DA, Venkat C, et al. The physician-patient relationship and quality of life: Lessons from chronic lymphocytic leukemia. Leuk Res. 2009;33(2):263-270. Epub 2008 Jul 25. 5. Rozman C, Bosch F, Montserrat E. Chronic lymphocytic leukemia: A changing natural history? Leukemia. 1997;11(6):775-778. 6. Zent CS, Kay NE. Management of patients with chronic lymphocytic leukemia with a high risk of adverse outcome: The Mayo Clinic approach. Leuk Lymphoma. 2011;52(8):1425-1434. Epub 2011 Jun 8. 7. Shanafelt TD, Rabe KG, Kay NE, et al. Age at diagnosis and the utility of prognostic testing in patients with chronic lymphocytic leukemia. Cancer. 2010;116(20):4777-4787. 8. Molica S, Alberti A. Prognostic value of the lymphocyte doubling time in chronic lymphocytic leukemia. Cancer. 1987;60(11):2712-2716. 9. Bergmann MA, Eichhorst BF, Busch R, et al. Prospective Evaluation of Prognostic Parameters in Early Stage Chronic Lymphocytic Leukemia (CLL): REFERENCES Expert Testimony Other Remuneration Results of the CLL1-Protocol of the German CLL Study Group (GCLLSG). ASH Annual Meeting Abstracts. 2007;110(11):625. 10. Wierda WG, O’Brien S, Wang X, et al. Prognostic nomogram and index for overall survival in previously untreated patients with chronic lymphocytic leukemia. Blood. 2007;109(11):4679-4685. Epub 2007 Feb 13. 11. Damle RN, Wasil T, Fais F, et al. Ig V gene mutation status and CD38 expression as novel prognostic indicators in chronic lymphocytic leukemia. Blood. 1999;94(6):1840-1847. 12. Hamblin TJ, Davis Z, Gardiner A, et al. Unmutated Ig V(H) genes are associated with a more aggressive form of chronic lymphocytic leukemia. Blood. 1999;94(6):1848-1854. 13. Hamblin TJ, Orchard JA, Ibbotson RE, et al. CD38 expression and immunoglobulin variable region mutations are independent prognostic variables in chronic lymphocytic leukemia, but CD38 expression may vary during the course of the disease. Blood. 2002;99(3):1023-1029. 14. Dohner H, Stilgenbauer S, Benner A, et al. Genomic aberrations and survival in chronic lymphocytic leukemia. N Engl J Med. 2000;343(26):1910- 1916. Epub 2008 Mar 26. 15. Krober A, Seiler T, Benner A, et al. V(H) mutation status, CD38 expression level, genomic aberrations, and survival in chronic lymphocytic leukemia. Blood. 2002;100(4):1410-1416. 16. Crespo M, Bosch F, Villamor N, et al. ZAP-70 expression as a surrogate for immunoglobulin-variable-region mutations in chronic lymphocytic leukemia. N Engl J Med. 2003;348(18):1764-1775. 397
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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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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
Page 585 and 586:
Page 587 and 588:
Page 589 and 590:
ROLE OF HCT FOR INDOLENT LYMPHOMA T
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ROLE OF HCT FOR INDOLENT LYMPHOMA T
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ROLE OF HCT FOR INDOLENT LYMPHOMA e
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CONTROVERSIES IN MYELOMA: INDUCTION
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TRANSPLANTATION FOR MYELOMA Alterna
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TRANSPLANTATION FOR MYELOMA compare
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TRANSPLANTATION FOR MYELOMA autolog
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CURRENT STATUS OF MYELOMA THERAPY K
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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
Page 619 and 620:
THERAPIES FOR PATIENTS WITH METASTA
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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
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INCIDENCE AND PREVALENCE OF CHEMOTH
Page 639 and 640:
New Frontiers in Mucositis By Dougl
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MUCOSAL INJURY CAUSED BY CANCER THE
Page 643 and 644:
Page 645 and 646:
Page 647 and 648:
Short- and Long-term Cardiovascular
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Recent Advances in Cardiotoxicity o
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CARDIOTOXICITY OF ANTICANCER THERAP
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CARDIOTOXICITY OF ANTICANCER THERAP
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The Oncologist as the Patient with
Page 657 and 658:
THE ONCOLOGIST AS THE PATIENT OR RE
Page 659 and 660:
Prolonged Febrile Neutropenia in th
Page 661 and 662:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 663 and 664:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 665 and 666:
TREATMENT APPROACHES IN CHILDREN wh
Page 667 and 668:
TREATMENT APPROACHES IN CHILDREN th
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GENETIC COUNSELING OF THE PATIENT W
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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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