2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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has been intensively studied. These studies have proposed and validated a number of resistance mechanisms in small numbers of patient tumor samples including: (1) Mutations of NRAS, the protein upstream of BRAF in the MAPK pathway. 33 (2) Activation of downstream signaling proteins including MEK1 through mutation or activation by overexpression of MAP kinases 34,35 (3) The expression of alternate shortened forms of the BRAFV600 mutated molecule that are capable of binding together and reactivating the pathway even in the presence of vemurafenib. 36 All three of these mechanisms appear to reactivate the MAPK pathway, providing a direction to pursue in order to effectively delay or overcome these forms of resistance. (4) Alternatively, activation or overexpression of alternate pathways through activation of receptor tyrosine kinases, such as IGFR1 or PDGFRb. Both of these RTK appear to signal at least in part through the PI3K/Akt/mTOR pathway. 33,37 Ongoing trials are combining BRAF and MEK inhibitors with the goal of delaying or overcoming resistance as a result of reactivation of the MAPK pathway. On the other hand, combinations of BRAF-inhibitor therapy with either PI3 kinase, PI3 kinase/mTOR, Akt, mTORC1- and mTORC2dual inhibitors could be effective inhibiting mechanisms of resistance involving alternate pathways and different receptor tyrosine kinases. Although BRAF inhibitors induce rapid disease regression and symptom benefit in patients with bulky disease, markedly delay progression, and improve overall survival for the overall metastatic melanoma population, there is clearly need for further improvement of these outcomes. For patients with BRAFV600E/K mutant melanoma, there is a choice of therapy between new and older immunotherapy approaches, including high dose IL-2, ipilimumab, or a clinical trial investigating anti-PD1 compared with a BRAF inhibitor. It is apparent that patients with symptomatic, bulky, rapidly growing, and high-serum LDH– associated melanoma are much more likely to have rapid clinical improvement when treated with vemurafenib. The improvement may be relatively short term but can last up to 12 months in some patients. These patients are unlikely to benefit from immunotherapy, in part, because immunebased treatments can take a period of time and some experience progression initially before later improvement. Furthermore, the percent of patients having an objective clinical response is much lower with IL-2 (15% to 20%) or ipilimumab (5% to 10%) than with vemurafenib (� 50%). The greater dilemma surrounds the patient with BRAFmutant melanoma who has nonbulky, asymptomatic disease, and with a normal LDH. These patients have a choice. If young enough, with excellent organ function and at a treatment center with extensive experience, IL-2 may be the first choice. Or, in others who do not fulfill IL-2 criteria, ipilimumab. However, because of the delay in beneficial effect, it may require waiting up to 4 to 6 months before one can be certain that the melanoma is not responsive. Also, in this subset of patients, the response rate to vemurafenib is above 60% in the phase II trial, and overall survival is quite long with a median of 15.9 months. 31 This compares to 10 months on the previously treated trial and 11.2 months on the treatment-naive trial with ipilimumab. The definite answer to the question of which drug to use first will only be answered through trials including combinations of the two agents. 528 Treatment Options for BRAF WT Melanoma BRAF WT melanoma is a heterogeneous disease that includes patients with NRAS mutated melanoma (about one-third of these BRAF WT patients) as well as very small subset of patients with CKIT mutant melanoma from mucosal, acral, and chronic sun-damaged sites. Characterizing these mutations can be justified currently for the purposes of directing patients to relevant clinical trials. There is supporting literature showing that a fraction of patients with L597 or K642 mutations in CKIT are responsive to imatinib, some of which the results are quite durable (� 12 months). 38,39 NRAS approaches will be discussed below. Immunotherapy remains a strong consideration in BRAF WT patients. Those who are eligible for IL-2 should consider this treatment at an experienced center. Since it has the longest follow-up, we are confident of both its response rate and the frequency of extremely durable disease responses. Those patients are frequently assessed at 7 to 8 weeks and again at 11 to 12 weeks and in the case of progression or even stable disease, this treatment is rarely continued. Toxicities are acute and rarely, if ever, delayed. For these reasons, we believe that consideration of ipilimumab should come after these patients have received IL-2 if the treatment is appropriate. As stated previously, new trials with anti- PD1 antibodies are ongoing and demonstrate exciting, early results with response rates over 20% of which most are durable lasting over 12 months. It is critical to continue efforts to define other driver kinases within the BRAF WT population that could be targeted with drug therapy. For now, efforts are underway to investigate approaches to NRAS mutant melanoma, These include MEK inhibitors (GSK 1120212, TAK733, or others) alone or in combination with inhibitors of the PI3K/ AKT, mTOR pathway. These trials are still in dose-finding phases, but soon phase II efforts will be undertaken in NRAS mutant melanoma. Finally, chemotherapy still represents an option for patients without either good standard options, as listed above, or clinical phase I and II trial options. Because of its limited long-term benefit, chemotherapy is best considered for patients who are symptomatic or with rapidly growing disease with a goal of improving quality of life. Agents, including dacarbazine, temozolomide, and taxane-based regimens, have all demonstrated similar antitumor activity with below 20% response rates. Rarely, long-lasting responses are observed. Conclusion FLAHERTY, SOSMAN, AND ATKINS Given the current availability of multiple treatment options, patients and physicians now often have choices regarding initial treatment and the sequence of various treatments. For patients with BFAFV600E mutant melanoma, options could include HD IL-2, ipilimumab or vemurafenib. At the moment, there appears to be only limited information to guide this choice. Although vemurafenib appears to be equally active in patients whose disease has progressed following IL 2-based immunotherapy, there is no data on its activity following resistance to ipilimumab. Similarly, there is no data on the activity of ipilimumab (or even the feasibility of stopping vemurafenib and administering ipilimumab) following disease progression on vemurafenib. It is conceivable that patients treated initially with
THERAPIES FOR PATIENTS WITH METASTATIC MELANOMA ipilimumab may get the benefit of a durable response (up to 25%) without compromising the benefit of subsequent vemurafenib for those patients who exhibit disease progression, whereas those started on vemurafenib may not be able to benefit from subsequent ipilimumab at time of progression. It is also possible that the high response rate and prolonged progression free survival associated with vemurafenib therapy relative to ipilimumab may overwhelm any benefit that might be achieved with initial ipilimumab therapy. Further, it is possible that subsets of patients, defined by tumor and/or clinical characteristics (for example, PTEN loss, immune infiltration, high serum LDH), might do better with one initial therapy or sequence than with the other. A randomized phase III trial of ipilimumab (followed by vemurafenib) versus vemurafenib (followed by ipilimumab) is being planned within the Cooperative Group mechanism in an effort to obtain real data to address these important therapeutic questions and guide future treatment choices for this patient population. In addition, this population repre- Authors’ Disclosures of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role Keith T. Flaherty Genentech; GlaxoSmithKline; Metamark Genetics Jeff A. Sosman GlaxoSmithKline; Roche Michael B. Atkins Bristol-Myers Squibb; Celgene; Curetech; Genentech; Merck; Novartis; Prometheus 1. Siegel R, Ward E, Brawley O, et al. Cancer Statistics, 2011: the impact of eliminating socioeconomic and racial disparities on premature cancer deaths. CA Cancer J Clin. 2011;61:212-236. 2. Atkins MB, Lotze MT, Dutcher JP, et al. High-dose recombinant interleukin 2 therapy for patients with metastatic melanoma: analysis of 270 patients treated between 1985 and 1993. J Clin Oncol. 1999;17:2105-2116. 3. Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature. 2002;417:949-954. 4. Tsai J, Lee JT, Wang W, et al. Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity. Proc Natl Acad SciUSA.2008;105:3041-3046. 5. Neal SE, Eccleston JF, Webb MR. Hydrolysis of GTP by p21NRAS, the NRAS protooncogene product, is accompanied by a conformational change in the wild-type protein: use of a single fluorescent probe at the catalytic site. Proc Natl Acad Sci USA.1990;87:3562-3565. 6. Curtin JA, Fridlyand J, Kageshita T, et al. Distinct sets of genetic alterations in melanoma. N Engl J Med. 2005;353:2135-2147. 7. Curtin JA, Busam K, Pinkel D, et al. Somatic activation of KIT in distinct subtypes of melanoma. J Clin Oncol. 2006;24:4340-4346. 8. Davies MA, Stemke-Hale K, Tellez C, et al. A novel AKT3 mutation in melanoma tumours and cell lines. Br J Cancer. 2008;99:1265-1268. 9. Stahl JM, Sharma A, Cheung M, et al. Deregulated Akt3 activity promotes development of malignant melanoma. Cancer Res. 2004;64:7002- 7010. 10. Tsao H, Goel V, Wu H, et al. Genetic interaction between NRAS and BRAF mutations and PTEN/MMAC1 inactivation in melanoma. J Invest Dermatol. 2004;122:337-341. 11. Dankort D, Curley DP, Cartlidge RA, et al. Braf(V600E) cooperates with Pten loss to induce metastatic melanoma. Nat Genet. 2009;41:544-552. 12. Dhomen N, Reis-Filho JS, da Rocha Dias S, et al. Oncogenic Braf sents an ideal group for combination treatment approaches. Studies involving selective BRAF inhibitors with immunotherapy (ipilimumab, HD IL-2, PD1 pathway blockers), VEGF pathway inhibitors, or other molecularly targeted agents (MEK or PI3Kinase inhibitors or apoptosis inducers) are currently underway and represent opportunities to further advance treatment results. Options are more limited for patients with BRAF WT melanoma. For the few patients with mutations in C-Kit, imatinib or participation in a C-kit-inhibitor clinical trial seems to represent the best choice. For those with NRAS mutations, HD IL-2 might be a reasonable option, although data supporting this selection requires validation. Additional research is needed to determine the activity of ipilimumab or other immunotherapies in this population. Efforts are also underway to identify potential therapeutic targets downstream of NRAS or for BRAF, NRAS, or CKIT triple WT tumors that may allow for development of personalized treatment options for this patient population. Stock Ownership Honoraria Genentech; GlaxoSmithKline REFERENCES Roche Research Funding Expert Testimony Other Remuneration induces melanocyte senescence and melanoma in mice. Cancer Cell. 2009;15: 294-303. 13. Schwartzentruber DJ, Lawson DH, Richards JM, et al. Gp100 peptide vaccine and interleukin-2 in patients with advanced melanoma. N Engl J Med. 2011;364:2119-2127. 14. Rosenberg SA, Yang JC, Sherry RM, et al. Durable complete responses in heavily pretreated patients with metastatic melanoma using T-cell transfer immunotherapy. Clin Cancer Res. 2011;17:4550-4557. 15. Hodi FS, O’Day SJ, McDermott DF, et al. Improved survival with ipilimumab in patients with metastatic melanoma. N Engl J Med. 2010;363: 711-723. 16. Wolchok JD, Neyns B, Linette G, et al. Ipilimumab monotherapy in patients with pretreated advanced melanoma: A randomised, double-blind, multicentre, phase 2, dose-ranging study. Lancet Oncol. 2010;11:155-64. 17. Lawrence DPH, McDermott DF. Phase II trial of ipilimumab monotherapy in melanoma patients with brain metastasis. J Clin Oncol. 2010;28 (suppl; abstr 8523). 18. Wolchok JD, Hoos A, O’Day S, et al. Guidelines for the evaluation of immune therapy activity in solid tumors: immune-related response criteria. Clin Cancer Res. 2009;15:7412-7420. 19. Robert C, Thomas L, Bondarenko I, et al. Ipilimumab plus dacarbazine for previously untreated metastatic melanoma. N Engl J Med. 364:2517-2526. 20. Sharpe AHW, EJ, Ahmed R, Freeman GJ. The function of programmed cell death 1 and its ligands in regulating autoimmunity and infection. Nat Immun. 2007;8:239-245. 21. Brahmer JRD, Wollner I, Powderly JD, et al. Phase I study of singleagent anti-programmed death-1 (MDX-1106) in refractory solid tumors: safety, clinical activity, pharmacodynamics, and immunologic correlates. J Clin Oncol. 2010;28:3167-3175. 22. Sznol MH, Margolin K, McDermott D, et al. Phase I study of BMS- 529
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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American Society of Clinical Oncolo
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American Society of Clinical Oncolo
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New Looks and Challenges for Cooper
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Genitourinary Cancer Best Use of Im
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Research and Standard of Care: Lung
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Practice Management and Information
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2012 ASCO Annual Meeting Disclosure
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Matti S. Aapro, MD Clinique De Geno
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Hedy Lee Kindler, MD The University
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Douglas E. Wood, MD University of W
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Mary Lou Smith, JD, MBA Research Ad
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ASCO and Conquer Cancer Foundation
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Letter from the Editor The theme of
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Adjuvant Therapy for Older Women wi
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TREATMENT FOR OLDER WOMEN WITH BREA
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MANAGEMENT OF T1 BREAST CANCERS the
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MANAGEMENT OF T1 BREAST CANCERS Tab
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MANAGEMENT OF T1 BREAST CANCERS Tab
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MANAGEMENT OF T1 BREAST CANCERS 93.
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MANAGEMENT OF T1 BREAST CANCERS 1 c
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ADJUVANT ENDOCRINE THERAPY reductio
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ADJUVANT ENDOCRINE THERAPY which ra
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ADJUVANT ENDOCRINE THERAPY assay is
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A DICKENS TALE OF THE TREATMENT OF
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TREATMENT OF ADVANCED BREAST CANCER
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A FRESH LOOK AT DUCTAL CARCINOMA IN
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DCIS: OPPORTUNITIES AND UNCHARTED W
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DCIS: OPPORTUNITIES AND UNCHARTED W
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Ductal Carcinoma In Situ, and the I
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DCIS AND INFLUENCE OF RISK FACTORS
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KEY QUESTIONS IN THE LOCO-REGIONAL
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POSTMASTECTOMY RADIATION AND PARTIA
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The Appropriate Extent of Surgery f
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SURGERY FOR EARLY-STAGE BREAST CANC
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BIOLOGY AND LOCAL THERAPY DECISIONS
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Clinical and Imaging Surveillance F
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SURVEILLANCE FOLLOWING BREAST CANCE
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SURVEILLANCE FOLLOWING BREAST CANCE
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Advanced Imaging Techniques for the
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IMAGING TECHNIQUES FOR BREAST CANCE
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IMAGING TECHNIQUES FOR BREAST CANCE
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Update of the Oxford Overview: New
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UPDATE OF THE OXFORD OVERVIEW Fig.
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UPDATE OF THE OXFORD OVERVIEW Overv
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Gene Patents and Personalized Medic
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GENE PATENTS AND EFFECTS ON PERSONA
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Chemoprevention for Breast Cancer:
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CHEMOPREVENTION FOR BREAST CANCER T
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CHEMOPREVENTION FOR BREAST CANCER C
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CONTROVERSIES IN PROSTATE CANCER: P
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PROSTATE CANCER RISK REDUCTION men
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PROSTATE CANCER RISK REDUCTION Auth
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PSA SCREENING: HARMS WITHOUT CLEAR
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PSA SCREENING: HARMS WITHOUT CLEAR
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GLIOBLASTOMA: TAKING THE STANDARD O
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GLIOBLASTOMA: BIOLOGY, GENETICS AND
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FUTURE DIRECTIONS IN GBM THERAPY pr
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FUTURE DIRECTIONS IN GBM THERAPY Ch
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ESTABLISHING TREATMENTS FOR GLIOBLA
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Current Concepts in Brain Tumor Ima
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CONCEPTS IN BRAIN TUMOR IMAGING tum
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CONCEPTS IN BRAIN TUMOR IMAGING Aut
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PERSPECTIVES ON HEADLINE-MAKING NEW
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TTF THERAPY IN GLIOBLASTOMA Fig. 1.
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TTF THERAPY IN GLIOBLASTOMA istics.
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TTF THERAPY IN GLIOBLASTOMA because
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Limitations of Adaptive Clinical Tr
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LIMITATIONS OF ADAPTIVE CLINICAL TR
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LIMITATIONS OF ADAPTIVE CLINICAL TR
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Capturing the Patient Perspective:
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PATIENT-REPORTED OUTCOMES AS TRIAL
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PATIENT-REPORTED OUTCOMES AS TRIAL
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NEW LOOKS AND CHALLENGES FOR COOPER
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NCI NATIONAL CLINICAL TRIALS NETWOR
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Successful Integration of Cooperati
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COG: GIVING NEW MEANING TO COOPERAT
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A Critical Review of the Enrollment
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BLACK PATIENTS AND CANCER CLINICAL
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BLACK PATIENTS AND CANCER CLINICAL
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Trastuzumab Emtansine (T-DM1): Hitc
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T-DM1 AND THERAPEUTIC ANTIBODIES ag
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TARGETING CD30 IN HODGKIN LYMPHOMA
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TARGETING CD30 IN HODGKIN LYMPHOMA
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EARLY DRUG DEVELOPMENT: CASTING A W
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Table 1. Response Rates in Expanded
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Drug Development in the Era of Pers
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that the core pathway is not comple
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This situation is not surprising, g
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Practical Management of Immune-Rela
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the anterior pituitary axis is invo
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TARGETING CRITICAL MOLECULAR ABERRA
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Abl suppression; and 3) the early e
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50% 50% 100% Change in Tumor Size m
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vanced solid tumors, even if they a
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Targeting Molecular Aberrations in
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date. With the advent of gene expre
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consortium to facilitate the testin
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ETHICAL CHALLENGES OF HEALTH CARE R
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HEALTH CARE REFORM AND ONCOLOGY dev
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HEALTH CARE REFORM AND ONCOLOGY aut
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INTERNATIONAL VARIATION IN UNDERSTA
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midcareer physician; in one cross-s
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Table 1. Recommendations for Person
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stances (e.g., stage of career, fam
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elationship” is also acknowledged
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Conclusion In more individualistic
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The Oncologist’s Duty to Provide
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an external observer, but to the pe
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MEDICAL ERRORS IN CANCER CARE: PREV
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DISCLOSING MEDICAL ERRORS Disclosur
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DISCLOSING MEDICAL ERRORS Author’
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PREVENTING MEDICAL ERRORS more diff
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“PERSONALIZED” ONCOLOGY FOR COL
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0.001), progression-free survival (
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mately 40% of patients with colorec
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Table 1. Tumor Marker Utility Gradi
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treatment (tx) for metastatic color
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The Interventional Radiologist Role
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effect. The most common drug that h
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gone forever, no further therapy is
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is irrelevant if it is already rese
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Resection and Thermal Ablation of L
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Author’s Disclosures of Potential
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Minimally Invasive Surgery of Recta
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outcomes; local, wound-site, and di
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Authors’ Disclosures of Potential
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CAO/ARO 04 study—which added oxal
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STAGE III COLON CANCER: WHAT WORKS,
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Table 1. Comparison of Fluoropyrimi
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tients with stages II and III color
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ized by high fruit, vegetable, poul
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Exercise Change trial: a randomized
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A New Direction for Pancreatic Canc
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Table 1. FOLFIRINOX versus Gemcitab
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The Southwest Oncology Group (SWOG)
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A Matter of Timing: Is There a Role
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an OS benefit with radiation therap
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a dose of 50.4 Gy to 59.4 Gy of rad
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more commonly given for APC, specia
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subcutaneous bolus or infusion. Hal
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patients are cared for completely w
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Varying Lymphadenectomies for Gastr
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Table 1. Regional Lymph Nodes of th
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Conclusion There are clear differen
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Will Disease Heterogeneity Help Def
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prematurely due to poor accrual. 18
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Adjuvant Treatments for Localized A
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ADJUVANT TREATMENT FOR GASTRIC CANC
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LIVER-DIRECTED THERAPEUTIC OPTIONS
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ated with unique dose distributions
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HCC, with encouraging outcomes in e
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tion. Advanced computer-based image
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a 5-year survival rate of 70% follo
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THE MANAGEMENT OF LESS COMMON BUT C
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Fig 1. PubMed publications and clin
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of therapeutic options, patient sel
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less informative than the GRETCH an
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Table 3. New Agents/Regimens under
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combined with concurrent transarter
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to optimize the use of erlotinib by
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Optimal Use of Imaging to Guide Tre
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enhancement seen. Furthermore, the
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CASTRATION-RESISTANT PROSTATE CANCE
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Fig. 1. FDA regulatory approvals in
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Prognostic, Predictive, and Surroga
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adhesion molecule and further chara
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and treatment options are expanding
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KIDNEY CANCER BIOLOGY AND THERAPEUT
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Prognostic Factors in Advanced RCC
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cell immunotherapy in which a small
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New Developments in Urothelial Canc
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Novel Approaches in Advanced Urothe
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10. Albers P, Park SI, Niegisch G,
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700 at a dose of 400 mg twice daily
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therapy for nonmetastatic prostate
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ADJUVANT THERAPY FOR OLDER PATIENTS
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Adjuvant Systemic Therapy Adjuvant
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with early-stage breast cancer were
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clinical trials to generate additio
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Adjuvant Treatment of Older Patient
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OLDER PATIENTS WITH LUNG CANCER Fig
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OLDER PATIENTS WITH LUNG CANCER adj
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Considerations and Controversies in
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OLDER PATIENTS WITH ADVANCED CANCER
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RECENT CLINICAL HIGHLIGHTS IN GYNEC
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GLOBAL ADVANCES IN GYNECOLOGIC ONCO
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GLOBAL ADVANCES IN GYNECOLOGIC ONCO
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The European Society of Gynaecologi
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ESGO EDUCATIONAL AND RESEARCH ACTIV
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UPFRONT TREATMENT OF OVARIAN CANCER
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ANTIANGIOGENICS AND PARP INHIBITORS
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ANTIANGIOGENICS AND PARP INHIBITORS
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Intraperitoneal Treatment in Ovaria
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INTRAPERITONEAL TREATMENT IN OVARIA
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Dose-Dense Chemotherapy and Neoadju
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CHEMOTHERAPY FOR OVARIAN CANCER Fig
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CHEMOTHERAPY FOR OVARIAN CANCER whi
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UTERINE SARCOMA: CHALLENGING CASES
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HISTOLOGIC FEATURES AND MANAGEMENT
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SURGICAL OPTIONS FOR UTERINE SARCOM
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SURGICAL OPTIONS FOR UTERINE SARCOM
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PATIENTS WITH HPV-POSITIVE OROPHARY
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HPV-INDUCED OROPHARYNX CANCER analy
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HPV-INDUCED OROPHARYNX CANCER fract
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Important Early Advances in Squamou
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EARLY ADVANCES IN SCCHN Fig 1. Targ
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Application of Genomic and Proteomi
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GENOMIC AND PROTEOMIC TECHNOLOGIES
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GENOMIC AND PROTEOMIC TECHNOLOGIES
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TREATMENT OF THYROID CANCERS: NEW I
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EVALUATION OF ADVANCED THYROID CANC
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EVALUATION OF ADVANCED THYROID CANC
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Systemic Therapeutic Approaches to
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APPROACHES TO ADVANCED THYROID CANC
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AVOIDING OVERDIAGNOSIS AND OVERTREA
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Table 1. Prevalence of Prostate Can
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Table 3. Potential Risks and Benefi
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Overdiagnosis and Overtreatment of
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een reached by other modeling effor
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east cancer community have FDA-appr
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COSTS OF CANCER CARE: AFFORDABILITY
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REDUCING THE COST OF CANCER CARE Fi
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REDUCING THE COST OF CANCER CARE Th
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REDUCING THE COST OF CANCER CARE de
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Why Hasn’t Genomic Testing Change
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tigators should develop prospective
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MANAGEMENT OF CHRONIC LYMPHOCYTIC L
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PREDICTIVE PARAMETERS IN CLL Table
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PREDICTIVE PARAMETERS IN CLL patien
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Transplant in Chronic Lymphocytic L
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WHEN TO OFFER TRANSPLANTATION IN CL
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WHEN TO OFFER TRANSPLANTATION IN CL
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NEW DEVELOPMENTS IN MYELOPROLIFERAT
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SMALL-MOLECULE INHIBITORS FOR MPN S
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SMALL-MOLECULE INHIBITORS FOR MPN L
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Insights into the Molecular Genetic
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GENETICS OF MYELOPROLIFERATIVE NEOP
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Classification of Myeloproliferativ
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CLASSIFICATION AND PROGNOSIS OF MPN
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CLASSIFICATION AND PROGNOSIS OF MPN
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AROUND THE WORLD IN ALMOST 80 MINUT
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LUNG CANCER IN BRAZIL Fig. 1. Relat
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LUNG CANCER IN BRAZIL Fig. 3. Chara
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LUNG CANCER IN BRAZIL Author’s Di
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LUNG CANCER IN CHINA Fig 1. Chinese
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LUNG CANCER IN CHINA well equipped
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Research and Standard of Care: Lung
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LUNG CANCER IN ROMANIA ● Protecti
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LUNG CANCER IN ROMANIA reimbursemen
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A New Model: Physician-Patient Coll
Page 539 and 540:
PHYSICIAN ENGAGEMENT IN ONLINE PATI
Page 541 and 542:
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
Page 547 and 548:
LUNG CANCER SCREENING Fig. 1. Guide
Page 549 and 550:
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
Page 571 and 572: SYSTEMIC TREATMENT OF THYMOMA Study
Page 573 and 574: SYSTEMIC TREATMENT OF THYMOMA cance
Page 575 and 576: What Is the Best Strategy for Incor
Page 577 and 578: 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 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
Page 603 and 604: CURRENT STATUS OF MYELOMA THERAPY K
Page 605 and 606: CURRENT STATUS OF MYELOMA THERAPY F
Page 607 and 608: CURRENT STATUS OF MYELOMA THERAPY T
Page 609 and 610: Maintenance Therapy for Myeloma: Ho
Page 611 and 612: MAINTENANCE THERAPY FOR MULTIPLE MY
Page 617 and 618: NEW OPTIONS, NEW QUESTIONS: HOW TO
Page 619 and 620: THERAPIES FOR PATIENTS WITH METASTA
Page 621: THERAPIES FOR PATIENTS WITH METASTA
Page 625 and 626: ANTIEMETICS: CURRENT STANDARDS, EME
Page 627 and 628: ANTIEMETICS: ASCO GUIDELINE UPDATE
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 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 673 and 674:
CANCER PREDISPOSITION IN CHILDHOOD
Page 675 and 676:
Page 677 and 678:
Page 679 and 680:
HOW TO MANAGE VERY RARE PEDIATRIC C
Page 681 and 682:
RARE CANCER IN CHILDREN Registries
Page 683 and 684:
Genetic Alterations in Childhood Me
Page 685 and 686:
GENETIC ALTERATIONS IN CHILDHOOD ME
Page 687 and 688:
Desmoid-Type Fibromatosis in Childr
Page 689 and 690:
CHEMOTHERAPY FOR DESMOID TUMOR Tabl
Page 691 and 692:
CHEMOTHERAPY FOR DESMOID TUMOR 14.
Page 693 and 694:
Targeting the Insulin-Like Growth F
Page 695 and 696:
TARGETING THE IGF SYSTEM Fig. 1. Th
Page 697 and 698:
TARGETING THE IGF SYSTEM malignanci
Page 699 and 700:
Hedgehog Pathway in Pediatric Cance
Page 701 and 702:
HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 703 and 704:
HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 705 and 706:
Development and Refinement of Augme
Page 707 and 708:
ABFM THERAPY FOR PEDIATRIC ALL than
Page 709 and 710:
ABFM THERAPY FOR PEDIATRIC ALL Auth
Page 711 and 712:
RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 713 and 714:
RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 715 and 716:
Role of Doxorubicin in Rhabdomyosar
Page 717 and 718:
DOXORUBICIN IN RHABDOMYOSARCOMA 8.
Page 719 and 720:
Identification of Novel Biologic Ta
Page 721 and 722:
NOVEL TARGETS IN THE TREATMENT OF D
Page 723 and 724:
Is Biopsy Safe in Children with New
Page 725 and 726:
SAFETY OF DIPG BIOPSY IN CHILDREN F
Page 727 and 728:
SAFETY OF DIPG BIOPSY IN CHILDREN 1
Page 729 and 730:
CHILDREN WITH DIFFUSE INTRINSIC PON
Page 731 and 732:
Communication and Decision Support
Page 733 and 734:
COMMUNICATION AND DECISION SUPPORT
Page 735 and 736:
Page 737 and 738:
Page 739 and 740:
Planning for the Future: The Role o
Page 741 and 742:
present in the office suite but doe
Page 743 and 744:
Summary and Care Plan are provided.
Page 745 and 746:
DOING IT RIGHT, AND FOR LESS: IMPLE
Page 747 and 748:
CLINICAL PATHWAYS STANDARDIZING PER
Page 749 and 750:
CLINICAL PATHWAYS STANDARDIZING PER
Page 751 and 752:
The Future of Oncology Care with Pe
Page 753 and 754:
quantity. Determining the appropria
Page 755 and 756:
THE ASCO QUALITY ONCOLOGY PRACTICE
Page 757 and 758:
IMPROVING VALUE OF CARE IN ONCOLOGY
Page 759 and 760:
Page 761 and 762:
Page 763 and 764:
PHYSICIAN WELLNESS: COPING WITH REP
Page 765 and 766:
also provides insight on how clinic
Page 767 and 768:
good resource for exploring the pri
Page 769 and 770:
of death or following death and inc
Page 771 and 772:
telephone call to the family, sendi
Page 773 and 774:
New Insights in Cross-Cultural Comm
Page 775 and 776:
CROSS-CULTURAL COMMUNICATION Sideba
Page 777 and 778:
THE ONCOLOGIST, THE PATIENT, AND TH
Page 779 and 780:
estimate of the proportion of their
Page 781 and 782:
exactly the same treatment, even th
Page 783 and 784:
How to Decide Whether to Offer and
Page 785 and 786:
NONSTANDARD THERAPIES FOR ADVANCED
Page 787 and 788:
NONSTANDARD THERAPIES FOR ADVANCED
Page 789 and 790:
TARGETED THERAPIES IN TARGETED OR U
Page 791 and 792:
TARGETED THERAPY IN SARCOMA rates a
Page 793 and 794:
TARGETED THERAPY IN SARCOMA seen in
Page 795 and 796:
TARGETED THERAPY IN SARCOMA recepto
Page 797 and 798:
Adjuvant Treatment of Gastrointesti
Page 799 and 800:
ADJUVANT THERAPY IN HIGH-RISK GASTR
Page 801 and 802:
Management of Tyrosine Kinase Inhib
Page 803 and 804:
TKI-RESISTANT GIST Primary Imatinib
Page 805 and 806:
TKI-RESISTANT GIST Table 2. Clinica
Page 807 and 808:
BIOLOGIC PRINCIPLES OF TARGETED COM
Page 809 and 810:
COMBINING TARGETED AGENTS IN CLINIC
Page 811 and 812:
COMBINING TARGETED AGENTS IN CLINIC
Page 813 and 814:
Combination Therapies Building on t
Page 815 and 816:
COMBINATIONS FOR MELANOMA agents th
Page 817 and 818:
MECHANISMS OF RESISTANCE TO TARGETE
Page 819 and 820:
RESISTANCE MECHANISMS TO MAPK INHIB
Page 821 and 822:
RESISTANCE MECHANISMS TO MAPK INHIB
Page 823 and 824:
Mechanisms of Resistance to Targete
Page 825 and 826:
RESISTANCE TO TARGETED THERAPIES IN
Page 827 and 828:
RESISTANCE TO TARGETED THERAPIES IN
Page 829 and 830:
Translating PI3K-Delta Inhibitors t
Page 831 and 832:
THE STORY OF CAL-101 6% of patients
Page 833 and 834:
PI3 Kinase in Cancer: From Biology
Page 835 and 836:
PI3 KINASE IN CANCER Fig. 1. The PI
Page 837 and 838:
PI3 KINASE IN CANCER Fig. 3. In viv
Page 840:
This publication is supported by an
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2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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