2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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Table 1. RANO Criteria for Response Assessment Incorporating MRI and Clinical Factors† Complete response Requires all of the following: complete disappearance of all enhancing measurable and nonmeasurable disease sustained for at least 4 wk; no new lesions; stable or improved nonenhancing (T2/FLAIR) lesions; patients must be off corticosteroids (or on physiologic replacement doses only); and stable or improved clinically. Note: Patients with nonmeasurable disease only cannot have a complete response; the best response possible is stable disease Partial response Requires all of the following: � 50% decrease compared with baseline in the sum of products of perpendicular diameters of all measurable enhancing lesions sustained for at least 4 wk; no progression of nonmeasurable disease; no new lesions; stable or improved nonenhancing (T2/FLAIR) lesions on same or lower dose of corticosteroids compared with baseline scan; the corticosteroid dose at the time of the scan evaluation should be no greater than the dose at time of baseline scan; and stable or improved clinically. Note: Patients with nonmeasurable disease only cannot have a partial response; the best response possible is stable disease Stable disease Requires all of the following: does not qualify for complete response, partial response, or progression; stable nonenhancing (T2/FLAIR) lesions on same or lower dose of corticosteroids compared with baseline scan. In the event that the corticosteroid dose was increased for new symptoms and signs without confirmation of disease progression on neuroimaging, and subsequent follow-up imaging shows that this increase in corticosteroids was required because of disease progression, the last scan considered to show stable disease will be the scan obtained when the corticosteroid dose was equivalent to the baseline dose Progressive disease Defined by any of the following: � 25% increase in sum of the products of perpendicular diameters of enhancing lesions compared with the smallest tumor measurement obtained either at baseline (if no decrease) or best response, on stable or increasing doses of corticosteroids*; significant increase in T2/FLAIR nonenhancing lesion on stable or increasing doses of corticosteroids compared with baseline scan or best response after initiation of therapy* not caused by comorbid events (eg, radiation therapy, demyelination, ischemic injury, infection, seizures, postoperative changes, or other treatment effects); any new lesion; clear clinical deterioration not attributable to other causes apart from the tumor (eg, seizures, medication adverse effects, complications of therapy, cerebrovascular events, infection, and so on) or changes in corticosteroid dose; failure to return for evaluation as a result of death or deteriorating condition; or clear progression of nonmeasurable disease Abbreviations: MRI, magnetic resonance imaging; FLAIR, fluid-attenuated inversion recovery. † All measurable and nonmeasurable lesions must be assessed using the same techniques as at baseline. * Stable doses of corticosteroids include patients not on corticosteroids. Reprinted with permission. 6 © 2010 by American Society of Clinical Oncology. the results of ongoing studies are needed to determine whether it improves overall survival. Some data suggest that anti-VEGF therapies may prolong survival by virtue of potently reducing vascular permeability. 43 This is a wellknown effect of antiangiogenic treatment that likely accounts for the reduction in contrast enhancement typically seen within days of the first dose of bevacizumab or similar agents. 44 Although antiangiogenic drugs are generally welltolerated and lack the toxicities that are typical of cytotoxic agents, substantial preclinical data obtained since the late 1990s suggest that blocking VEGF signaling promotes an infiltrative tumor growth pattern based on co-option of existing cerebral vasculature. 45-48 Several uncontrolled, retrospective clinical studies reported that high-grade gliomas treated with bevacizumab showed increased infiltrative tumor growth on T2/FLAIR sequences. 49-52 Indeed, patients for whom there is MRI evidence of prolonged disease control on bevacizumab sometimes experience clinical progression that seems consistent with this phenomenon. In a small study that pathologically characterized the areas of nonenhancing, infiltrative tumor, there were thin-walled, relatively normal-appearing blood vessels and elevated levels of insulin-like growth factor binding protein-2 and matrix metalloprotease-2. 53 Some recent data challenge the assumption that antiangiogenic therapy promotes an infiltrative growth pattern. In one study, patients treated with bevacizumab-treated were compared with matched pairs of patients treated with conventional therapies. 54 The rates of distant or diffuse recurrence were approximately 20% in both groups with no significant difference detected. Another study examined preand posttreatment recurrence patterns in patients with recurrent GBM treated with bevacizumab or bevacizumab/ irinotecan on the BRAIN trial. 55 Among patients treated 122 NORDEN, POPE, AND CHANG with bevacizumab alone, 16% experienced a change in recurrence pattern from local to diffuse. For reasons that are unclear, a higher proportion (39%) of patients treated with bevacizumab and irinotecan experienced this change. In a retrospective report that examined recurrence patterns in 80 patients with GBM who were treated with bevacizumab, there was no significant difference in recurrence pattern after bevacizumab treatmentas compared with before bevacizumab treatment. 56 Approximately 70% to 80% of recurrences were described as local, which is consistent with older data. 57 Whether antiangiogenic therapy actually promotes infiltrative tumor growth or merely unmasks it is an unanswered question. By controlling peritumoral edema and durably reducing contrast enhancement, bevacizumab may lead to the false impression of increased nonenhancing tumor progression compared with the prebevacizumab era. Further data are required to address this. Regardless, there is no question that bevacizumab therapy renders the radiological diagnosis of progressive disease more challenging than before. There does appear to be a subset of patients with recurrent high-grade glioma whose tumors progress primarily in a nonenhancing fashion who would be missed when the conventional Macdonald criteria is applied. The RANO criteria for progressive disease therefore include “. . . significant increase in T2/FLAIR nonenhancing lesion on stable or increasing doses of corticosteroids not caused by comorbid events (eg, radiation therapy, demyelination, ischemic injury, infection, seizures, postoperative changes, or other treatment effects).” 6 Although the ability to determine the etiology of T2/FLAIR changes is challenging, these criteria represent an important step toward optimally assessing progressive disease in the current era of antiangiogenic therapy.
CONCEPTS IN BRAIN TUMOR IMAGING Authors’ Disclosures of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role Stock Ownership Honoraria Research Funding Andrew D. Norden* Whitney B. Pope Genentech Susan M. Chang Novartis; Schering-Plough *No relevant relationships to disclose. 1. Lauterbur PC. Image formation by induced local interactions. Examples employing nuclear magnetic resonance. 1973. Clin Orthop Relat Res. 1989; 3-6. 2. Doyle FH, Gore JC, Pennock JM, et al. Imaging of the brain by nuclear magnetic resonance. Lancet. 1981;2:53-57. 3. Carr DH, Gadian DG. Contrast agents in magnetic resonance imaging. Clin Radiol. 1985;36:561-568. 4. Bilaniuk LT, Zimmerman RA, Wehrli FW, et al. Cerebral magnetic resonance: comparison of high and low field strength imaging. Radiology. 1984;153:409-414. 5. Kates R, Atkinson D, Brant-Zawadzki M. Fluid-attenuated inversion recovery (FLAIR): clinical prospectus of current and future applications. Top Magn Reson Imaging 1996;8:389-396. 6. Wen PY, Macdonald DR, Reardon DA, et al. Updated response assessment criteria for high-grade gliomas: response assessment in neuro-oncology working group. J Clin Oncol. 2010;28:1963-1972. 7. Pope WB, Sayre J, Perlina A, et al. MR imaging correlates of survival in patients with high-grade gliomas. AJNR Am J Neuroradiol. 2005;26:2466- 2474. 8. Rees JH, Smirniotopoulos JG, Jones RV, et al. Glioblastoma multiforme: radiologic-pathologic correlation. Radiographics. 1996;16:1413-1438; quiz 1462-1463. 9. Clarke JL, Chang S. Pseudoprogression and pseudoresponse: challenges in brain tumor imaging. Curr Neurol Neurosci Rep. 2009;9:241-246. 10. Brandsma D, van den Bent MJ. Pseudoprogression and pseudoresponse in the treatment of gliomas. Curr Opin Neurol. 2009;22:633-638. 11. Hirai T, Murakami R, Nakamura H, et al. Prognostic value of perfusion MR imaging of high-grade astrocytomas: long-term follow-up study. AJNR Am J Neuroradiol. 2008;29:1505-1510. 12. Law M, Young RJ, Babb JS, et al. Gliomas: predicting time to progression or survival with cerebral blood volume measurements at dynamic susceptibility-weighted contrast-enhanced perfusion MR imaging. Radiology. 2008;247:490-498. 13. Mangla R, Singh G, Ziegelitz D, et al. Changes in relative cerebral blood volume 1 month after radiation-temozolomide therapy can help predict overall survival in patients with glioblastoma. Radiology. 2010;256:575-584. 14. Sorensen AG, Batchelor TT, Zhang WT, et al. A “vascular normalization index” as potential mechanistic biomarker to predict survival after a single dose of cediranib in recurrent glioblastoma patients. Cancer Res. 2009;69:5296-5300. 15. Bidault F, Sahnoun, M., Rousseau, V., et al.: High-Grade Gliomas Treated with Bevacizumab: Assessment of Tumor Response with Dynamic Susceptibility Contrast Perfusion MRI (DSC-MRI) presented at the Radiological Society of North America Annual Meeting, Chicago, IL., 2011. 16. Sawlani RN, Raizer J, Horowitz SW, et al. Glioblastoma: A method for predicting response to antiangiogenic chemotherapy by using MR perfusion imaging-pilot study. Radiology. 2010;255:622-8. 17. Barajas RF Jr, Chang JS, Segal MR, et al. Differentiation of recurrent glioblastoma multiforme from radiation necrosis after external beam radiation therapy with dynamic susceptibility-weighted contrast-enhanced perfusion MR imaging. Radiology. 2009;253:486-496. 18. Hu LS, Baxter LC, Smith KA, et al. Relative cerebral blood volume values to differentiate high-grade glioma recurrence from posttreatment radiation effect: direct correlation between image-guided tissue histopathology and localized dynamic susceptibility-weighted contrast-enhanced perfusion MR imaging measurements. AJNR Am J Neuroradiol. 2009;30:552-558. 19. Sugahara T, Korogi Y, Tomiguchi S, et al. Posttherapeutic intraaxial brain tumor: the value of perfusion-sensitive contrast-enhanced MR imaging for differentiating tumor recurrence from nonneoplastic contrast-enhancing tissue. AJNR Am J Neuroradiol. 2000;21:901-909. 20. Lev MH, Ozsunar Y, Henson JW, et al. Glial tumor grading and outcome prediction using dynamic spin-echo MR susceptibility mapping compared with conventional contrast-enhanced MR: confounding effect of REFERENCES Expert Testimony Other Remuneration elevated rCBV of oligodendrogliomas [corrected]. AJNR Am J Neuroradiol. 2004;25:214-221. 21. Ellingson BM, Malkin MG, Rand SD, et al. Validation of functional diffusion maps (fDMs) as a biomarker for human glioma cellularity. J Magn Reson Imaging 2010;31:538-548. 22. Moffat BA, Chenevert TL, Meyer CR, et al. The functional diffusion map: an imaging biomarker for the early prediction of cancer treatment outcome. Neoplasia. 2006;8:259-267. 23. Hamstra DA, Chenevert TL, Moffat BA, et al. Evaluation of the functional diffusion map as an early biomarker of time-to-progression and overall survival in high-grade glioma. Proc Natl Acad Sci USA.2005;102: 16759-16764. 24. Hamstra DA, Galbán CJ, Meyer CR, et al. Functional diffusion map as an early imaging biomarker for high-grade glioma: correlation with conventional radiologic response and overall survival. J Clin Oncol. 2008;26:3387- 3394. 25. Ellingson B, Malkin M, Rand S, et al. Functional diffusion maps applied to FLAIR abnormal areas are valuable for the clinical monitoring of recurrent brain tumors. Proc Intl Soc Mag Reson Med. 2009;102:17:285. 26. Ellingson BM, Rand SD, Malkin MG, et al. Utility of functional diffusion maps to monitor a patient diagnosed with gliomatosis cerebri. J Neurooncol. 2010;97:419-423. 27. Ellingson BM, Malkin MG, Rand SD, et al. Comparison of cytotoxic and anti-angiogenic treatment responses using functional diffusion maps in FLAIR abnormal regions. Proc Intl Soc Mag Reson Med. 2009;102:17:1010. 28. Ellingson BM, Malkin MG, Rand SD, et al. Volumetric analysis of functional diffusion maps is a predictive imaging biomarker for cytotoxic and anti-angiogenic treatments in malignant gliomas. J Neurooncol. 2011:102;95- 103. 29. Pope WB, Kim HJ, Huo J, et al. Recurrent glioblastoma multiforme: ADC histogram analysis predicts response to bevacizumab treatment. Radiology. 2009;252:182-189. 30. Pope WB, et al. Title forthcoming. J Neurooncol. In press. 31. Macdonald DR, Cascino TL, Schold SC Jr, et al. Response criteria for phase II studies of supratentorial malignant glioma. J Clin Oncol. 1990;8: 1277-1280. 32. Watling CJ, Lee DH, Macdonald DR, et al. Corticosteroid-induced magnetic resonance imaging changes in patients with recurrent malignant glioma. J Clin Oncol. 1994;12:1886-1889. 33. Stupp R, Mason WP, van den Bent MJ, et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med. 2005;352:987-996. 34. Brandes AA, Franceschi E, Tosoni A, et al. MGMT promoter methylation status can predict the incidence and outcome of pseudoprogression after concomitant radiochemotherapy in newly diagnosed glioblastoma patients. J Clin Oncol. 2008;26:2192-2197. 35. Taal W, Brandsma D, de Bruin HG, et al. Incidence of early pseudoprogression in a cohort of malignant glioma patients treated with chemoirradiation with temozolomide. Cancer. 2008;113:405-410. 36. Chamberlain MC, Glantz MJ, Chalmers L, et al. Early necrosis following concurrent Temodar and radiotherapy in patients with glioblastoma. J Neurooncol. 2007;82:81-83. 37. de Wit MC, de Bruin HG, Eijkenboom W, et al. Immediate postradiotherapy changes in malignant glioma can mimic tumor progression. Neurology. 2004;63:535-537. 38. Hegi ME, Diserens AC, Gorlia T, et al. MGMT gene silencing and benefit from temozolomide in glioblastoma. N Engl J Med. 2005;352:997-1003. 39. Ulmer S, Braga TA, Barker FG 2nd, et al. Clinical and radiographic features of peritumoral infarction following resection of glioblastoma. Neurology. 2006;67:1668-1670. 40. Scott JN, Brasher PM, Sevick RJ, et al. How often are nonenhancing supratentorial gliomas malignant? A population study. Neurology. 2002;59: 947-949. 123
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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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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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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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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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Page 511 and 512:
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Classification of Myeloproliferativ
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CLASSIFICATION AND PROGNOSIS OF MPN
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CLASSIFICATION AND PROGNOSIS OF MPN
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AROUND THE WORLD IN ALMOST 80 MINUT
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LUNG CANCER IN BRAZIL Fig. 1. Relat
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LUNG CANCER IN BRAZIL Fig. 3. Chara
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LUNG CANCER IN BRAZIL Author’s Di
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LUNG CANCER IN CHINA Fig 1. Chinese
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LUNG CANCER IN CHINA well equipped
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Research and Standard of Care: Lung
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LUNG CANCER IN ROMANIA ● Protecti
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LUNG CANCER IN ROMANIA reimbursemen
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A New Model: Physician-Patient Coll
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PHYSICIAN ENGAGEMENT IN ONLINE PATI
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PHYSICIAN ENGAGEMENT IN ONLINE PATI
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LUNG CANCER SCREENING 101 CHAIR Chr
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LUNG CANCER SCREENING The concern i
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LUNG CANCER SCREENING Fig. 1. Guide
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LUNG CANCER SCREENING Fig. 2. Guide
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LUNG CANCER SCREENING 19. Montes RP
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Molecular Testing of Non-Small Cell
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MOLECULAR TESTING AND NSCLC Fig 1.
Page 557 and 558:
MOLECULAR TESTING AND NSCLC logic d
Page 559 and 560:
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
Page 583 and 584:
TREATMENT OPTIONS IN INDOLENT LYMPH
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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
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 613 and 614:
Page 615 and 616:
Page 617 and 618:
NEW OPTIONS, NEW QUESTIONS: HOW TO
Page 619 and 620:
THERAPIES FOR PATIENTS WITH METASTA
Page 621 and 622:
Page 623 and 624:
Page 625 and 626:
ANTIEMETICS: CURRENT STANDARDS, EME
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ANTIEMETICS: ASCO GUIDELINE UPDATE
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Page 631 and 632:
Page 633 and 634:
Page 635 and 636:
Chemotherapy-Induced Nausea and Vom
Page 637 and 638:
INCIDENCE AND PREVALENCE OF CHEMOTH
Page 639 and 640:
New Frontiers in Mucositis By Dougl
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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
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
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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