2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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TARGETED TREATMENT OF NEWLY DIAGNOSED DISEASE DNA repair, or various selection pressures, advanced cancers accumulate multiple genetic and/or molecular derangements over time, conferring various phenotypic advantages on each subpopulation. 28,29 Metastatic tumors from breast, lung, and gastrointestinal cancers have more genetic abnormalities than do their primary tumors, and often display considerable heterogeneity compared with primary lesions, including discordant clinically utilized biomarkers. 30,31 A counter argument to the conventional wisdom that solid tumors are genetically more complex and heterogenous than CML is the efficacy of targeted agents (e.g., vemurafenib and crizotinib) in selected patients with advanced disease. In the phase III vemurafenib trial, the overwhelming majority of previously untreated patients with advanced melanoma had tumor regression, although 48% of the evaluable patients met criteria for response. 32 An example of response rates of targeted therapy in advanced solid tumors degrading with increasing stage of disease is lapatinib, an oral dual EGFR-erbB2 TKI. When evaluated in patients with newly diagnosed metastatic HER2-positive breast cancer, lapatinib achieved an response rate of 24%. 33 Among patients with previously treated, metastatic HER2-positive breast cancer, the response rate declined to 7%. 34 These trials cannot be directly compared but do suggest an improvement in response rates with earlier use of targeted therapy, similar to the CML experience. Thus, although it appears likely that targeted agents perform better in untreated patients than patients with relapsed metastatic disease, we believe that this experience cannot be compared with newly diagnosed CML, as untreated metastatic solid tumors are analogous to untreated CML blastic phase. Interestingly, the results attained in metastatic solid tumors (either untreated or previously treated) are remarkably similar to those achieved in patients with CML blastic phase (either untreated or previously treated): 1) many patients have some regression; 2) a partial or complete response is achieved in a small subset of patients ; 3) resistance develops in most patients; and 4) the increase in survival can be measured in months, not years. Mutations as a Mechanism of Resistance in Solid Tumors Although other pathways may be relevant for disease progression, much of the resistance to imatinib in CML is due to BCR-ABL kinase domain mutations. 35,36 Resistance to targeted therapy of solid tumors is less well characterized, but preliminary evidence suggests a similar phenomenon may occur, i.e., mutation of the original critical target. 37,38 It is not clear if this dependence on the initial oncologic driver is more pronounced early, or is constant throughout the disease course. In CML blastic phase, the minimal and transient efficacy of Bcr-Abl TKIs, including those able to overcome many common mutations, would be an arguement for a substantial change in disease biology away from initial driver dependence with disease progression. When a crizotinib-resistant model of ALK-rearranged lung cancer was generated with serial exposure, the most common mechanisms of resistance were amplification of the EML4-ALK gene and a “gatekeeper” mutation within the kinase domain. 37 As with CML, this finding suggests that the driving abnormality remains critical to the survival of the cancer cells, even in disease resistant to targeted therapy. In contrast, early studies of vemurafenib resistance in V600E mutant melanoma cell lines have not identified mutations in BRAF. 39 In lieu of mutating the kinase domain, these vemurafenib-resistant cells were able to activate the MAPK pathway in a BRAF-independent fashion, but remained sensitive to targeting the pathway farther downstream. The use of EGFR inhibitors in EGFR-mutated lung cancer provides corroborating evidence of both resistance mechanisms. Mutations in exon 19 and 21 of EGFR are known to be associated with increased sensitivity to EGFR TKIs. In previously untreated patients with advanced lung cancer who have an EGFR mutation, treatment with an EGFR inhibitor typically yields median progression-free survivals of approximately 9 months. 40 When resistance develops, the most common mechanisms are the development of a secondary point mutation in EGFR (T790M), which reduces the ability of TKIs to inhibit EGFR, or amplification of the MET gene. 38,40,41 Together, these preliminary data suggest that a portion of solid tumors may gave resistance mechanisms to targeted therapy similar to those in CML, even while there is continued dependence on the initial genetic driver. If so, a CMLlike approach of developing second-generation targeted agents with activity in resistant populations with mutated, yet functional target kinase, or in targeting the critical pathway at multiple points, could demonstrate efficacy by either resensitizing resistant disease or blocking development of resistance. Conclusion Cancer claims more than half a million lives annually and is now the leading cause of death under age 85 in the United States. 42 Globally, an estimated 12.7 million new cancer diagnoses and 7.6 million cancer deaths occurred in 2008, and these numbers are expected to nearly double in the next 25 years. 43,44 In order to make a substantial impact on this global health crisis, we believe it is beneficial to re-examine one of oncology’s greatest success stories–imatinib in CML. Like solid tumors, CML accumulates new genetic aberrations throughout its course and eventually reaches a stage where therapy targeted against its driving aberration has markedly reduced effectiveness. It is our contention that CML blastic phase is the equivalent of metastatic disease in solid tumors. Both CML blastic phase and metastatic solid tumors are difficult to eradicate because of their molecular complexity. Deciphering this complexity and determining how to best treat it is perceived as a staggeringly complicated task. Indeed, although the survival of patients with CML blastic phase has increased in the imatinib era, it remains at about 1 year. Yet, outcomes in chronic phase CML have been transformed, with overall survival from diagnosis increasing from approximately 4 years to more than 25 years. As seen in CML, the true leap forward in outcomes occurred only after investigators used Bcr-Abl TKIs in the earliest stage of the disease. Importantly, delaying therapy even slightly, to later chronic phase and certainly to accelerated phase CML, is associated with a precipitous fall in response rates and much poorer outcomes. It is therefore plausible, if the CML paradigm holds true, that administering targeted therapies to patients with ad- 183
vanced solid tumors, even if they are untreated, will continue to result in only incremental improvements. Newly diagnosed metastatic disease is already genetically complex and likely analogous to newly diagnosed CML blastic phase, and not to newly diagnosed chronic phase CML. Timing may therefore be a crucial missing component in the optimal application of targeted therapies to solid tumors. The les- Authors’ Disclosures of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role sons of CML suggest that once a targeted therapy has shown some activity in advanced disease, it may have the potential for a high rates of functional cures but only if given at the time of diagnosis of early stage disease. The current strategy of using targeted therapy for patients with metastatic solid tumors may therefore underestimate, perhaps dramatically, the ultimate effectiveness of active targeted agents. Stock Ownership Honoraria Research Funding Jason R. Westin* Hagop Kantarjian Novartis Bristol-Myers Squibb; Cyclacel; Genzyme; Novartis; Pfizer Razelle Kurzrock AstraZeneca; Health Advances; Johnson & Johnson; Merck; SAIC-Frederick *No relevant relationships to disclose. 1. Lemonick MD, Park A. New hope for cancer. TIME. May, 28, 2001. 2. Kurzrock R, Gutterman JU, Talpaz M. The molecular genetics of Philadelphia chromosome-positive leukemias. N Engl J Med. 1988 Oct 13;319:990-998. 3. Deininger M, O’Brien, SG, Guilhot F, et al. International randomized study of interferon vs STI571 (IRIS) 8-year follow up: sustained survival and low risk for progression or events in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP) treated with imatinib. Blood. 2009;114:22 (suppl; abstr 1126). 4. Druker BJ, Guilhot F, O’Brien SG, et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med. 2006;355: 2408-2417. 5. Kantarjian HM, Talpaz M, O’Brien S, et al. Survival benefit with imatinib mesylate versus interferon-alpha-based regimens in newly diagnosed chronic-phase chronic myelogenous leukemia. Blood. 2006;108:1835- 1840. 6. Björkholm M, Ohm L, Eloranta S, et al. Success story of targeted therapy in chronic myeloid leukemia: a population-based study of patients diagnosed in Sweden from 1973 to 2008. J Clin Oncol. 2011;29:2514-2520. 7. Kantarjian H, O’Brien S, Jabbour E. Improved survival in chronic myeloid leukemia since the introduction of imatinib therapy: a singleinstitution historical experience. Blood. 2012;119:1981-1987. 8. Kantarjian HM, Cortes J, O’Brien S, et al. Imatinib mesylate (STI571) therapy for Philadelphia chromosome-positive chronic myelogenous leukemia in blast phase. Blood. 2002;99:3547-3553. 9. Cortes J, Kim DW, Raffoux E, et al. Efficacy and safety of dasatinib in imatinib-resistant or -intolerant patients with chronic myeloid leukemia in blast phase. Leukemia. 2008;22:2176-2183. 10. Giles FJ, Kantarjian HM, le Coutre PD, et al. Nilotinib is effective in imatinib-resistant or -intolerant patients with chronic myeloid leukemia in blastic phase. Leukemia. Epub 2011 Dec 13. 11. Sawyers CL, Hochhaus A, Feldman E, et al. Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. Blood. 2002;99:3530- 3539. 12. Talpaz M, Silver RT, Druker BJ, et al. Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase 184 REFERENCES Amgen; AstraZeneca; Enzon; Exelixis; Genentech; Johnson & Johnson; Maxygen; Merck; Myriad; Nereus; Pfizer; Pharmion; Roche; SAIC- Frederick Amgen; AmpliMed; AstraZeneca; Callisto; Centocor Ortho Biotech; CuraGen; Enzon; Exelixis; GlaxoSmithKline; Globomax; Merck; Myriad Genetics; Nereus; Novartis; Pfizer; Roche WESTIN, KANTARJIAN, AND KURZROCK Expert Testimony Other Remuneration Exelixis; Nova Research Co.; Pfizer; Roche chronic myeloid leukemia: results of a phase 2 study. Blood. 2002;99:1928- 1937. 13. Guilhot F, Apperley J, Kim DW, et al. Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase. Blood. 2007;109: 4143-4150. 14. Kantarjian HM, Hochhaus A, Saglio G, et al. Nilotinib versus imatinib for the treatment of patients with newly diagnosed chronic phase, Philadelphia chromosome-positive, chronic myeloid leukaemia: 24-month minimum follow-up of the phase 3 randomised ENESTnd trial. Lancet Oncol. 2011;12: 841-851. 15. Kantarjian HM, Shah NP, Cortes JE, et al. Dasatinib or imatinib in newly diagnosed chronic phase chronic myeloid leukemia: 2-year follow-up from a randomized phase 3 trial (DASISION). Blood. Epub 2011 Dec 9. 16. Jain RK, Lee JJ, Hong D, et al. Phase I oncology studies: evidence that in the era of targeted therapies patients on lower doses do not fare worse. Clin Cancer Res. 2010;16:1289-1297. 17. Druker BJ, Talpaz M, Resta DJ, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med. 2001;344:1031-1037. 18. Jabbour E, Issa JP, Garcia-Manero G, et al. Evolution of decitabine development: accomplishments, ongoing investigations, and future strategies. Cancer. 2008;112:2341-2351. 19. Fenaux P, Mufti GJ, Hellstrom-Lindberg E, et al. Efficacy of azacitidine compared with that of conventional care regimens in the treatment of higher-risk myelodysplastic syndromes: a randomised, open-label, phase III study. Lancet Oncol. 2009;10:223-232. 20. Shah NP, Nicoll JM, Nagar B, et al. Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell. 2002;2:117-125. 21. Santos FP, Quintás-Cardama A. New drugs for chronic myelogenous leukemia. Curr Hematol Malig Rep. 2011;6:96-103. 22. Heidel F, Solem FK, Breitenbuecher F, et al. Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain. Blood. 2006;107:293-300. 23. Wheeler DL, Dunn EF, Harari PM. Understanding resistance to EGFR
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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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Page 229 and 230: midcareer physician; in one cross-s
Page 231 and 232: Table 1. Recommendations for Person
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Page 235 and 236: elationship” is also acknowledged
Page 237 and 238: Conclusion In more individualistic
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Page 243 and 244: MEDICAL ERRORS IN CANCER CARE: PREV
Page 245 and 246: DISCLOSING MEDICAL ERRORS Disclosur
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Page 253 and 254: 0.001), progression-free survival (
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effect. The most common drug that h
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gone forever, no further therapy is
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is irrelevant if it is already rese
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Resection and Thermal Ablation of L
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Author’s Disclosures of Potential
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Minimally Invasive Surgery of Recta
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outcomes; local, wound-site, and di
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Authors’ Disclosures of Potential
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CAO/ARO 04 study—which added oxal
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STAGE III COLON CANCER: WHAT WORKS,
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Table 1. Comparison of Fluoropyrimi
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tients with stages II and III color
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ized by high fruit, vegetable, poul
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Exercise Change trial: a randomized
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A New Direction for Pancreatic Canc
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Table 1. FOLFIRINOX versus Gemcitab
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The Southwest Oncology Group (SWOG)
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A Matter of Timing: Is There a Role
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an OS benefit with radiation therap
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a dose of 50.4 Gy to 59.4 Gy of rad
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more commonly given for APC, specia
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subcutaneous bolus or infusion. Hal
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patients are cared for completely w
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Varying Lymphadenectomies for Gastr
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Table 1. Regional Lymph Nodes of th
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Conclusion There are clear differen
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Will Disease Heterogeneity Help Def
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prematurely due to poor accrual. 18
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Adjuvant Treatments for Localized A
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ADJUVANT TREATMENT FOR GASTRIC CANC
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LIVER-DIRECTED THERAPEUTIC OPTIONS
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ated with unique dose distributions
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HCC, with encouraging outcomes in e
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tion. Advanced computer-based image
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a 5-year survival rate of 70% follo
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THE MANAGEMENT OF LESS COMMON BUT C
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Fig 1. PubMed publications and clin
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of therapeutic options, patient sel
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less informative than the GRETCH an
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Table 3. New Agents/Regimens under
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combined with concurrent transarter
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to optimize the use of erlotinib by
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Optimal Use of Imaging to Guide Tre
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enhancement seen. Furthermore, the
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CASTRATION-RESISTANT PROSTATE CANCE
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Fig. 1. FDA regulatory approvals in
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Prognostic, Predictive, and Surroga
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adhesion molecule and further chara
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and treatment options are expanding
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KIDNEY CANCER BIOLOGY AND THERAPEUT
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Prognostic Factors in Advanced RCC
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cell immunotherapy in which a small
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New Developments in Urothelial Canc
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Novel Approaches in Advanced Urothe
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10. Albers P, Park SI, Niegisch G,
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700 at a dose of 400 mg twice daily
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therapy for nonmetastatic prostate
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ADJUVANT THERAPY FOR OLDER PATIENTS
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Adjuvant Systemic Therapy Adjuvant
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with early-stage breast cancer were
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clinical trials to generate additio
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Adjuvant Treatment of Older Patient
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OLDER PATIENTS WITH LUNG CANCER Fig
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OLDER PATIENTS WITH LUNG CANCER adj
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Considerations and Controversies in
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OLDER PATIENTS WITH ADVANCED CANCER
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RECENT CLINICAL HIGHLIGHTS IN GYNEC
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GLOBAL ADVANCES IN GYNECOLOGIC ONCO
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GLOBAL ADVANCES IN GYNECOLOGIC ONCO
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The European Society of Gynaecologi
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ESGO EDUCATIONAL AND RESEARCH ACTIV
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UPFRONT TREATMENT OF OVARIAN CANCER
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ANTIANGIOGENICS AND PARP INHIBITORS
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ANTIANGIOGENICS AND PARP INHIBITORS
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Intraperitoneal Treatment in Ovaria
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INTRAPERITONEAL TREATMENT IN OVARIA
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Dose-Dense Chemotherapy and Neoadju
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CHEMOTHERAPY FOR OVARIAN CANCER Fig
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CHEMOTHERAPY FOR OVARIAN CANCER whi
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UTERINE SARCOMA: CHALLENGING CASES
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HISTOLOGIC FEATURES AND MANAGEMENT
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SURGICAL OPTIONS FOR UTERINE SARCOM
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SURGICAL OPTIONS FOR UTERINE SARCOM
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PATIENTS WITH HPV-POSITIVE OROPHARY
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HPV-INDUCED OROPHARYNX CANCER analy
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HPV-INDUCED OROPHARYNX CANCER fract
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Important Early Advances in Squamou
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EARLY ADVANCES IN SCCHN Fig 1. Targ
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Application of Genomic and Proteomi
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GENOMIC AND PROTEOMIC TECHNOLOGIES
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GENOMIC AND PROTEOMIC TECHNOLOGIES
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TREATMENT OF THYROID CANCERS: NEW I
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EVALUATION OF ADVANCED THYROID CANC
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EVALUATION OF ADVANCED THYROID CANC
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Systemic Therapeutic Approaches to
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APPROACHES TO ADVANCED THYROID CANC
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AVOIDING OVERDIAGNOSIS AND OVERTREA
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Table 1. Prevalence of Prostate Can
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Table 3. Potential Risks and Benefi
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Overdiagnosis and Overtreatment of
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een reached by other modeling effor
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east cancer community have FDA-appr
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COSTS OF CANCER CARE: AFFORDABILITY
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REDUCING THE COST OF CANCER CARE Fi
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REDUCING THE COST OF CANCER CARE Th
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REDUCING THE COST OF CANCER CARE de
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Why Hasn’t Genomic Testing Change
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tigators should develop prospective
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MANAGEMENT OF CHRONIC LYMPHOCYTIC L
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PREDICTIVE PARAMETERS IN CLL Table
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PREDICTIVE PARAMETERS IN CLL patien
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Transplant in Chronic Lymphocytic L
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WHEN TO OFFER TRANSPLANTATION IN CL
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WHEN TO OFFER TRANSPLANTATION IN CL
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NEW DEVELOPMENTS IN MYELOPROLIFERAT
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SMALL-MOLECULE INHIBITORS FOR MPN S
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SMALL-MOLECULE INHIBITORS FOR MPN L
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Insights into the Molecular Genetic
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GENETICS OF MYELOPROLIFERATIVE NEOP
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Classification of Myeloproliferativ
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CLASSIFICATION AND PROGNOSIS OF MPN
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CLASSIFICATION AND PROGNOSIS OF MPN
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AROUND THE WORLD IN ALMOST 80 MINUT
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LUNG CANCER IN BRAZIL Fig. 1. Relat
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LUNG CANCER IN BRAZIL Fig. 3. Chara
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LUNG CANCER IN BRAZIL Author’s Di
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LUNG CANCER IN CHINA Fig 1. Chinese
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LUNG CANCER IN CHINA well equipped
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Research and Standard of Care: Lung
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LUNG CANCER IN ROMANIA ● Protecti
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LUNG CANCER IN ROMANIA reimbursemen
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A New Model: Physician-Patient Coll
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PHYSICIAN ENGAGEMENT IN ONLINE PATI
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PHYSICIAN ENGAGEMENT IN ONLINE PATI
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LUNG CANCER SCREENING 101 CHAIR Chr
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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
Page 583 and 584:
TREATMENT OPTIONS IN INDOLENT LYMPH
Page 585 and 586:
Page 587 and 588:
Page 589 and 590:
ROLE OF HCT FOR INDOLENT LYMPHOMA T
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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
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 613 and 614:
Page 615 and 616:
Page 617 and 618:
NEW OPTIONS, NEW QUESTIONS: HOW TO
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THERAPIES FOR PATIENTS WITH METASTA
Page 621 and 622:
Page 623 and 624:
Page 625 and 626:
ANTIEMETICS: CURRENT STANDARDS, EME
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ANTIEMETICS: ASCO GUIDELINE UPDATE
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Page 631 and 632:
Page 633 and 634:
Page 635 and 636:
Chemotherapy-Induced Nausea and Vom
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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
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
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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
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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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