2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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Table 1. Investigational Therapies in GIST Drug Type Drug Target(s) Trial Information Tyrosine kinase inhibitors Imatinib KIT, PDGFR FDA approved Sunitinib KIT, PDGFR, VEGFR FDA approved Nilotinib KIT, PDGFR Phase III NCT00785785 Dasatanib KIT, PDGFR Phase II NCT00568750 Sorafenib KIT, PDGFR, VEGFR Phase II NCT01091207 Regorafenib KIT, PDGFR, VEGFR Phase III NCT01271712 Vatalanib KIT, PDGFR, VEGFR Phase II NCT00117299 Masitinib (AB1010) KIT, PDGFR Phase III NCT00812240 Pazopanib KIT, PDGFR, VEGFR Phase II NCT01323400 Crenolanib PDGFR Phase II NCT01243346 Dovitinib VEGFR, PDGFR, FGFR Phase II NCT01478373 HSP90 inhibitors STA-9090 HSP90 Phase II NCT01039519 AT-13387 HSP90 Phase II NCT01294202 AUY922 HSP90 Phase II NCT01404650 Monoclonal antibody IMC-3G3 (Olaratumab) PDGFR Phase II NCT01316263 Bevacizumab VEGFR Phase III NCT00324987 mTOR inhibitor Everolimus mTOR Phase II NCT00510354 Miscellaneous Perifosine AKT (PI3K pathway) Phase II NCT00455559 BKM120 PI3K pathway Phase I NCT1468688 TH-302 Tumor hypoxia Phase I NCT01381822 (histone deacetylase inhibitors). These medications are sometimes used in combination with KIT inhibitors. For example, multiple heat shock protein 90 (Hsp90) inhibitors are in phase II trials in GIST. Hsp90 is an important chaperone protein for oncoproteins such as KIT. Inhibition of this target leads to preferential degradation of activated forms of KIT (as well as other activated kinases). There is strong preclinical data showing that Hsp90 inhibitors have activity against imatinib-resistant GIST in vitro; 21 however, there is not yet strong clinical data for the use of these medications in GIST. In addition, there is evidence to suggest that the downstream PI3K-mTOR pathway is perhaps the most important signaling pathway in GIST 3 and inhibitors of this pathway including everolimus, BKM120, and perifosine are currently in phase II clinical trials (Table 1). In addition to clinical strategies to inhibit downstream pathways, multiple TKIs are currently in trials for TKIresistant GIST. Of note, a novel agent, crenolanib, is being tested in a phase II study for treatment of PDGFRA D842Vmutant GIST. As noted above, this particular mutation is strongly resistant to imatinib (and sunitinib as well). 22 In terms of FDA-approved KIT/PDGFRA kinase inhibitors, a number of these have been tested in phase II studies of drug-resistant GIST. For example, nilotinib has been 666 studied in a several clinical studies against drug-resistant GIST. 23 Nilotinib is structurally very similar to imatinib and, like sunitinib, lacks the ability to overcome any of the activation loop mutations in exons 17 or 18. In addition, like imatinib, it also has limited potency against ATP binding pocket mutations. Because of this, nilotinib has shown limited activity in imatinib- and sunitinib-resistant GIST. In a phase III trial, 248 patients were randomly assigned to nilotinib versus best supportive care for third-line therapy. 24 There was no statistical difference in overall survival between nilotinib and best supportive care. Sorafenib has more promising data for treatment of drug-resistant GIST, with an approximate 20-week PFS in the third-line, and even fourth-line setting. 25 This may be due to its apparent ability to overcome some exon 17 mutations in vitro. However, it appears that this agent has been supplanted in clinical development by its closely related analog, regorafenib. In a recent phase II trial, regorafenib showed a promising 10-month PFS in the third- or fourth-line setting. 26 Based on these results, a randomized, double-blind, placebo-controlled phase III study was initiated for patients who were intolerant of or who had progression during prior first- and second-line therapy. The study completed enrollment in mid-2011 and the final study analysis is planned for sometime in early 2012. The National Comprehensive Cancer Network guidelines suggest consideration of a clinical study or off-label treatment with sorafenib, nilotinib, or dasatinib for physicians with patients with imatinib- and sunitinib-resistant GIST. 20 In addition, reintroduction of imatinib can be considered. Fumagalli and colleagues have published data supporting rechallenging patients with imatinib or sunitinib after failure of standard and investigational agents. 27 Most GIST experts believe that life-long continuation of TKI therapy should be considered an essential component of best supportive care. As noted above, GIST patients often harbor deposits of quiescent, drug-sensitive tumor cells that will become clinically active following discontinuation of TKI therapy. These lesions can add to overall disease burden and patient symptoms. In addition, there is evidence to suggest that some secondary drug resistance mutations result in relative rather than absolute resistance to TKI therapy; continued TKI treatment may slow (but not arrest) such clones, potentially palliating symptoms. Role of Surgery in Advanced GIST BARNETT AND HEINRICH Given that there can be significant heterogeneity in secondary mutations and therefore mixed responses with TKI treatment of advanced GIST, many patients inquire about surgery to control their disease. Raut and colleagues published a study about their series of 69 patients who underwent surgery while receiving TKI therapy, with the majority receiving front-line imatinib (but a minority on second-line sunitinib). Notably, only those patients with overall stable disease (i.e., disease controlled by TKIs) strongly benefited from surgery in terms of disease control (Table 2). 28 In another study, 50 patients receiving second-line sunitinib underwent surgery for their disease and median PFS was a mere 5.8 months, and was independent of the immediate presurgical sunitinib clinical response status. That is, sunitinib-responding patients did not have better PFS after surgery than patients with frank progression on sunitinib before surgery. 29 In addition, over half of the patients had
TKI-RESISTANT GIST Table 2. Clinical outcomes following surgery for TKI treated patients (pts) with advanced GIST. Median progression-free and overall-survival data are tabulated based on the immediate pre-surgery response status of patients to TKI therapy. a Progression-Free Survival Overall Survival Study Pt # Treatment Status Stableb Limitc Gend Stableb Limitc Gend Raut (28) 69 IM 45 pts IM 3 SU 21 pts �40 mo. 8 mo. 3 mo. �40 mo. 30 mo. 6 mo. Dematteo (30) 40 IM 37 pts IM 3 SU 3 pts �48 mo. 12 mo. 3 mo. �48 mo. 19 mo. 11 mo. Raut (29) 50 IM 3 SU 50 pts 11 mo. 4 mo. 4 mo. �36 mo. 19 mo. 9 mo. a IM (surgery during front-line imatinib therapy). IM 3 SU (surgery during second-line sunitinib). b Stable or responsive disease prior to surgery. c Limited or focal disease progression prior to surgery. d Generalized disease progression prior to surgery. complications from surgery, and it is important to keep in mind that surgical complications usually lead to a delay in restarting systemic therapy. Therefore, only for patients with primary disease, or for symptom control in advanced disease, is surgery generally recommended as a treatment strategy. Conclusion The knowledge of the biology of GIST has made this cancer a model of targeted therapy with tyrosine kinase Authors’ Disclosures of Potential Conflicts of Interest Employment or Leadership Positions Consultant or Advisory Role Author Christine M. Barnett* Michael C. Heinrich MolecularMD; Novartis; Pfizer *No relevant relationships to disclose. 1. Corless CL, Fletcher JA, Heinrich MC. Biology of gastrointestinal stromal tumors. J Clin Oncol. 2004;22:3813-3825. 2. Miettinen M, Sobin LH, Sarlomo-Rikala M. Immunohistochemical spectrum of GISTs at different sites and their differential diagnosis with a reference to CD117 (KIT). Mod Pathol. 2000;13:1134-1142. 3. Corless CL, Barnett CM, Heinrich MC. Gastrointestinal stromal tumours: origin and molecular oncology. Nat Rev Cancer. 2011;11:865-878. 4. Duensing A, Joseph NE, Medeiros F, et al. Protein Kinase C theta (PKCtheta) expression and constitutive activation in gastrointestinal stromal tumors (GISTs). Cancer Res. 2004;64:5127-5131. 5. Druker BJ, Tamura S, Buchdunger E, et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med. 1996;2:561-566. 6. Heinrich MC, Griffith DJ, Druker BJ, et al. Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. Blood. 2000;96:925-932. 7. Tuveson DA, Willis NA, Jacks T, et al. STI571 inactivation of the gastrointestinal stromal tumor c-KIT oncoprotein: biological and clinical implications. Oncogene. 2001;20:5054-5058. 8. van Oosterom AT, Judson I, Verweij J, et al. Safety and efficacy of imatinib (STI571) in metastatic gastrointestinal stromal tumours: a phase I study. Lancet. 2001;358:1421-1423. 9. Blanke CD, Demetri GD, von Mehren M, et al. Long-term results from a randomized phase II trial of standard- versus higher-dose imatinib mesylate for patients with unresectable or metastatic gastrointestinal stromal tumors expressing KIT. J Clin Oncol. 2008;26:620-625. 10. Comparison of two doses of imatinib for the treatment of unresectable or metastatic gastrointestinal stromal tumors: A meta-analysis of 1,640 patients. J Clin Oncol. 2010;28:1247-1253. 11. Le Cesne A, Ray-Coquard I, Bui BN, et al. Discontinuation of imatinib in patients with advanced gastrointestinal stromal tumours after 3 years of treatment: an open-label multicentre randomised phase 3 trial. Lancet Oncol. 2010;11:942-949. 12. von Mehren M, Heinrich MC, Joensuu H, et al. Follow-up results after 9 years (yrs) of the ongoing, phase II B2222 trial of imatinib mesylate (IM) in inhibitors. Currently, the mainstay of treatment for this disease is TKI-based therapy with enrollment in a clinical trial if multiple TKIs fail to control disease. Understanding the mechanisms of disease persistence and drug resistance has helped identify new targets for therapy. Hopefully, our increased understanding of GIST biology will not only help us improve current treatment, but ultimately help create new treatments that might cure patients with advanced disease. Stock Ownership Honoraria Research Funding MolecularMD Novartis ARIAD; Arog; ImClone Systems; Novartis; Pfizer REFERENCES Expert Testimony Other Remuneration patients (pts) with metastatic or unresectable KIT� gastrointestinal stromal tumors (GIST). J Clin Oncol. 2011;29 (suppl; abstr 10016). 13. Heinrich MC, Corless CL, Demetri GD, et al. Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. J Clin Oncol. 2003;21:4342-4349. 14. Demetri GD, Wang Y, Wehrle E, et al. Imatinib plasma levels are correlated with clinical benefit in patients with unresectable/metastatic gastrointestinal stromal tumors. J Clin Oncol. 2009;27:3141-3147. 15. Antonescu CR, Besmer P, Guo T, et al. Acquired resistance to imatinib in gastrointestinal stromal tumor occurs through secondary gene mutation. Clin Cancer Res. 2005;11:4182-4190. 16. Liegl B, Kepten I, Le C, et al. Heterogeneity of kinase inhibitor resistance mechanisms in GIST. J Pathol. 2008;216:64-74. 17. Demetri GD, van Oosterom AT, Garrett CR, et al. Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial. Lancet. 2006;368:1329- 1338. 18. George S, Blay JY, Casali PG, et al. Clinical evaluation of continuous daily dosing of sunitinib malate in patients with advanced gastrointestinal stromal tumour after imatinib failure. Eur J Cancer. 2009;45:1959-1968. 19. Gramza AW, Corless CL, Heinrich MC. Resistance to tyrosine kinase inhibitors in gastrointestinal stromal tumors. Clin Cancer Res. 2009;15:7510- 7518. 20. Demetri GD, von Mehren M, Antonescu CR, et al. NCCN Task Force report: update on the management of patients with gastrointestinal stromal tumors. J Natl Compr Canc Netw. 2010;8 Suppl 2:S1-41; quiz S2-4. 21. Bauer S, Yu LK, Demetri GD, et al. Heat shock protein 90 inhibition in imatinib-resistant gastrointestinal stromal tumor. Cancer Res. 2006;66:9153- 9161. 22. Heinrich MC, Corless CL, Duensing A, et al. PDGFRA activating mutations in gastrointestinal stromal tumors. Science. 2003;299:708-710. 23. Demetri GD, Casali PG, Blay JY, et al. A phase I study of single-agent nilotinib or in combination with imatinib in patients with imatinib-resistant gastrointestinal stromal tumors. Clin Cancer Res. 2009;15:5910-5916. 24. Reichardt P, Blay J, Gelderblom H, et al. Phase III trial of nilotinib in 667
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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
Page 533 and 534:
LUNG CANCER IN ROMANIA ● Protecti
Page 535 and 536:
LUNG CANCER IN ROMANIA reimbursemen
Page 537 and 538:
A New Model: Physician-Patient Coll
Page 539 and 540:
PHYSICIAN ENGAGEMENT IN ONLINE PATI
Page 541 and 542:
PHYSICIAN ENGAGEMENT IN ONLINE PATI
Page 543 and 544:
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
Page 551 and 552:
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 585 and 586:
Page 587 and 588:
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 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
Page 627 and 628:
ANTIEMETICS: ASCO GUIDELINE UPDATE
Page 629 and 630:
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
Page 641 and 642:
MUCOSAL INJURY CAUSED BY CANCER THE
Page 643 and 644:
Page 645 and 646:
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:
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 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: TKI-RESISTANT GIST Primary Imatinib
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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