2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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Addition of Monoclonal Antibodies to RIC SCT GVHD remains the major concern after RIC SCT and attempts have been made to utilize monoclonal antibodies to reduce the incidence of GVHD without increasing the subsequent risk of relapse. Excellent results have been obtained at MDACC using RIC based on a combination of fludarabine and cyclophosphamide with the addition of rituximab, an approach designed to maximize GVL by early tapering of immune suppression with use of rituximab and DLI. Among 39 patients treated, median age 57 (range, 34 to 70), median time from diagnosis to transplantation was 4.5 years. 33 All patients had recurrent advanced disease, were heavily pretreated with a median of three (range, 2 to 8) chemotherapy regimens, and had been previously treated with fludarabine/ rituximab-based regimens. At transplant, 34 patients (87%) had active disease, including nine (23%) with evidence of Richter’s transformation. In this series, only four of the donors were unrelated. Fourteen patients required immunomodulation with rituximab and DLI for persistent disease after SCT. Only one patient died early, and among the 38 evaluable patients, 27 (71%) achieved CR with a 48% estimated OS at 4 years and current PFS of 44%. Acute grade 2 through 4 GVHD was observed in 45%, but chronic extensive GVHD was reduced without concomitant increased risk of relapse. GVHD can be decreased using alemtuzumab in the conditioning regimen to reduce donor lymphocytes, but this is associated with delayed immune reconstitution, increases the risk of infective complications, and appears to impair GVL. In 41 consecutive patients with CLL (24 HLA-matched sibling donors and 17 unrelated volunteer donors, including 4 mismatched) treated with the conditioning regimen alemtuzumab with fludarabine and melphalan had impressive antitumor effects with 100% of patients with chemotherapysensitive disease and 86% with chemotherapy-refractory disease responding. 32 The TRM rate was 26%, OS was 51%, and relapse risk was 29% at 2 years. GVHD rates were relatively low with acute GVHD occurring in 17 (41%) and chronic GVHD in 13 (33%). The unexpectedly high TRM rate was because of a high incidence of fungal and viral infections. How to Select Who and When to Offer Allogeneic SCT All studies of SCT have enrolled younger patients with “high-risk” disease. This term is very loosely defined and it is difficult to determine precisely the risk factors used in each of the reported studies. EBMT guidelines have been established outlining indications for SCT in CLL, which conclude that there is a evidence base for the efficacy of allogeneic SCT in CLL and that this procedure is indicated in patients with high-risk CLL. 38 Patients at high risk are defined in Table 3 and include those requiring treatment who have TP53 abnormalities (who merit allogeneic SCT in first response), patients who fail to achieve CR, who progress within 12 months after fludarabine, who relapse within 24 months after having achieved a response with combination therapy, those who have relapsed after prior autologous SCT, or those patients who are fludarabine refractory. It should be noted that the only category that requires assessment of biologic risk is detection of TP53 abnormalities. Ongoing prospective clinical studies will determine the ef- 402 JOHN G. GRIBBEN Table 3. EBMT Guidelines for Transplantation in CLL 38 Allo-SCT is a reasonable treatment option in poor-risk CLL including: ● Fludarabine resistance—nonresponse or early relapse (� 12 months) after purine analogue-based therapy ● Relapse � 24 months after purine analogue combinations or auto-SCT (plus high-risk genetics) ● p53 mutation with treatment indication Auto-SCT indicated in clinical trial only Abbreviation: EBMT, European Blood and Marrow Transplantation; Allo-SCT, allogeneic stem cell transplantation; CLL, chronic lymphocytic leukemia; auto- SCT, autologous SCT. fect of biomarkers including IgV H mutational status and other cytogenetic abnormalities in identification of patients at sufficiently high risk to merit use of allogeneic SCT in first CR. The definition of “refractory” CLL is of particular importance and the terms “refractory” CLL and “fludarabinerefractory” CLL are often used interchangeably. But with the large number of treatment options, the consideration of treatment context is important. The type of therapy to which patients fail to respond and previous therapies received are of major importance. The clinical importance of refractory CLL is based on the fact that these patients have very poor prognosis (median 1–2 years OS in most studies) despite various and intense salvage therapy strategies. 2,39-40 Most trials of investigational agents use this definition as an entry point for early drug development. The most recent CLL guidelines define refractory CLL as treatment failure (less than partial remission [PR]) or disease progression within 6 months of the last antileukemic therapy. 3 These still correspond to the definition coined when CLL treatment was based on chlorambucil or fludarabine monotherapy. In current standard practice, patients eligible to consider allogeneic SCT are most likely to have received combination chemoimmunotherapy. There is accumulating evidence that patients who are formally not refractory based on the current definition but relapse within 3 years after chemoimmunotherapy also have very poor outcome and are unlikely to have durable responses to subsequent chemotherapy. 2 The guidelines suggest three groups of patients who may be offered therapy. The first group is those with TP53 loss, and these are the patients who have the poorest response and shortest duration of remission. Allogeneic SCT is considered appropriate in first response after initial therapy for these patients. Those patients who failed to achieve CR to FCR and/or have very short (� 24 months) response to prior FCR can be added to this very high-risk group. These patients are prime candidates for drugs with proven activity in TP53 deleted/mutant cells, investigational agents in clinical trials, and then for allogeneic SCT if they respond. A second scenario of “high-risk” CLL is identification of subgroups destined to relapse relatively early after standard treatment and it is in this group that biomarker analysis will prove useful. Candidates within this group include patients with high beta-2-microglobulin or thymidine kinase, unmutated immunoglobulin heavy chain variable region (IgVH) or 11q deletion. 9,41 These patients are the ones who gained most by the addition of rituximab to FC. 9 Biomarker analysis will also be useful to identify those patients in whom allogeneic SCT should not be offered (no 11q deletion, no TP53 deletion/mutation, mutated IGHV, low beta-2-MG, no prior therapy) who have very favorable outcome despite progressing to indication for treatment.
WHEN TO OFFER TRANSPLANTATION IN CLL The results of phase II studies of RIC allogeneic SCT suggest that whereas patients with refractory disease may respond to the GVL effect, optimal outcome will be achieved by consideration of transplant for those patients with highrisk disease before they become truly refractory and those patients in whom minimal disease state cannot be achieved. We have demonstrated that CLL cells are inherently immunosuppressive even to allogeneic donor T cells, and this may explain why better results are obtained when patients receive RIC allogeneic SCT with low tumor bulk, which can only be achieved if patients are offered this approach before truly refractory disease occurs. 42 Conclusion SCT has a role to play in selected patients with CLL, with major focus now on the use of RIC allogeneic SCT. Future Author’s Disclosure of Potential Conflicts of Interest Author Employment or Leadership Positions Consultant or Advisory Role approaches to the management of this disease must take into account the balance between the increased morbidity and mortality of SCT in CLL with the curative potential that these approaches potentially offer, in the setting of the outcome improvements that can now be seen using chemoimmunotherapy. Although RIC allogeneic SCT results in high response rates and eradication of polymerase chain reaction–detectable MRD and is potentially curative, the follow-up of most clinical trials remains too short to assess whether SCT can really cure CLL. In the absence of any other treatment modalities currently capable of improving outcome in this disease, SCT should be considered as a treatment approach for younger patients with high-risk CLL early in the course of the disease, ideally in the setting of well-designed clinical trials assessing the treatment’s effect on outcome in these patients. Several such trials are underway. Stock Ownership Honoraria John G. Gribben Celgene; Merck Mundipharma; Roche 1. Gribben JG, O’Brien S. Update on therapy of chronic lymphocytic leukemia. J Clin Oncol. 2011;29:544-550. 2. Stilgenbauer S, Zenz T. Understanding and managing ultra high-risk chronic lymphocytic leukemia. Hematology Am Soc Hematol Educ Program. 2010;2010:481-488. 3. Hallek M, Cheson BD, Catovsky D, et al. Guidelines for the diagnosis and treatment of chronic lymphocytic leukemia: a report from the International Workshop on Chronic Lymphocytic Leukemia updating the National Cancer Institute-Working Group 1996 guidelines. Blood. 2008;111:5446-5456. 4. Rai KR, Peterson BL, Appelbaum FR, et al. Fludarabine compared with chlorambucil as primary therapy for chronic lymphocytic leukemia. N Engl J Med. 2000;343:1750-1757. 5. Eichhorst BF, Busch R, Hopfinger G, et al. Fludarabine plus cyclophosphamide versus fludarabine alone in first-line therapy of younger patients with chronic lymphocytic leukemia. Blood. 2006;107:885-891. 6. Flinn IW, Neuberg DS, Grever MR, et al. Phase III trial of fludarabine plus cyclophosphamide compared with fludarabine for patients with previously untreated chronic lymphocytic leukemia: US Intergroup Trial E2997. J Clin Oncol. 2007;25:793-798. 7. Catovsky D, Richards S, Matutes E, et al. Assessment of fludarabine plus cyclophosphamide for patients with chronic lymphocytic leukaemia (the LRF CLL4 Trial): a randomised controlled trial. Lancet. 2007;370:230-239. 8. Tam CS, O’Brien S, Wierda W, et al. Long-term results of the fludarabine, cyclophosphamide, and rituximab regimen as initial therapy of chronic lymphocytic leukemia. Blood. 2008;112:975-980. 9. Hallek M, Fischer K, Fingerle-Rowson G, et al. Addition of rituximab to fludarabine and cyclophosphamide in patients with chronic lymphocytic leukaemia: a randomised, open-label, phase 3 trial. Lancet. 2010;376:1164- 1174. 10. Dohner H, Stilgenbauer S, Benner A, et al. Genomic aberrations and survival in chronic lymphocytic leukemia. N Engl J Med. 2000;343:1910-1916. 11. Damle RN, Wasil T, Fais F, et al. Ig V gene mutation status and CD38 expression as novel prognostic indicators in chronic lymphocytic leukemia. Blood. 1999;94:1840-1847. 12. Rassenti LZ, Huynh L, Toy TL, et al. ZAP-70 compared with immunoglobulin heavy-chain gene mutation status as a predictor of disease progression in chronic lymphocytic leukemia. N Engl J Med. 2004;351:893-901. 13. Rassenti LZ, Jain S, Keating MJ, et al. Relative value of ZAP-70, CD38, and immunoglobulin mutation status in predicting aggressive disease in chronic lymphocytic leukemia. Blood. 2008;112:1923-1930. 14. Gribben JG. Are prognostic factors in CLL overrated? Oncology (Williston Park). 2011;25:703, 706. 15. Gribben JG, Zahrieh D, Stephans K, et al. Autologous and allogeneic REFERENCES Research Funding Expert Testimony Other Remuneration stem cell transplantation for poor-risk chronic lymphocytic leukemia. Blood. 2005;106:4389-4396. 16. Milligan DW, Fernandes S, Dasgupta R, et al. Results of the MRC pilot study show autografting for younger patients with chronic lymphocytic leukemia is safe and achieves a high percentage of molecular responses. Blood. 2005;105:397-404. 17. Jantunen E, Itala M, Siitonen T, et al. Autologous stem cell transplantation in patients with chronic lymphocytic leukaemia: the Finnish experience. Bone Marrow Transplant. 2006;37:1093-1098. 18. Montserrat E, Gribben JG. Autografting CLL: the game is over! Blood 2011;117:6057-6058. 19. Dreger P, Stilgenbauer S, Benner A, et al. The prognostic impact of autologous stem cell transplantation in patients with chronic lymphocytic leukemia: a risk-matched analysis based on the VH gene mutational status. Blood. 2004;103:2850-2858. 20. Michallet M, Dreger P, Sutton L, et al. Autologous hematopoietic stem cell transplantation in chronic lymphocytic leukemia: Results of European intergroup randomized trial comparing autografting versus observation. Blood. 2011;117:1516-1521. 21. Sutton L, Chevret S, Tournilhac O, et al. Autologous stem cell transplantation as a first-line treatment strategy for chronic lymphocytic leukemia: a multicenter, randomized, controlled trial from the SFGM-TC and GFLLC. Blood. 2011;117:6109-6119. 22. Brion A, Mahe B, Kolb B, et al. Autologous transplantation in CLL patients with B and C Binet stages: Final results of the prospective randomized GOELAMS LLC 98 trial. Bone Marrow Transplant. Epub 2011 Jul 4. 23. Zenz T, Ritgen M, Dreger P, et al. Autologous graft-versus-host diseaselike syndrome after an alemtuzumab-containing conditioning regimen and autologous stem cell transplantation for chronic lymphocytic leukemia. Blood. 2006;108:2127-2130. 24. Montillo M, Tedeschi A, Miqueleiz S, et al. Alemtuzumab as consolidation after a response to fludarabine is effective in purging residual disease in patients with chronic lymphocytic leukemia. J Clin Oncol. 2006;24:2337-2342. 25. Michallet M, Archimbaud E, Bandini G, et al. HLA-identical sibling bone marrow transplantation in younger patients with chronic lymphocytic leukemia. European Group for Blood and Marrow Transplantation and the International Bone Marrow Transplant Registry. Ann Internal Med. 1996; 124:311-315. 26. Khouri I, Champlin R. Allogenic bone marrow transplantation in chronic lymphocytic leukemia. Ann Intern Med. 1996;125:780-787. 27. Doney KC, Chauncey T, Appelbaum FR. Allogeneic related donor hematopoietic stem cell transplantation for treatment of chronic lymphocytic leukemia. Bone Marrow Transplant. 2002;29:817-823. 403
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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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TREATMENT OF ADVANCED BREAST CANCER
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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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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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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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PROSTATE CANCER RISK REDUCTION men
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PSA SCREENING: HARMS WITHOUT CLEAR
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GLIOBLASTOMA: TAKING THE STANDARD O
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FUTURE DIRECTIONS IN GBM THERAPY pr
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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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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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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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Targeting Molecular Aberrations in
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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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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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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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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 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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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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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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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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Page 521 and 522: LUNG CANCER IN BRAZIL Fig. 1. Relat
Page 523 and 524: LUNG CANCER IN BRAZIL Fig. 3. Chara
Page 525 and 526: LUNG CANCER IN BRAZIL Author’s Di
Page 527 and 528: LUNG CANCER IN CHINA Fig 1. Chinese
Page 529 and 530: LUNG CANCER IN CHINA well equipped
Page 531 and 532: 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
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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
Page 553 and 554:
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
Page 561 and 562:
MANAGEMENT OF THYMIC CARCINOMA recu
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MANAGEMENT OF THYMIC CARCINOMA Refe
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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
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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
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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 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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