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MANAGING OLDER PATIENTS WITH ALL FIGURE 4. Preliminary Results of Reduced Intensity Allografting from United Kingdom ALL XIV Overall survival post-transplant. TABLE 3. Major Demographic Characteristics and Outcomes for 60 RIC Allografts Registered for RIC transplant 91 Transplant data available 60 Median age 49 Sibling donor 36 (60%) ECOG PS 1-2 24 (40%) WBC 30 10e9/L 12 (20%) High-risk cytogenetics 27/51* Median time to transplant from diagnosis 5.4 months (4-9) Acute GVHD grade 2-4 29% Chronic GVHD 14 (23%) Donor lymphocyte infusions 16/41** Relapse 4 (2 survive) Transplant-related mortality 6 Total deaths 8 Abbreviations: RIC; reduced intensity conditioning; ECOG; Eastern Cooperative Oncology Group; PS, performance status; WBC, white blood count; GVHD, graft versus host disease. *Nine patients did not have evaluable cytogenetics. **Data only available on 41 patients currently (10 for mixed chimerism and six for persistent or rising minimum residual disease). show it to be an effective way of eradicating disease, uses moderate doses of chemotherapy and involves a short period of neutropenia, mild mucositis, and is generally not very debilitating. A transplant may be seen as providing a more rapid recovery than consolidation, intensifıcation, and longer than 2 years of maintenance chemotherapy. It is important to avoid severe graft versus host disease (GVHD) in this older age group, but RIC allografts do rely on a graft-versusleukemia effect. The main evidence for a graft-versusleukemia effect is that relapse is less common in patients with grade 2 to grade 4 acute GVHD and/or chronic GVHD. However, this effect is most operative in patients with low levels of disease. Full intensity conditioning causes excessive TRM in this age group and is seldom indicated. It should be noted that RIC allografts are mainstream therapy in older patients with AML with many studies showing acceptable TRM in selected patients. Two registry-based comparisons with full intensity conditioning show adjusted survival and event-free survival to be similar to full-intensity conditioning (Fig. 4). 20,21 Unsurprisingly, relapse rates are increased and TRM only marginally decreased. The optimum conditioning regimen and GVHD prophylaxis strategy are yet to be defıned. The United Kingdom ALL XIV trial is prospectively examining the role of RIC sibling and unrelated donor allografting. All patients older than age 40 are considered high risk and are eligible for allografts if they are fıt, in CR, and have a matched sibling or 8/8 molecularly matched unrelated donor. (Patients with high-risk cytogenetics or persistent MRD are permitted to have a 7/8 match). Sixty-two percent of the fırst 374 patients are eligible, and we have data on the fırst 60 allografts. Survival with a median follow-up of 12 months exceeds 80%, and the current TRM of 9% shows that the procedure can be performed safely on a multicenter basis. The rates of acute and chronic GVHD are modest (Table 3). Mixed chimerism is a common outcome of fludarabine, melphalan, and alemtuzamab allografts; 10 patients received donor lymphocyte infusions for this and six additional patients received donor lymphocyte infusions for persistent or progressive MRD. Fifteen of these 16 patients currently survive, but follow-up is short. FUTURE DEVELOPMENTS The newer agents, blinatumomab and inotuzumab, 14,16 have not been tested specifıcally in this age group, but there will be some data from the ongoing phase III studies (Inovate and Tower). Both drugs have been tested mainly in the relapsed/ refractory setting, but blinatumomab is very impressive at converting persistent MRD positivity (after 3 months of chemotherapy) to negativity (78% of 116 patients in the phase II study). 22,23 As most older patients have dose reductions that may result in higher incidences of persistent MRD positivity, it is attractive to add in a 28-day course of blinatumomab to deepen remission states before further consolidative or maintenance chemotherapy. However, fırst we need data comparing this agent with conventional chemotherapy and to know if older patients tolerate the cytokine release syndrome and neurotoxicity. Similarly, the effıcacy and safety of inotuzumab will need to be compared with conventional salvage therapy before we can assess the place of this drug in older patients. In the United Kingdom, we are working to establish a backbone of chemotherapy that older patients can tolerate, with reasonable CR rates and 1-year survival. We then plan to add in novel agents to improve those outcomes without increasing toxicity and NRM. The collection of diagnostic specimens in these patients and correlation with clinical data may improve our understanding of the biologic differences that exist in older patients with ALL. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e349
DAVID I. MARKS Chimeric antigen receptor T cells directed against CD19 have shown remarkable effıcacy in a relatively small number of children but are likely to be tested in younger adults before any trials in the older-patient population. 24 A proportion of patients experience severe cytokine release syndrome requiring ICU admission; this could be a limiting factor in the older age group. CONCLUSION Effective management of older patients with ALL is a major unmet need. The different biology of the disease and the patient is recognized, and we now need the systematic trials that have improved the outcome of ALL in children and adults to be applied to the older age group. Many fıt patients between age 50 and 65 will be able to tolerate conventional aggressive chemotherapy with reasonable outcomes and acceptable NRM. However, older and less-fıt patients require lessaggressive chemotherapy, and strategies are needed to improve CR rates in this group. It is essential that we better understand the comorbidities that affect tolerance to chemotherapy so that we can rationally adjust therapy and not rely on end-of-the-bed impressions. Trials such as the United Kingdom ALL 60 study that assess comorbidities and include objective and subjective QOL endpoints will hopefully advance the fıeld. Leukemia physicians are urged to enter older patients into trials in order that we may improve the outcome of this diffıcult clinical management problem. ACKNOWLEDGEMENT David I. Marks would like to thank Adele Fielding for helpful discussions and kindly permitting access to unpublished work. Jenny Bird reviewed the manuscript, making helpful suggestions. Disclosures of Potential Conflicts of Interest Relationships are considered self-held and compensated unless otherwise noted. Relationships marked “L” indicate leadership positions. Relationships marked “I” are those held by an immediate family member; those marked “B” are held by the author and an immediate family member. Institutional relationships are marked “Inst.” Relationships marked “U” are uncompensated. Employment: None. Leadership Position: None. Stock or Other Ownership Interests: None. Honoraria: None. Consulting or Advisory Role: David I. Marks, Amgen. Speakers’ Bureau: None. Research Funding: None. Patents, Royalties, or Other Intellectual Property: None. Expert Testimony: None. Travel, Accommodations, Expenses: None. Other Relationships: None. References 1. Rowe JM, Buck G, Burnett AK, et al. Induction therapy for adults with acute lymphoblastic leukemia: results of more than 1500 patients from the international ALL trial: MRC UKALL XII/ECOG 2993. Blood. 2005; 106:3760-3767. 2. Pulte D, Gondos A, Brenner H. Improvement in survival in younger patients with acute lymphoblastic leukemia from the 1980s to the early 21st century. Blood. 2009;113:1408-1411. 3. Larson RA. Acute lymphoblastic leukemia: older patients and newer drugs. Hematology Am Soc Hematol Educ Program. 2005;131- 136. 4. Marks DI. Treating the “older” adult with acute lymphoblastic leukemia. ‘Hematology 2010’ 30 th edition. American Society of Hematology Education Program Book. 2010;13-20. 5. Gökbuget N. How I treat older patients with ALL. Blood. 2013;122:1366- 1375. 6. Goldstone AH, Richards SM, Lazarus HM, et al. In adults with standard-risk acute lymphoblastic leukemia, the greatest benefıt is achieved from a matched sibling allogeneic transplantation in fırst complete remission, and an autologous transplantation is less effective than conventional consolidation/maintenance chemotherapy in all patients: fınal results of the International ALL Trial (MRC UKALL XII/ECOG E2993). Blood. 2008;111:1827-1833. 7. Moorman AV, Harrison CJ, Buck GA, et al. Karyotype is an independent prognostic factor in acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial. Blood. 2007;109:3189-3197. 8. Moorman AV, Chilton L, Wilkinson J, et al. A population-based cytogenetic study of adults with acute lymphoblastic leukemia. Blood. 2010; 115:206-214. 9. Daenen S, van der Holt B, Dekker AW, et al. Intensive chemotherapy to improve outcome in patients with acute lymphoblastic leukemia over the age of 40: a phase II study for effıcacy and feasibility by HOVON. Leukemia. 2012;26:1726-1729. 10. Sive JI, Buck G, Fielding A, et al. Outcomes in older adults with acute lymphoblastic leukaemia (ALL): results from the international MRC UKALL XII/ECOG2993 trial. Br J Haematol. 2012;157:463-471. 11. Klepin HD, Geiger AM, Tooze JA, et al. Geriatric assessment predicts survival for older adults receiving induction chemotherapy for acute myelogenous leukemia. Blood. 2013;121:4287-4294. 12. Larson RA, Dodge RK, Linker CA, et al. A randomized controlled trial of fılgrastim during remission induction and consolidation chemotherapy for adults with acute lymphoblastic leukemia: CALGB study 9111. Blood. 1998;92:1556-1564. 13. Thomas DA, O’Brien S, Kantarjian HM. Monoclonal antibody therapy with rituximab for acute lymphoblastic leukemia. Hematol Oncol Clin North Am. 2009;23:949-971, v. 14. Topp MS, Kufer P, Gökbuget N, et al. Targeted therapy with the T-cellengaging antibody blinatumomab of chemotherapy-refractory minimal residual disease in B-lineage acute lymphoblastic leukemia patients results in high response rate and prolonged leukemia-free survival. J Clin Oncol. 2011;29:2493-2498. 15. Gökbuget N, Basara N, Baurmann H, et al. High single-drug activity of nelarabine in relapsed T-lymphoblastic leukemia/lymphoma offers cu- e350 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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Controversies in Neoadjuvant Therap
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Managing Ovarian Cancer in the Olde
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2015 ASCO Annual Meeting Disclosure
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2015 Educational Book Expert Panel
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James Marshall, PhD Roswell Park Ca
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2015 Annual Meeting Supporters* MIS
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David Yurman Corporate Allies Conqu
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DAVID W. SCOTT FIGURE 3. The Lymph2
Page 652 and 653:
DAVID W. SCOTT 10. Shaffer AL 3rd,
Page 654 and 655:
CHEAH, OKI, AND FANALE Novel Treatm
Page 656 and 657:
CHEAH, OKI, AND FANALE an ongoing G
Page 658 and 659:
CHEAH, OKI, AND FANALE a similar me
Page 660 and 661:
CHEAH, OKI, AND FANALE TABLE 3. Sel
Page 662 and 663:
CHEAH, OKI, AND FANALE eral T cell
Page 664 and 665:
CHEAH, OKI, AND FANALE 77. Cairns R
Page 666 and 667:
STEPHEN ANSELL associated with pati
Page 668 and 669:
STEPHEN ANSELL Disclosures of Poten
Page 670 and 671:
MATEOS AND SAN MIGUEL Smoldering Mu
Page 672 and 673:
MATEOS AND SAN MIGUEL years. This f
Page 674 and 675:
MATEOS AND SAN MIGUEL previously me
Page 676 and 677:
MATEOS AND SAN MIGUEL TABLE 2. Risk
Page 678 and 679:
MATEOS AND SAN MIGUEL 30. Rajkumar
Page 680 and 681:
BHUTANI, LANDGREN, AND USMANI of th
Page 682 and 683:
BHUTANI, LANDGREN, AND USMANI bette
Page 684 and 685:
BHUTANI, LANDGREN, AND USMANI fıne
Page 686 and 687:
BHUTANI, LANDGREN, AND USMANI FIGUR
Page 688 and 689:
BHUTANI, LANDGREN, AND USMANI 15. K
Page 690 and 691:
MOREAU AND TOUZEAU Multiple Myeloma
Page 692 and 693:
MOREAU AND TOUZEAU other effıcacy
Page 694 and 695:
MOREAU AND TOUZEAU was able to indu
Page 696 and 697:
MOREAU AND TOUZEAU Group consensus
Page 698 and 699:
LYMPHOMA AND PLASMA CELL DISORDERS
Page 700 and 701:
MANAGEMENT OF CLL Up-Front Manageme
Page 702 and 703:
MANAGEMENT OF CLL than 17p-/TP53mut
Page 704 and 705:
MANAGEMENT OF CLL could be associat
Page 706 and 707:
MANAGEMENT OF CLL tion by nonmalign
Page 708 and 709:
MANAGEMENT OF CLL fludarabine and c
Page 710 and 711:
MANAGEMENT OF CLL lymphocytic leuke
Page 712 and 713:
PROGNOSTIC FACTORS AND ADJUVANT RAD
Page 714 and 715:
Page 716 and 717:
Page 718 and 719:
MERKEL CELL CARCINOMA Merkel Cell C
Page 720 and 721:
MERKEL CELL CARCINOMA tions in PIK3
Page 722 and 723:
MERKEL CELL CARCINOMA treating MCC
Page 724 and 725:
MERKEL CELL CARCINOMA 32. Leonard J
Page 726 and 727:
MELANOMA/SKIN CANCERS Locoregional
Page 728 and 729:
PERFUSION AND INFUSION IN THE ERA O
Page 730 and 731:
Page 732 and 733:
Page 734 and 735:
NEOADJUVANT THERAPY OF MELANOMA Neo
Page 736 and 737:
NEOADJUVANT THERAPY OF MELANOMA TAB
Page 738 and 739:
NEOADJUVANT THERAPY OF MELANOMA ity
Page 740 and 741:
NEOADJUVANT THERAPY OF MELANOMA 4.
Page 742 and 743:
MELANOMA/SKIN CANCERS Targeted Mole
Page 744 and 745:
SULLIVAN ET AL FIGURE 1. Relevant S
Page 746 and 747:
SULLIVAN ET AL Resistance to BRAF i
Page 748 and 749:
SULLIVAN ET AL TABLE 1. Clinical Tr
Page 750 and 751:
SULLIVAN ET AL 17. Halait H, Demart
Page 752 and 753:
SULLIVAN ET AL NRAS-mutant melanoma
Page 754 and 755:
KLEPIN, RODIN, AND HURRIA Treating
Page 756 and 757:
KLEPIN, RODIN, AND HURRIA plication
Page 758 and 759:
KLEPIN, RODIN, AND HURRIA plan was
Page 760 and 761:
KLEPIN, RODIN, AND HURRIA patient-s
Page 762 and 763:
KLEPIN, RODIN, AND HURRIA 62. Blanc
Page 764 and 765:
PERIPHERAL NEUROTOXICITY IN CANCER
Page 766 and 767:
Page 768 and 769:
Page 770 and 771:
Page 772 and 773:
PARTRIDGE, JACOBSEN, AND ANDERSEN C
Page 774 and 775:
PARTRIDGE, JACOBSEN, AND ANDERSEN c
Page 776 and 777:
PARTRIDGE, JACOBSEN, AND ANDERSEN w
Page 778 and 779:
PARTRIDGE, JACOBSEN, AND ANDERSEN v
Page 780 and 781:
LESLIE R. SCHOVER Sexual Healing in
Page 782 and 783:
LESLIE R. SCHOVER tinuous ADT in pr
Page 784 and 785:
LESLIE R. SCHOVER 12. Potosky AL, H
Page 786 and 787:
CATHERINE H. VAN POZNAK TABLE 1. Wo
Page 788 and 789:
CATHERINE H. VAN POZNAK (tamoxifen,
Page 790 and 791:
CATHERINE H. VAN POZNAK TABLE 3. FD
Page 792 and 793:
CATHERINE H. VAN POZNAK premenopaus
Page 794 and 795:
SHARI GOLDFARB KEY POINTS Brea
Page 796 and 797:
SHARI GOLDFARB and friction with va
Page 798 and 799:
SHARI GOLDFARB importance both duri
Page 800 and 801:
PATIENT AND SURVIVOR CARE Moving Su
Page 802 and 803:
MAYER ET AL TABLE 1. Quality Metric
Page 804 and 805:
MAYER ET AL to enhance the quality
Page 806 and 807:
MAYER ET AL FIGURE 2. (A) Infertili
Page 808 and 809:
MAYER ET AL efıcial suggests that
Page 810 and 811:
PATIENT AND SURVIVOR CARE The Chall
Page 812 and 813:
BRUERA AND PAICE Choice of Opioid a
Page 814 and 815:
BRUERA AND PAICE toxicity and proce
Page 816 and 817:
BRUERA AND PAICE effective. Basic s
Page 818 and 819:
PEDIATRIC ONCOLOGY Real-Time Molecu
Page 820 and 821:
CARROLL, RAETZ, AND MEYER KEY POINT
Page 822 and 823:
CARROLL, RAETZ, AND MEYER most are
Page 824 and 825:
CARROLL, RAETZ, AND MEYER markers a
Page 826 and 827:
PEDIATRIC ONCOLOGY Translating Surv
Page 828 and 829:
REDUCING THE BURDEN OF LATE EFFECTS
Page 830 and 831:
Page 832 and 833:
Page 834 and 835:
Page 836 and 837:
PROFESSIONAL DEVELOPMENT The Challe
Page 838 and 839:
ADVANCES IN WEBSITE INFORMATION RES
Page 840 and 841:
Page 842 and 843:
Page 844 and 845:
Page 846 and 847:
COMMUNICATION AND TECHNOLOGY: IT’
Page 848 and 849:
Page 850 and 851:
Page 852 and 853:
PATIENT-REPORTED OUTCOMES IN ONCOLO
Page 854 and 855:
PATIENT-REPORTED OUTCOMES IN ONCOLO
Page 856 and 857:
PROFESSIONAL DEVELOPMENT Trends, An
Page 858 and 859:
CLINICAL ONCOLOGY PRACTICE 2015 FIG
Page 860 and 861:
CLINICAL ONCOLOGY PRACTICE 2015 (6.
Page 862 and 863:
CLINICAL ONCOLOGY PRACTICE 2015 Pro
Page 864 and 865:
ADJUVANT/NEOADJUVANT MEDICAL THERAP
Page 866 and 867:
Page 868 and 869:
Page 870 and 871:
INDICATIONS FOR ADJUVANT RADIATION
Page 872 and 873:
Page 874 and 875:
Page 876 and 877:
Page 878 and 879:
SARCOMA Latest Advances in Systemic
Page 880 and 881:
SYSTEMIC THERAPY FOR OSTEOSARCOMA A
Page 882 and 883:
SYSTEMIC THERAPY FOR OSTEOSARCOMA A
Page 884 and 885:
RETHINKING TREATMENT FOR CHONDROSAR
Page 886 and 887:
Page 888 and 889:
Page 890 and 891:
Page 892 and 893:
BONE SARCOMAS IN ADULTS local disea
Page 894 and 895:
BONE SARCOMAS IN ADULTS structure a
Page 896 and 897:
SARCOMA Well-Differentiated and Ded
Page 898 and 899:
ABBAS MANJI ET AL ticular region. 7
Page 900 and 901:
ABBAS MANJI ET AL MYXOID (ROUND CEL
Page 902 and 903:
ABBAS MANJI ET AL versus doxorubici
Page 904 and 905:
SHLUSH AND HERSHKOVITZ Clonal Evolu
Page 906 and 907:
SHLUSH AND HERSHKOVITZ FIGURE 1. Ti
Page 908 and 909:
TUMOR BIOLOGY New Strategies to Und
Page 910 and 911:
KNAPP, DHAWAN, AND OSTRANDER in dog
Page 912 and 913:
KNAPP, DHAWAN, AND OSTRANDER TABLE
Page 914 and 915:
KNAPP, DHAWAN, AND OSTRANDER 14. Fe
Page 916 and 917:
SOURBIER, SRINIVASAN, AND LINEHAN M
Page 918 and 919:
SOURBIER, SRINIVASAN, AND LINEHAN F
Page 920 and 921:
SOURBIER, SRINIVASAN, AND LINEHAN T
Page 922:
Author Index Abbas Manji, Gulam ...
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