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TREATMENT OF PHILADELPHIA CHROMOSOME–POSITIVE ACUTE LYMPHOBLASTIC LEUKEMIA from the European Group for Blood and Marrow Transplantation. Blood. 2010;116:4439-4443. 45. Marks DI, Wang T, Pérez WS, et al. The outcome of full-intensity and reduced-intensity conditioning matched sibling or unrelated donor transplantation in adults with Philadelphia chromosome-negative acute lymphoblastic leukemia in fırst and second complete remission. Blood. 2010;116:366-374. 46. Pfeifer H, Wassmann B, Bethge W, et al. Randomized comparison of prophylactic and minimal residual disease-triggered imatinib after allogeneic stem cell transplantation for BCR-ABL1-positive acute lymphoblastic leukemia. Leukemia. 2013;27:1254-1262. 47. 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. 48. Wetzler M, Watson D, Stock W, et al. Autologous transplantation for Philadelphia chromosome-positive acute lymphoblastic leukemia achieves outcomes similar to allogeneic transplantation: results of CALGB Study 10001 (Alliance). Haematologica. 2014;99:111-115. 49. Giebel S, Stella-Holowiecka B, Krawczykk-Kulis M, et al. Status of minimal residual disease determines outcome of autologous hematopoietic SCT in adult ALL. Bone Marrow Transplant. 2010;45:1095-1101. 50. Mullighan CG, Su X, Zhang J, et al. Deletion of IKZF1 and prognosis in acute lymphoblastic leukemia. N Engl J Med. 2009;360:470-480. 51. Tavernier E, Boiron JM, Huguet F, et al. Outcome of treatment after fırst relapse in adults with acute lymphoblastic leukemia initially treated by the LALA-94 trial. Leukemia. 2007;21:1907-1914. 52. Gokbuget N, Stanze D, Beck J, et al. Outcome of relapsed adult lymphoblastic leukemia depends on response to salvage chemotherapy, prognostic factors, and performance of stem cell transplantation. Blood. 2012;120:2032-2041. 53. Ottmann OG, Larson RA, Kantarjian HM, et al. Phase II study of nilotinib in patients with relapsed or refractory Philadelphia chromosomepositive acute lymphoblastic leukemia. Leukemia. 2012;27:1411-1413. 54. Ottmann O, Dombret H, Martinelli G, et al. Dasatinib induces rapid hematologic and cytogenetic responses in adult patients with Philadelphia chromosome positive acute lymphoblastic leukemia with resistance or intolerance to imatinib: interim results of a phase 2 study. Blood. 2007;110:2309-2315. 55. Cortes JE, Kantarjian H, Shah NP, et al. Ponatinib in refractory Philadelphia chromosome-positive leukemias. N Engl J Med. 2012;367:2075- 2088. 56. Den Boer ML, van Slegtenhorst M, De Menezes RX, et al. A subtype of childhood acute lymphoblastic leukaemia with poor treatment outcome: a genome-wide classifıcation study. Lancet Oncol. 2009;10:125- 134. 57. Roberts KG, Li Y, Payne-Turner D, et al. Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia. N Engl J Med. 2014;371: 1005-1015. 58. Weston BW, Hayden MA, Roberts KG, et al. Tyrosine kinase inhibitor therapy induces remission in a patient with refractory EBF1-PDGFRBpositive acute lymphoblastic leukemia. J Clin Oncol. 2013;31:e413-e416. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e359
SADELAIN ET AL CD19 CAR Therapy for Acute Lymphoblastic Leukemia Michel Sadelain, MD, PhD, Renier Brentjens, MD, PhD, Isabelle Rivière, PhD, and Jae Park, MD OVERVIEW Chimeric antigen receptor (CAR) therapy is an emerging immunotherapy that shows great promise for cancer, in particular acute lymphoblastic leukemia (ALL). CARs are recombinant receptors for antigen, which, in a single molecule, redirect the specificity and function of T lymphocytes. Following their genetic transfer to patient T cells, the latter acquire the ability to recognize leukemia cells and destroy them. Several years ago, we identified CD19 as an attractive target for CAR therapy for most B cell malignancies, including ALL. We and others have reported remarkable clinical outcomes in adults and children with ALL, achieving a high complete remission rate irrespective of age, prior treatments, or other prognostic markers. Severe cytokine release may develop in patients with high tumor burdens. Several interventions are available to curb the cytokine release syndrome when it occurs. Based on the impressive results obtained with CD19 CAR therapy for ALL, it is realistic to expect that CD19 CARs will become part of the armamentarium for B cell-ALL and other B cell malignancies. Chimeric antigen receptors (CARs) are recombinant receptors for antigens, which in a single molecule, redirect the specifıcity and function of T lymphocytes. A general premise for their use in cancer immunotherapy is to rapidly generate tumor-targeted T cells, bypassing the barriers to and incremental kinetics of active immunization. 1 Second generation CARs not only redirect cytotoxicity, but also reprogram T cell function and longevity, thus conferring supraphysiological properties on T cells, which then become “living drugs” that exert both immediate and sustained therapeutic effects. 2 T cells normally recognize their target antigen through the T cell receptor (TCR), which binds to human leukocyte antigen (HLA)-peptide complexes displayed on the surface of target cells. The TCR does not itself signal, but it does determine, based on its affınity for the HLA-peptide complex, the strength of the activation signals the T cell generates on contacting the tumor. The strength of these signals is further modifıed by costimulatory receptors, which may be either activating (such as CD28 and 4–1BB) or inhibitory (such as CTLA-4 and PD-1). 3 The ligands for these receptors are not ubiquitously expressed, and therefore place costimulation under the control of the target cell engaged by the T cell. Thus, professional antigen presenting cells, such as B cells and dendritic cells, may express powerful ligands for CD28 and 4–1BB, but tumors typically do not, as is the case for ALL. The concept underlying second generation CARs is to provide costimulatory support to T cells irrespective of the presence of a ligand on tumor cells (Fig. 1). In this context, T cells that engage the tumor through the CAR are given a costimulatory signal within the tumor microenvironment itself, resulting in a pharmacologic boost that we thought would radically alter the functional profıle of T cells. 4 The CARs that have recently shown impressive clinical outcomes in patients with B cell malignancies, especially ALL, are indeed second generation CARs. CAR TARGETS AND THE CD19 PARADIGM Unlike the physiological TCR, which engages HLA-peptide complexes, CARs are able to engage native cell surface molecules and do not require any processing or HLA expression to be recognized. CARs therefore can recognize target antigens on any HLA background, in contrast to TCRs, which need to be matched to the patient’s HLA haplotype. Furthermore, CARs can target tumor cells that have downregulated HLA expression or proteasomal antigen processing, two mechanisms that contribute to tumor escape from TCR-mediated immunity. 5 Another attractive feature of CAR-mediated T cell responses is that they are not limited to proteins and may target carbohydrate and glycolipid structures. The target must, however, be found on the tumor cell surface. Identifying appropriate CAR targets is important to achieving complete tumor eradication, as is avoiding damage to normal tissues that express the same target antigen (“ontarget, off-tumor effect”). Two decades ago, we selected CD19 as the prime target for developing our CAR technology. CD19 is a cell-surface antigen found on most B lineage lymphomas and leukemias. 6 We chose CD19 not only because it is highly expressed in these tumors, but also for its highly restricted expression in normal tissues. CD19 is indeed known to be only expressed among normal tissues in From the Center for Cell Engineering and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Michel Sadelain, MD, PhD, Memorial Sloan Kettering Cancer Center, 1275 York Ave., New York, NY 10065; email: m-sadelain@ski.mskcc.org. © 2015 by American Society of Clinical Oncology. e360 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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American Society of Clinical Oncolo
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Controversies in Neoadjuvant Therap
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Clinical Trials of Precision Medici
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Managing Ovarian Cancer in the Olde
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PEDIATRIC ONCOLOGY Real-Time Molecu
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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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INVITED ARTICLES This year’s invi
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WONG, CAPASSO, AND ECKHARDT terize
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GILBERT ET AL tional scholars, lead
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ENG ET AL colorectal cancer. Indeed
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WILLIAM M. SIKOV gational treatment
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NASSER HANNA Current Standards and
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NASSER HANNA At the 2014 ASCO Annua
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NASSER HANNA culty of this task. Va
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LYMPHOMA AND PLASMA CELL DISORDERS
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CHEAH, OKI, AND FANALE Novel Treatm
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BHUTANI, LANDGREN, AND USMANI bette
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BHUTANI, LANDGREN, AND USMANI fıne
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BHUTANI, LANDGREN, AND USMANI FIGUR
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BHUTANI, LANDGREN, AND USMANI 15. K
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MOREAU AND TOUZEAU Multiple Myeloma
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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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