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LYMPHOMA AND PLASMA CELL DISORDERS Progress and Challenges in Chronic Lymphocytic Leukemia CHAIR Clive S. Zent, MD University of Rochester Rochester, NY SPEAKERS Stephan Stilgenbauer, MD Ulm University Ulm, Germany Richard R. Furman, MD Weill Cornell Medical College New York, NY
STILGENBAUER, FURMAN, AND ZENT Management of Chronic Lymphocytic Leukemia Stephan Stilgenbauer, MD, Richard R. Furman, MD, and Clive S. Zent, MD OVERVIEW Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) is usually diagnosed in asymptomatic patients with early-stage disease. The standard management approach is careful observation, irrespective of risk factors unless patients meet the International Workshop on CLL (IWCLL) criteria for “active disease,” which requires treatment. The initial standard therapy for most patients combines an anti-CD20 antibody (such as rituximab, ofatumumab, or obinutuzumab) with chemotherapy (fludarabine/cyclophosphamide [FC], bendamustine, or chlorambucil) depending on multiple factors including the physical fitness of the patient. However, patients with very high-risk CLL because of a 17p13 deletion (17p-) with or without mutation of TP53 (17p-/TP53mut) have poor responses to chemoimmunotherapy and require alternative treatment regimens containing B-cell receptor (BCR) signaling pathway inhibitors. The BCR signaling pathway inhibitors (ibrutinib targeting Bruton’s tyrosine kinase [BTK] and idelalisib targeting phosphatidyl-inositol 3-kinase delta [PI3K-delta], respectively) are currently approved for the treatment of relapsed/refractory CLL and all patients with 17p- (ibrutinib), and in combination with rituximab for relapsed/refractory patients (idelalisib). These agents offer great efficacy, even in chemotherapy refractory CLL, with increased tolerability, safety, and survival. Ongoing studies aim to determine the best therapy combinations with the goal of achieving long-term disease control and the possibility of developing a curative regimen for some patients. CLL is associated with a wide range of infectious, autoimmune, and malignant complications. These complications result in considerable morbidity and mortality that can be minimized by early detection and aggressive management. This active monitoring requires ongoing patient education, provider vigilance, and a team approach to patient care. Chronic lymphocytic leukemia/small lymphocytic lymphoma is the most prevalent lymphoid malignancy in many parts of the world, and approximately 90% of patients are diagnosed with asymptomatic, early-intermediate stage (Rai 0-I, Binet A) disease. 1-3 Many of these patients have indolent disease and could have a normal life expectancy, whereas others have rapid disease progression and poor outcome. There is no proven survival benefıt from early therapy in patients with CLL. 4,5 There are now multiple prognostic factors that can be used to predict the risk of disease progression including serum thymidine kinase (TK) and beta-2- microglobulin (2MG) levels, genomic aberrations assessed by fluorescence in situ hybridization (FISH), ZAP70, CD38, and CD49 expression, somatic hypermutation of the immunoglobulin heavy chain variable region genes (IGHV), and mutations of other genes, most prominently TP53. 6,7 Despite multiple published studies of these prognostic factors in early-stage CLL, none have been prospectively validated. 8-14 Moreover, there is currently no evidence that early, risk factor–guided intervention with chemoimmunotherapy can alter the natural course of early-stage CLL. 4,5 Therefore, “watch and wait” remains the standard of care for patients with early-stage, asymptomatic CLL. The intervals of monitoring can be adjusted to a patient’s risk profıle, that is, with 3-monthly follow-up for patients with high-risk markers such as 17p- with or without TP53mut, unmutated IGHV, 11q22.3 deletion (11q-), and high 2MG or TK serum levels. INITIAL MANAGEMENT OF CLL Early-Stage Asymptomatic Patients A small proportion of patients with early-stage CLL (approximately 3% to 5%) have 17p-/TP53mut, 15 which predicts a very high risk of disease progression 16-21 based on data from chemoimmunotherapy studies in patients who required treatment (discussed later). However, a small proportion of early-stage patients with 17p-/TP53mut CLL do not have early disease progression, 15,22 and 17p-/TP53mut at diagnosis in a patient who does not have active disease 1 is not an indication for treatment. However, these patients deserve a more extensive prognostic work-up and closer monitoring, including the discussion of allogeneic stem cell transplantation (ASCT) as an option in young/fıt patients when their disease progresses and treatment is indicated. In summary, outside of clinical trials, the decision to start therapy requires the presence of active disease and is not modifıed by the presence of any high-risk marker. Prognostic markers can, however, be very helpful in counseling patients and planning patient follow-up. From Ulm University, Ulm, Germany; Weill Cornell Medical College, New York, NY; University of Rochester, Rochester, NY. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Clive S. Zent, MD, Wilmot Cancer Institute, University of Rochester Medical Center, 601 Elmwood Ave., Box 704, Rochester, NY 14642; email: clive_zent@urmc.rochester.edu. © 2015 by American Society of Clinical Oncology. 164 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
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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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GYNECOLOGIC CANCER Managing Ovarian
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TREATMENT OF PHILADELPHIA CHROMOSOM
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CD19 CAR THERAPY FOR ALL FIGURE 1.
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NASSER HANNA culty of this task. Va
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LYMPHOMA AND PLASMA CELL DISORDERS
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NOWAKOWSKI AND CZUCZMAN sociated wi
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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
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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
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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
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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
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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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