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LYMPHOMA AND PLASMA CELL DISORDERS Diffuse Large B-Cell Lymphoma: Are We Ready for Molecular Subtype-Specific Therapy? CHAIR Grzegorz S. Nowakowski, MD Mayo Clinic Rochester, MN SPEAKERS David W. Scott, MBCHB, PhD BC Cancer Agency Vancouver, BC, Canada Myron S. Czuczman, MD Roswell Park Cancer Institute Buffalo, NY
MANAGEMENT OF DLBCL BASED ON MOLECULAR PROFILE ABC, GCB, and Double-Hit Diffuse Large B-Cell Lymphoma: Does Subtype Make a Difference in Therapy Selection? Grzegorz S. Nowakowski, MD, and Myron S. Czuczman, MD OVERVIEW Personalized therapy for the treatment of patients with cancer is rapidly approaching and is an achievable goal in the near future. A substantial number of novel targets have been developed into therapeutic agents. There is a substantial variability to antitumor activity by novel therapeutics because of the unique heterogeneity and biology that exists both between and within lymphoma subtypes. Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma (NHL). Approximately 40% of patients have refractory disease or disease that will relapse after an initial response, and the majority of patients with relapsed DLBCL will succumb to the disease. There are two major biologically distinct molecular subtypes of DLBCL: germinal center B-cell (GCB) and activated B-cell (ABC). ABC DLBCL is associated with substantially worse outcomes when treated with standard chemoimmunotherapy. In addition to GCB and ABC subtypes, double-hit lymphomas (approximately 5% to 10% of patients) and double-expressor lymphomas, which overexpress MYC and BCL2 protein, are aggressive DLBCLs and are also associated with a poor prognosis. Double-hit lymphomas have concurrent chromosomal rearrangements of MYC plus BCL2 (or less likely, BCL6). Advances in molecular characterization techniques and the development of novel agents targeting specific subtypes of DLBCL have provided a foundation for personalized therapy of DLBCL based on molecular subtype. A number of early clinical trials evaluating combinations of novel targeted agents with standard chemotherapy (R-CHOP) have been completed and have demonstrated the feasibility of this approach with encouraging efficacy. As such, molecular classification of DLBCL is not only important for prognostication, but moves to center stage for personalization of therapy for DLBCL. The addition of the anti-CD20 monoclonal antibody rituximab (R) to the standard CHOP regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) was a major breakthrough in the front-line treatment for patients with DLBCL, resulting in dramatic improvements in progression-free survival (PFS) and overall survival (OS). 1-3 However, despite these improvements approximately 40% of patients with DLBCL who are treated with R-CHOP or R-CHOP–like chemotherapy will relapse or develop refractory disease, 4,5 and the majority of patients with relapsed or refractory DLBCL will succumb to the disease. 1-3 Various strategies have been implemented to improve the outcome of DLBCL, including intensifıcation of chemotherapy and use of maintenance therapy. Regardless of molecular subtype, standard front-line treatment for DLBCL is a combination of R-CHOP or CHOP-like chemotherapy. Additional regimens and immunochemotherapy combinations are under investigation as alternatives to front-line R-CHOP, including dose-dense R-CHOP14, dose-adjusted R-EPOCH (rituximab plus etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin), and R-CEOP90 (rituximab, cyclophosphamide, etoposide, vincristine, prednisone). 6-8 In a phase III trial including 1,080 patients with previously untreated DLBCL, no additional clinical benefıt was observed in patients treated with R-CHOP every 14 days (R-CHOP14) versus every 21 days (R-CHOP21). 6 Although evaluation of some of these intensifıcation strategies is still ongoing, recent insight into the biology of DLBCL allowed the development of strategies based on the addition of novel agents (X) to R-CHOP in so-called XR-CHOP combinations 9 that target specifıc oncogenic pathways (Fig. 1). In the development of these strategies, molecular characterization of DLBCL and the development of biomarkers is a critical step to identify patients who might benefıt from the addition of novel agent(s). Indeed, because of the molecular heterogeneity of DLBCL, addition of a novel agent may benefıt only a subgroup of patients with DLBCL. In this regard, preclinical and clinical studies of novel agents as monotherapies in relapsed and refractory DLBCL often provide important initial indications regarding the subtype of DLBCL that might benefıt from specifıc targeted therapy. Gene expression profıling (GEP) of DLBCL resulted in the identifıcation of two major and clinically distinct subtypes that are classifıed based on cell of origin (COO) and are as- From the Division of Hematology, Mayo Clinic, Rochester, MN; Roswell Park Cancer Institute, Buffalo, NY. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Grzegorz S. Nowakowski, MD, Division of Hematology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905; email: nowakowski.grzegorz@mayo.edu. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e449
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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2015 Educational Book Expert Panel
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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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CD19 CAR THERAPY FOR ALL 5. Zhou G,
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MANAGEMENT OF CLL than 17p-/TP53mut
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MANAGEMENT OF CLL could be associat
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MERKEL CELL CARCINOMA Merkel Cell C
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MELANOMA/SKIN CANCERS Locoregional
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PERFUSION AND INFUSION IN THE ERA O
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SULLIVAN ET AL FIGURE 1. Relevant S
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SULLIVAN ET AL TABLE 1. Clinical Tr
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SULLIVAN ET AL 17. Halait H, Demart
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SULLIVAN ET AL NRAS-mutant melanoma
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KLEPIN, RODIN, AND HURRIA Treating
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KLEPIN, RODIN, AND HURRIA plication
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KLEPIN, RODIN, AND HURRIA plan was
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KLEPIN, RODIN, AND HURRIA patient-s
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KLEPIN, RODIN, AND HURRIA 62. Blanc
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PERIPHERAL NEUROTOXICITY IN CANCER
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PARTRIDGE, JACOBSEN, AND ANDERSEN C
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PARTRIDGE, JACOBSEN, AND ANDERSEN c
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PARTRIDGE, JACOBSEN, AND ANDERSEN w
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PARTRIDGE, JACOBSEN, AND ANDERSEN v
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LESLIE R. SCHOVER Sexual Healing in
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LESLIE R. SCHOVER tinuous ADT in pr
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LESLIE R. SCHOVER 12. Potosky AL, H
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CATHERINE H. VAN POZNAK TABLE 1. Wo
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CATHERINE H. VAN POZNAK (tamoxifen,
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CATHERINE H. VAN POZNAK TABLE 3. FD
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CATHERINE H. VAN POZNAK premenopaus
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SHARI GOLDFARB KEY POINTS Brea
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SHARI GOLDFARB and friction with va
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SHARI GOLDFARB importance both duri
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PATIENT AND SURVIVOR CARE Moving Su
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MAYER ET AL TABLE 1. Quality Metric
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MAYER ET AL to enhance the quality
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MAYER ET AL FIGURE 2. (A) Infertili
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MAYER ET AL efıcial suggests that
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PATIENT AND SURVIVOR CARE The Chall
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BRUERA AND PAICE Choice of Opioid a
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BRUERA AND PAICE toxicity and proce
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BRUERA AND PAICE effective. Basic s
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PEDIATRIC ONCOLOGY Real-Time Molecu
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CARROLL, RAETZ, AND MEYER KEY POINT
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CARROLL, RAETZ, AND MEYER most are
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CARROLL, RAETZ, AND MEYER markers a
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PEDIATRIC ONCOLOGY Translating Surv
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REDUCING THE BURDEN OF LATE EFFECTS
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PROFESSIONAL DEVELOPMENT The Challe
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ADVANCES IN WEBSITE INFORMATION RES
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COMMUNICATION AND TECHNOLOGY: IT’
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Page 850 and 851:
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PATIENT-REPORTED OUTCOMES IN ONCOLO
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PATIENT-REPORTED OUTCOMES IN ONCOLO
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PROFESSIONAL DEVELOPMENT Trends, An
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CLINICAL ONCOLOGY PRACTICE 2015 FIG
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CLINICAL ONCOLOGY PRACTICE 2015 (6.
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CLINICAL ONCOLOGY PRACTICE 2015 Pro
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ADJUVANT/NEOADJUVANT MEDICAL THERAP
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INDICATIONS FOR ADJUVANT RADIATION
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SARCOMA Latest Advances in Systemic
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SYSTEMIC THERAPY FOR OSTEOSARCOMA A
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SYSTEMIC THERAPY FOR OSTEOSARCOMA A
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RETHINKING TREATMENT FOR CHONDROSAR
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BONE SARCOMAS IN ADULTS local disea
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BONE SARCOMAS IN ADULTS structure a
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SARCOMA Well-Differentiated and Ded
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ABBAS MANJI ET AL ticular region. 7
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ABBAS MANJI ET AL MYXOID (ROUND CEL
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ABBAS MANJI ET AL versus doxorubici
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SHLUSH AND HERSHKOVITZ Clonal Evolu
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SHLUSH AND HERSHKOVITZ FIGURE 1. Ti
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TUMOR BIOLOGY New Strategies to Und
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KNAPP, DHAWAN, AND OSTRANDER in dog
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KNAPP, DHAWAN, AND OSTRANDER TABLE
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KNAPP, DHAWAN, AND OSTRANDER 14. Fe
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SOURBIER, SRINIVASAN, AND LINEHAN M
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SOURBIER, SRINIVASAN, AND LINEHAN F
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SOURBIER, SRINIVASAN, AND LINEHAN T
Page 922:
Author Index Abbas Manji, Gulam ...
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