LATEST CONCEPTS IN LARGE CELL AND HODGKIN LYMPHOMAS Morton Coleman, M.D. Director, Center for Lymphoma and Myeloma New York-Presbyterian Hospital Weill Cornell Medical Center Clinical Professor of Medicine Weill Cornell Medical College Chairman, Medical Affiliates Board Lymphoma Research Foundation

Disclosures for Morton Coleman, MD In compliance with ACCME policy, ASH requires the following disclosures to the session audience: Employment None Consultancy Celgene, Genzyme, GlaxoSmithKline, Millenium, Onyx, Spectrum Equity Ownership Immunomedics Research Funding Glaxo Smith Kline, Onyx Honoraria Patents & Royalties 2012 Clinical Research Training Institute Summer Workshop, La Jolla, CA

Disclosures for Morton Coleman, MD, con’t In compliance with ACCME policy, ASH requires the following disclosures to the session audience: Speakers Bureau None Membership on Board of Directors/Advisory Committee Immunomedics, Glaxo Smith Kline Other Presentation includes a description of the following off-label use of a drug or medical device 2012 Clinical Research Training Institute Summer Workshop, La Jolla, CA

THE THRUST OF CURRENT DEVELOPMENTS Identify subsets of patients with diffuse large B cell or Hodgkin lymphoma who are either destined to do well or fare poorly using techniques beyond the known clinical predictive factors, particuarly those techniques using molecular changes and/or PET scans. By applying our better understanding of the (molecular) biology of these diseases, can we not only identify these subsets, but also develop and individualize treatments using less therapy for those with a good prognosis and using novel therapies for those destined to do poorly.

R-CHOP-21/14 cures about 2/3 of “all comers”: Failure-free survival 533 438 355 224 102 25 1 Patients at Risk R-CHOP21 534 429 358 216 116 Years from randomisation Probability 0.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 2 3 4 5 6 0.99 (0.79–1.24) HR (95% CI) p=0.94 Log-rank test 75% 2-yr FFS 153 (28) 155 (29) Events, n (%) Cunningham et al, ASCO 2011

DLBCL patients who recur post R-CHOP-21 do not do well N=228 31% Gisselbrecht C, et al. J Clin Oncol 2009; 27(15s): Abstract 8509. 6

Core Medical Need (CM) 4/22/2017 11:20:39 AM Overall survival of patients with DLBCL refractory to second line therapy is very poor 0 5 10 15 20 25 0.00 0.25 0.50 0.75 1.00 Proportion of Patients Time (months) Elstrom et al , Clin Lymph Myel Leuk, 2010 DRAFT 7 7

Germinal center vs activated B cell DLBCL Rosenwald A et al. N Engl J Med. 2002;346:1937-1947

Outcome by GCB vs non-GCB gene signatures in DLBCL N=233 patients treated with R-CHOP PFS OS Lenz G, et al, NEJM November 27, 2008

GCB + CD10 - ? HGAL BCL6 BCL2 - + ? non-GCB MUM1 + - FOXP1

Non-GCB DLBCL is associated with high expression of target genes of NF-kB transcription factors Davis, et al, J Exp Med 2001

CHOP-R + bortezomib DLBCL PFS and OS by subtype (n = 40) Ruan et al, JCO 2010

Six treatment cycles q21 days Six treatment cycles q21 days PYRAMID study design DLBCL diagnosis & subtyping Hans method Non-GCB GCB Not enrolled R Vc-R-CHOP Bortezomib 1.3 mg/m2, d 1, 4 Rituximab 375 mg/m2, d 1 Cyclophosphamide 750 mg/m2, d 1 Doxorubicin 50 mg/m2, d 1 Vincristine 1.4 mg/m2, d 1 Prednisone 100 mg/d, d 1–5 Six treatment cycles q21 days R-CHOP Rituximab 375 mg/m2, d 1 Cyclophosphamide 750 mg/m2, d 1 Doxorubicin 50 mg/m2, d 1 Vincristine 1.4 mg/m2, d 1 Prednisone 100 mg/d, d 1–5 Six treatment cycles q21 days Follow up every 3 months for 2 yrs

What is a “double hit” lymphoma? Recurrent breakpoints activating multiple oncogenes, one being MYC BCL2+/MYC+ most common BCL6, CCND1 and BCL3 may also occur Can also have “triple hit”

Immunophenotype of “double hit” lymphoma CD10+, GCB phenotype Lack MUM1, ABC phenotype BCL2 + also present (with Myc) in a majority of cases High proliferative index median 90% Ki67+ Aukema et al, Blood 2011

Clinical features of “double hit” lymphoma Study N DH/ total N (%) DH w prior iNHL % Med age St III/IV % LDH > Nl % BM + % CNS + % > 1 ENS % IPI Hi/HiI % Bertrand 2007 10/17 (59%) 10% 58 70% NA 56% Johnson 2009 54/54 (100%) 46% 62 76% 50% 71% 35% Kanungo 2006 14/14 (100%) None 55 93% 79% 21% 57% Le Gouill 2007 16/16 (100%) 25% 61 100% 94% 88% 81% Macpherson 1999 15/39 (38%) 65 92% 80% 69% 62% 90% Niitsu 2009 19/19 (100%) 84% 63% 89% Snuderl 2010 20/20 (100%) 15% 64 95% 59% 45% 30% 85% Tomita 2009 27/27 (100%) 17% 51 96% 65% 9% 87% Aukema et al, Blood 2011

R-CHOP and MYC rearranged DLBCL 35 (14%) with MYC rearrangements 19 also had t(14;18) 3 also had BCL6 7 “triple hit” Therefore most “MYC+” are “double” or “triple” hit EFS OS Barrans et al, JCO 2010

DA-R-EPOCH and MYC+ DLBCL Similar risk by IPI High RR/PFS in BL EFS OS Dunleavy et al, Lugano 2011

ASH 2013, Abstract 40 Impact of Induction Regimen and Consolidative Stem Cell Transplantation in Patients with Double Hit Lymphoma (DHL): A Large Multicenter Retrospective Analysis Mitul Gandhi, Adam M. Petrich, Ryan Cassaday, Oliver Press, Khushboo A. Shah, Jeremy D. Whyman, Frederick Lansigan, Andrew Zelenetz, Namrata Shah, Timothy Fenske, Francisco J. Hernandez-Ilizaliturri, Lisa X. Lee, Stefan K. Barta, Shruthi Melinamani, Reem Karmali, Camille Adeimy, Scott Smith, Julie Vose, Neil Dalal, Chadi Nabhan, David Peace, Borko Jovanvoic, Aliyah Sohani, Andrew Evens, Jorge Castillo, Jeremy S. Abramson

DHL: Impact of R-EPOCH Results of chi-square analysis Improved CR compared to R-CHOP (p = .005) Trend towards improvement w/ other regimens (p = .07) Decreased PD compared to R-CHOP (p = .005) Decreased PD w/ other intensive regimens (p = .003)

DHL: Conclusions DHL has a poor prognosis, although a subset exists which can achieve durable CR R-EPOCH is associated with improved rates of CR and decreased rates of PD SCT does not clearly improve OS compared to observation alone in those achieving CR Novel approaches and agents are necessary to overcome unfavorable biology

ASH 2013, Abstract 371 A Phase III Study of Enzastaurin in Patients with High-risk Diffuse Large B Cell Lymphoma Following Response to Primary Treatment: The PRELUDE Trial Michael Crump; Sirpa Leppä; Luis Fayad; Je Jung Lee; Alice Di Rocco; Michinori Ogura; Hans Hagberg; Frederick Schnell; Robert Rifkin; Andreas Mackensen; Fritz Offner; Lauren Pinter-Brown; Sonali Smith; Kensei Tobinai; Su-Peng Yeh; Jun Zhu; Eric D. Hsi; Marjo Hahka-Kemppinen; Scott P. Myrand; Donald Thornton; Peipei Shi; Tuan Nguyen; Boris Lin; Brad Kahl; Norbert Schmitz; Kerry J. Savage; Thomas Habermann for PRELUDE Trial Investigators 23

Background Patients with DLBCL and an IPI score of 3-5 at diagnosis who relapse after R-CHOP can have a poor prognosis. Enzastaurin is a potent and selective competitive inhibitor of PKCβ.1,2 Enzastaurin was associated with freedom from progression in a phase II trial in a small subgroup of patients with relapsed or refractory DLBCL, thereby providing the rationale for this study.3 R-CHOP = rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone. The PRELUDE Trial 1Morgillo F, et al. Mol Cancer Ther 2008;7:1698-707; 2Dumstorf CA, et al. Mol Cancer Ther 2010;9:3158-63; 3Robertson MJ, et al. J Clin Oncol 2007;25:1741-6. 24

Background PKCβ is the major isoform expressed in normal and malignant B cells.1,2 BTK PI 3K AKT mTOR PLC2 PKCβ SYK P IKK NFKB PKCβ is required for B cell receptor signaling, activation of NFκB, and VEGF-mediated angiogenesis.3 Over-expression of PKCβ mRNA and protein is associated with a poor outcome in patients with DLBCL.1 DLBCL = diffuse large B cell lymphoma. 1Shipp MA, et al. Nat Med 2002;8:68-74; 2Graff JR, et al. Cancer Res 2005;65:7462-9; 3Robertson MJ, et al. J Clin Oncol 2007;25:1741-6. The PRELUDE Trial 25

Disease Free Survival by Treatment Arm for ITT Population 100 80 60 40 20 Enzastaurin Placebo Survival Probability HR (95% Cl): 0.92 (0.689, 1.216) P = 0.541 p=0.541 0 6 12 18 24 30 36 42 48 54 60 66 72 78 Patients at risk, n: Disease-Free Survival Time (months) Patients at Risk, (n): Disease-free Survival Time (months) Enza: Placebo: 504 383 348 259 157 45 254 197 165 138 74 18 The PRELUDE Trial 26

Disease-free Survival – GCB vs. Non-GCB by Hans’ Algorithm GCB (N=109) Non-GCB (N=106) Time (Months) 0 6 12 18 24 30 36 42 48 54 60 66 72 78 84 1.0 0.9 0.8 0.7 0.6 0.5 Survival Distribution Function HR (95% Cl): 0.92 (0.56, 1.52) P=0.74 GCB vs. non-GCB in the Combined Arm Survival Distribution Function Survival Distribution Function GCB vs. non-GCB in the Enzastaurin Arm GCB vs. non-GCB in the Placebo Arm 1.0 0.9 0.8 0.7 0.6 0.5 1.0 0.9 0.8 0.7 0.6 0.5 GCB, Enzastaurin (N=79) Non-GCB, Enzastaurin (N=66) GCB, Enzastaurin (N=79) GCB, Placebo (N=30) Non-GCB, Placebo (N=40) GCB, Placebo (N=30) Non-GCB, Enzastaurin (N=66) Non-GCB, Placebo (N=40) Time (Months) Time (Months) HR (95% Cl): 0.77 (0.42, 1.42) P=0.40 HR (95% Cl): 1.31 (0.56, 3.08) P=0.54 0 6 12 18 24 30 36 42 48 54 60 66 72 78 84 0 6 12 18 24 30 36 42 48 54 60 66 72 78 84 Cox regression determined associations between DFS and GCB/non-GCB status, adjusted for IPI score (3 vs. >3), age (≤60 vs. >60), and prior radiation (yes vs. no). The PRELUDE Trial 27

Discussion and Conclusions Enzastaurin did not improve DFS, EFS, or OS vs. placebo in patients with CR after initial treatment for DLBCL and an IPI score of ≥3 Safety results of PRELUDE were consistent with the established safety profile of enzastaurin when used as a single-agent therapy in lymphoma and other cancers Cell-of-origin (GCB vs. non-GCB) was not prognostic for DFS in patients with CR The PRELUDE Trial 28

BENDAMUSTINE (with rituximab, vitamin R) Three studies reported: Japan, NSH, Germany Doses of B were 120mgm/m2 days 1,2 + R 375 mgm/m2 every three weeks. German study was with unrx’ed elderly (E) Responses ranged from 58% to 69% (E) CR’s ranged from 19% to 54% (E) PFS/OS ranged from 6 to 7.7(E) months Significant toxicity

Approach to “variant” DLBCLs GCB vs non-GCB R-CHOP is standard Various randomized trials underway MYC+, DH, TH Consider FISH/IHC for MYC, BCL2, BCL6 Less favorable with R-CHOP Unclear if other approaches better Prospective studies underway, including R- EPOCH Intensive BL type regimens R-EPOCH Less favorable outcome than other DLBCL with R-CHOP Risk seems to be beyond age, IPI Less favorable at progression Rearrangements noted BCL2 31% BCL6 18% C-MYC 13% C-MYC worse PFS and OS

In Hodgkin lymphoma, what role do PET Scans play in lessening (toxicity) therapy and enhancing cure? May interim PET/CAT scans be of value or should scans be used only at the end of treatment?

FDG-PET: After one (two treatments) versus two cycles (four treatments) of therapy Early determination of treatment sensitivity in Hodgkin lymphoma: FDG-PET/CT after one cycle of therapy has a higher negative predictive value than after two cycles of therapy Hutchings, M., Kostakoglu,L., Coleman, M., et al. Submitted for publication

Participating Nations Denmark United States Italy Poland

Patient Population:126 Pts. Stage I 8% Stage 2 46% Stage 3 19% Stage4 27% B Sxs 56% Bulky 37%

Comparison of the prognostic value of PET 1 and PET 2: Progression Free Survival at 2 Years PET 1 PET2 Negative predictive value 98% 91% Positive predictive value 63% 85% Sensitivity 95% 61% Specificity 86% 97% Concordance >90%

The RAPID Trial in Patients With Clinical Stages IA/IIA Hodgkin Lymphoma and a “Negative” PET Scan After 3 Cycles ABVD Radford J, Barrington S, Counsell N, Pettengell R, Johnson P, Wimperis J, Coltart S, Culligan D, Lister A, Bessell E, Kruger A, Popova B, Hancock B, Hoskin P, Illidge T, O’Doherty M 36

RAPID Trial Design Initial treatment: ABVD x 3 Reassessment: if NR/PD, patient goes off study if CR/PR, FDG-PET scan performed PET-positive PET-negative 4th cycle ABVD then IFRT Randomization IFRT No further treatment Radford J, et al. Blood. 2012;120: Abstract 547. 37

Outcomes After Median Follow-Up of 45.7 Months PET negative; randomized to IFRT (n = 209) PET negative; randomized to NFT (n = 211) PET positive; 4th cycle ABVD/IFRT (n = 145) Progressions 9 20 11 Deaths 6 1 8 PFS at 3 years 93.8% 90.7% 85.9% OS at 3 years 97.0% 99.5% 93.9% Radford J, et al. Blood. 2012;120: Abstract 547.

Summary 602 pts registered between 2003 and 2010 75% PET-negative at central review after ABVD x 3 In the randomized PET-negative population, 3 yr PFS is 93.8% IFRT and 90.7% NFT Risk difference -3% is within the maximum allowable difference of -7% Radford J, et al. Blood. 2012;120: Abstract 547. 39

Conclusion Patients with a negative PET scan after 3 cycles ABVD have an excellent prognosis without further treatment, and for these patients RT can be avoided Radford J, et al. Blood. 2012;120: Abstract 547.

Commentary These data are similar to those reported from Argentina several years ago. Would the slightly higher rate of false negative PET scans at cycle 3 seen in those patients not receiving adjuvant radiotherapy been avoided had the PET been performed at cycle 2, or better yet, cycle 1 Response-adapted therapy based on quality- controlled/assured PET imaging may become the future standard of care in early-stage HL Radford J, et al. Blood. 2012;120: Abstract 547.

An Individual Patient-Data Comparison of German Hodgkin Study Group HD10 and HD11 Combined Modality Therapy and NCIC Clinical Trials Group HD.6 ABVD Alone Hay AE, Klimm B, Chen BE, Goergen H, Shepherd LE, Fuchs M, Gospodarowicz M, Borchmann P, Connors JM, Markova J, Crump M, Lohri A, Winter JN, Dorken B, Pearcey RG, Volker D, Horning SJ, Eich HT, Engert A, Meyer RM 42

Comparison of NCIC CTG HD Comparison of NCIC CTG HD.6 and GHSG HD10 and HD11 Staging, Eligibility and Preferred Arms 2 ABVD + 20 Gy IFRT 4 ABVD + 30 Gy IFRT Early, favorable HD10 Early, unfavorable HD11 Advanced GHSG 4 – 6 ABVD alone NCIC CTG HD.6 Favorable Unfavorable Advanced Not necessarily to scale Hay AE, et al. Blood. 2012;120: Abstract 549. 43

Comparison of NCIC CTG HD Comparison of NCIC CTG HD.6 and GHSG HD10 and HD11 Staging, Eligibility and Preferred Arms Very good prognosis B or Bulk Early, favorable HD10 Early, unfavorable HD11 Advanced GHSG NCIC CTG HD.6 Favorable Unfavorable Advanced Not necessarily to scale Hay AE, et al. Blood. 2012;120: Abstract 549. 44

Outcomes: All Patients Endpoint Number Med. F/U GHSG HD10/11 406 7.6 Years NCIG CTG HD.6 182 11.2 Years HR (95% CI) GHSG PD/OS NCIC CTG 8-yr TTP 93% 87% 0.44 (0.24, 0.78) 25/0 23/0 8-yr PFS 89% 86% 0.71 (0.42, 1.18) 25/13 23/4 8-yr OS 95% 1.09 (0.49, 2.40) 19 10 Hay AE, et al. Blood. 2012;120: Abstract 549. 45

Combined modality therapy (CMT) improves disease control by 4%-7% Overall Summary Combined modality therapy (CMT) improves disease control by 4%-7% Superior long-term overall survival with CMT is highly unlikely The relatively long term outcomes associated with IFRT remain to be clarified Hay AE, et al. Blood. 2012;120: Abstract 549.

What’s new for refractory/relalpsing disease? Evolving Data on Brentuximab Vedotin

Brentuximab Vedotin Mechanism of Action Brentuximab vedotin (SGN-35) ADC monomethyl auristatin E (MMAE), potent antitubulin agent protease-cleavable linker anti-CD30 monoclonal antibody ADC binds to CD30 ADC-CD30 complex traffics to lysosome MMAE is released G2/M cell cycle arrest MMAE disrupts microtubule network Apoptosis

Long-Term Survival Analyses of an Ongoing Phase 2 Study of Brentuximab Vedotin in Patients with Relapsed or Refractory Hodgkin Lymphoma R Chen, AK Gopal, SE Smith, SM Ansell, JD Rosenblatt, KJ Savage, JM Connors, A Engert, EK Larsen, EL Sievers, A Younes 49

Overall survival after treatment with Brentuximab vedotin Median observation time from 1st dose: All patients = 29.5 months (range, 1.8 to 36.9) CR patients = 29.1 months (range, 2.6 to 34.3) 60/102 patients (59%) remain alive; median OS has not been reached (95% CI: 28.7, NE) Estimated 24-month survival rate* = 65% (95% CI: 55, 74)

Overall Survival by Cycle 4 PET Status

Conclusions Achievement of CR Negative PET scan at Cycle 4 After a median observation time of ~2.5 years from first brentuximab vedotin dose, 60 of 102 patients (59%) remain alive at last follow up Median OS has not yet been reached; the estimated 24-mo survival rate was 65% Improved OS strongly correlated with both: Achievement of CR Negative PET scan at Cycle 4 Prolonged OS was observed in patients with both long and short progression-free intervals after auto-SCT

What are we doing new for Advanced-Stage HL How can we improve the cure rate and reduce the toxicity for advanced stage disease?

Ansell SM, Connors JM, Park SI, O’Meara M, Younes A Frontline Therapy With Brentuximab Vedotin Combined with ABVD or AVD in Patients with Newly Diagnosed Advanced-Stage Hodgkin Lymphoma Ansell SM, Connors JM, Park SI, O’Meara M, Younes A 54

Study Design Phase I, multicenter, dose-escalation study Major eligibility criteria Treatment-naïve HL patients Age ≥18 to ≤60 years Stage IIA bulky disease or Stage IIB-IV disease Treatment design 28-day cycles (up to 6 cycles) with dosing on Days 1 and 15 Dose escalation cohorts – I-6, II-13, III-6, IV-6, expansion-20 Cycle 1 Cycle 2 Cycle 3 Brentuximab Vedotin A(B)VD 6 Cycles +/- XRT 2 4 6 8 10 12 Weeks Ansell SM, et al. Blood. 2012;120: Abstract 798.

Response Results at End of Front-Line Therapy Response per Investigatora ABVD with brentuximab vedotin N = 22 AVD with brentuximab vedotin N = 25 Response at end of front-line therapy, n (%) Complete remission 21 (95) 24 (96) Progressive disease 1 (4) Not evaluable due to AEs 1b (5) Response Results at End of Front-Line Therapy Response results at end of front-line therapy: ABVD cohorts: 21 of 22 CR (95%) AVD cohorts: 24 of 25 CR (96%) In addition, 1 patient withdrew consent and 3 patients were lost to follow-up prior to completion of front-line therapy and were not evaluable for response Ansell SM, et al. Blood. 2012;120: Abstract 798.

Carde et al. J Clin Oncol 30, 2012 (suppl; abs 8002)

Study Design HL Stages III-IV IPS ≥ 3 Randomized Phase III Trial Carde et al. J Clin Oncol 30, 2012 (suppl; abs 8002)

Progression-Free Survival (Not a predefined study endpoint) Carde et al. J Clin Oncol 30, 2012 (suppl; abs 8002)

Treatment Discontinuations for Toxicity ABVD n = 272 BEACOPP n = 269 Toxicity 10 28 Respiratory related (not including infections) 7 5 Hematological 4 Infection / meningitis / septicemia Septic / toxic shock 1 Hepatic 2 Cardiac Neurological Allergy to etoposide Carde et al. J Clin Oncol 30, 2012 (suppl; abs 8002)

Event-Free Survival Carde et al. J Clin Oncol 30, 2012 (suppl; abs 8002)

Overall Survival Carde et al. J Clin Oncol 30, 2012 (suppl; abs 8002)

CONCLUSIONS EFS (primary endpoint) is similar between treatment arms. However, more progressions / relapses were observed with ABVD while early discontinuations were more frequent with BEACOPP In this high-risk group, conventional dose escalation with BEACOPP 4+4 provides a better PFS compared to ABVD, yet not good enough to improve OS Additional considerations (treatment burden & cost, fertility issues, risk of relapse, risk of salvage, immediate & late morbidities) may guide physician / patient decisions toward ABVD or BEACOPP, which currently may share the claim for “current standard of care” Carde et al. J Clin Oncol 30, 2012 (suppl; abs 8002)

CONCLUSIONS A GENERAL SURVEY OF STUDIES COMPARING BEACOPP TO ABVD ALMOST ALL CONSISTENTLY SHOW A SUPERIOR PROGRESSION FREE SURVIVAL FOR BEACOPP BUT LONG TERM SURVIVAL SEEMS TO BE COMPARABLE DUE TO THE TOXICITY OF BEACOPP. AS WITH LIMITED STAGE DISEASE, CAN INTERIM PET SCANS BE USED TO SELECT OUT THOSE PATIENTS NOTNEEDING MORE AGGRESSIVE THERAPY AND THEREBY AVOID ALL THE UNNECESSARY TOXICITY OF BEACOPP? IS GENETIC INSTABILITY ADVANCED BY DR DIEHL TRULY OPERATIVE EVEN AS EARLY AS (A PET SCAN AFTER) ONE CYCLE

SUMMARY 3 cycles of ABVD without IFRT has an excellent outcome for favorable stage IA/IIA patients who are at the conclusion of treatment are PET neg. Disease control may be slightly better for CMT as compared with CT (3%- 7%), although a survival difference is unlikely although long-term effects of IF (reduced) RT are unknown. BV + AVD results are comparable, if not superior, to ABVD for patients with stage III/IV HL. Phase III comparison has opened. BV has been shown effective in relapsing/refractory patients including those failing transplant. It is being incorporated into many strategies for the rx of ‘difficult’ HL pts. The overall results with ABVD are at least equal to BEACOPP with less toxicity. Interim PET scans may prove valuable in the rx strategies for HL.

Acknowledgment Elizabeth Hyjek, M.D., Ph.D. Amy Chadburn, M.D. (Northwestern) Wayne Tam, M.D. Acknowledgment Clinical Research Jia Ruan, M.D., Ph.D. Richard Furman, M.D. John P. Leonard, M.D. Peter Martin, M.D. Maureen Joyce, R.N. Patricia Glenn, R.N. Jamie Ketas Jessica Hansen Karen Weil Jennifer O’Loughlin Rebecca Elstrom, M.D. (Gen.) Lale Kostakoglu, M.D. (Sinai) Stanley Goldsmith, M.D. Translational Core Maureen Lane, Ph.D. (Cornell) Maureen Ward Biostatistician Ken Chueng, Ph.D. (Columbia) Madhu Mazumdar, Ph.D. (Cornell) Lymphoma Research Foundation ASCO Foundation (YIA, CDA) NIH / NHLBI Laboratory Research Ari Milneck, M.D., Ph.D.(Cornell) Katherine Hajjar, M.D. (Cornell) Shahin Rafii, M.D. (Cornell)

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