1. 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

2. 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

3. 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

4. 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.

5. 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

6. 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

7. Core Medical Need (CM)
4/22/ :20:39 AM
Overall survival of patients with DLBCL refractory to second line therapy is very poor
Proportion of Patients
Time (months)
Elstrom et al , Clin Lymph Myel Leuk, 2010
DRAFT 7 7

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

9. 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

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

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

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

13. 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

14. 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”

15. 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

16. 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

17. 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

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

19. 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

21. 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)

22. 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

23. 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

24. 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: ; 2Dumstorf CA, et al. Mol Cancer Ther 2010;9: ; 3Robertson MJ, et al. J Clin Oncol 2007;25: 24

25. 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:
The PRELUDE Trial 25

26. 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
Patients at risk, n:
Disease-Free Survival Time (months)
Patients at Risk, (n):
Disease-free Survival Time (months)
Enza:
Placebo:
The PRELUDE Trial 26

27. Disease-free Survival – GCB vs. Non-GCB by Hans’ Algorithm
GCB (N=109)
Non-GCB (N=106)
Time (Months)
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
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

28. 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

29. 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

30. 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

31. 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?

32. 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

33. Participating Nations
Denmark
United States
Italy
Poland

34. Patient Population:126 Pts.
Stage I 8%
Stage %
Stage %
Stage %
B Sxs %
Bulky %

35. 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 % 61%
Specificity % 97%
Concordance >90%

36. 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

37. 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

38. 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.

39. 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

40. 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.

41. 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.

42. 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

43. 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

44. 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

45. 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

46. 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.

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

48. 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

49. 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

50. 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)

51. Overall Survival by Cycle 4 PET Status

52. 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

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

54. 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

55. 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.

56. 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.

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

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

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

60. 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)

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

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

63. 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)

64. 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

65. 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.

66. 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)

67. THANK YOU FOR
YOUR ATTENTION