latest concepts in large cell and hodgkin lymphomas

LATEST CONCEPTS IN LARGE CELL AND HODGKIN LYMPHOMAS

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

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


Disclosures for Morton Coleman, MD

Employment None

ConsultancyCelgene, Genzyme, GlaxoSmithKline, Millenium, Onyx, Spectrum

Equity Ownership Immunomedics

Research Funding Glaxo Smith Kline, Onyx

Honoraria None

Patents & Royalties None

In compliance with ACCME policy, ASH requires the following disclosures to the session audience:

2012

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Disclosures for Morton Coleman, MD, con’t

Speakers Bureau None

Membership on Board of Directors/Advisory Committee Immunomedics, Glaxo Smith Kline

Other None

Presentation includes a description of the following off-label use of a drug or medical device

None

In compliance with ACCME policy, ASH requires the following disclosures to the session audience:

2012

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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

R-CHOP14 533 438 355 224 102 25 1

Patients at Risk

R-CHOP21 534 429 358 216 116 25 1

Years from randomisation

R-CHOP21

R-CHOP14

Pro

babi

lity

0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1.0

0 1 2 3 4 5 6

0.99 (0.79–1.24)HR (95% CI)

p=0.94Log-rank test

75%75%2-yr FFS

153 (28)155 (29)Events, n (%)

R-CHOP14R-CHOP21

Cunningham et al, ASCO 2011

N=22831%

Gisselbrecht C, et al. J Clin Oncol 2009; 27(15s): Abstract 8509.

DLBCL patients who recur post R-CHOP-21 do not do well

Overall survival of patients with DLBCL refractory to

second line therapy is very poor

Elstrom et al , Clin Lymph Myel Leuk, 2010

0 5 10 15 20 250 5 10 15 20 25

0.00

0.

25

0.50

0.

75

1.00

0.00

0.

25

0.50

0.

75

1.00

Pro

po

rtio

n o

f P

atie

nts

Pro

po

rtio

n o

f P

atie

nts

Time (months)Time (months)

Rosenwald A et al. N Engl J Med. 2002;346:1937-1947

Germinal center vs activated B cell DLBCL

Lenz G, et al, NEJM November 27, 2008

Outcome by GCB vs non-GCB gene signatures in DLBCL

N=233 patients treated with R-CHOP

PFS OS

CD10+

-

BCL6

-

GCB

non-GCB+

MUM1+ -

?

?

BCL2

FOXP1

HGAL

Non-GCB DLBCL is associated with high expression of target genes of

NF-kB transcription factors

Davis, et al, J Exp Med 2001

Ruan et al, JCO 2010

CHOP-R + bortezomib DLBCL PFS and OS by subtype (n = 40)

PYRAMID study designDLBCL

diagnosis & subtyping

GCB

Not enrolled

Non-GCB

R

Vc-R-CHOPBortezomib 1.3 mg/m2, d 1, 4

Rituximab 375 mg/m2, d 1Cyclophosphamide 750 mg/m2, d 1

Doxorubicin 50 mg/m2, d 1Vincristine 1.4 mg/m2, d 1

Prednisone 100 mg/d, d 1–5Six treatment cycles q21 days

R-CHOPRituximab 375 mg/m2, d 1

Cyclophosphamide 750 mg/m2, d 1Doxorubicin 50 mg/m2, d 1Vincristine 1.4 mg/m2, d 1

Prednisone 100 mg/d, d 1–5Six treatment cycles q21 days

Follow up every 3 months for 2 yrs

Hans method

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

Aukema et al, Blood 2011

StudyN 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 NA NA NA 56%

Johnson 2009

54/54 (100%)

46% 62 76% 50% 71% NA 35% 70%

Kanungo 2006

14/14 (100%)

None 55 NA 93% 79% 21% 57% NA

Le Gouill 2007

16/16 (100%)

25% 61 100% 100% 94% 50% 88% 81%

Macpherson 1999

15/39 (38%)

46% 65 92% 80% 69% NA 62% 90%

Niitsu 2009 19/19 (100%)

None 61 100% 100% 84% 21% 63% 89%

Snuderl 2010

20/20 (100%)

15% 64 95% 100% 59% 45% 30% 85%

Tomita 2009 27/27 (100%)

17% 51 96% 93% 65% 9% 65% 87%

R-CHOP and MYC rearranged DLBCL

Barrans et al, JCO 2010

EFS

OS

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

DA-R-EPOCH and MYC+ DLBCL

Dunleavy et al, Lugano 2011

EFS

OS

9 MYC+ DLBCL

99 MYC- DLBCL

Similarrisk by IPI

High RR/PFS inBL

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

ASH 2013, Abstract 40

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

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

ASH 2013, Abstract 371

Background

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.

R-CHOP = rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone.

The PRELUDE Trial

• 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

Background

• PKCβ is the major isoform expressed in normal and malignant B cells.1,2

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.

• 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.

BTK

PI 3K

AKT

mTOR

PLC2

PKCβ

SYK

PP

IKK

NFKB

The PRELUDE Trial

Disease Free Survival by Treatment Arm for ITT Population

p=0.541

Enzastaurin

Placebo

HR (95% Cl): 0.92 (0.689, 1.216)P = 0.541

Su

rviv

al P

rob

abil

ity

Disease-Free Survival Time (months)Patients at Risk, (n):

504 383 348 259 157 45254 197 165 138 74 18

0 6 12 18 24 30 36 42 48 54 60 66 72 78

Disease-free Survival Time (months)Patients at risk, n:

Enza:Placebo:

100

80

60

40

20

0

The PRELUDE Trial

Disease-free Survival – GCB vs. Non-GCB by Hans’ Algorithm

GCB vs. non-GCB in the Enzastaurin Arm GCB vs. non-GCB in the Placebo Arm

GCB vs. non-GCB in the Combined Arm

GCB, Enzastaurin (N=79)

Non-GCB, Enzastaurin (N=66)

GCB, Placebo (N=30)

Non-GCB, Placebo (N=40)GCB, Enzastaurin (N=79)

Non-GCB, Enzastaurin (N=66)

GCB, Placebo (N=30)

Non-GCB, Placebo (N=40)

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

1.0

0.9

0.8

0.7

0.6

0.5

1.0

0.9

0.8

0.7

0.6

0.5

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

GCB (N=109)

Non-GCB (N=106)

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

HR (95% Cl): 0.92 (0.56, 1.52)P=0.74

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

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

Initial treatment: ABVD x 3

Reassessment: if NR/PD, patient goes off studyif CR/PR, FDG-PET scan performed

4th cycle ABVD then IFRT Randomization

IFRT No further treatment

PET-positive PET-negative

RAPID Trial Design

Radford J, et al. Blood. 2012;120: Abstract 547.

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%

Outcomes After Median Follow-Up of 45.7 Months


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%


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


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


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

2 ABVD + 20 Gy IFRT

Comparison of NCIC CTG HD.6 and GHSG HD10 and HD11 Staging, Eligibility and

Preferred Arms

4 ABVD + 30 Gy IFRT

4 – 6 ABVD alone

Early, unfavorable

HD11

Early, favorable

HD10

AdvancedHD.6

FavorableUnfavorable

NCIC CTG

GHSG

Advanced

Not necessarily to scale

Hay AE, et al. Blood. 2012;120: Abstract 549.

Very good prognosis B or Bulk

Early, unfavorable

HD11

Early, favorable

HD10

AdvancedHD.6

FavorableUnfavorable

NCIC CTG

GHSG

Advanced

Not necessarily to scale


Comparison of NCIC CTG HD.6 and GHSG HD10 and HD11 Staging, Eligibility and Preferred ArmsComparison of NCIC CTG HD.6 and GHSG HD10 and HD11 Staging, Eligibility and Preferred Arms

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

PD/OS

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% 95% 1.09 (0.49, 2.40) 19 10

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


What’s new for refractory/relalpsing disease?

Evolving Data on Brentuximab Vedotin

Brentuximab Vedotin Mechanism of Action

Brentuximab vedotin (SGN-35) ADCmonomethyl auristatin E (MMAE), potent antitubulin agent

protease-cleavable linker

anti-CD30 monoclonal antibody

ADC binds to CD30

MMAE disruptsmicrotubule network

ADC-CD30 complex traffics to lysosome

MMAE is released

Apoptosis

G2/M cellcycle arrest

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

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

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?

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

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

A(B)VD

Brentuximab Vedotin

Cycle 1 Cycle 2 Cycle 3

6 Cycles +/- XRT

Weeks0 2 4 6 8 10 12

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 0 1 (4)

Not evaluable due to AEs 1b (5) 0

• 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


Progression-Free Survival(Not a predefined study endpoint)


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 10

Septic / toxic shock 1 4

Hepatic 2 2

Cardiac 1

Neurological 1

Allergy to etoposide 1Carde et al. J Clin Oncol 30, 2012 (suppl; abs 8002)

Event-Free Survival


Overall Survival


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”


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

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.

SUMMARY

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 KetasJessica HansenKaren WeilJennifer O’LoughlinRebecca Elstrom, M.D. (Gen.)Lale Kostakoglu, M.D. (Sinai)Stanley Goldsmith, M.D.

Biostatistician

Ken Chueng, Ph.D. (Columbia)

Madhu Mazumdar, Ph.D. (Cornell)

Translational Core Maureen Lane, Ph.D. (Cornell)Maureen Ward

Laboratory Research Ari Milneck, M.D., Ph.D.(Cornell)Katherine Hajjar, M.D. (Cornell)Shahin Rafii, M.D. (Cornell)


ASCO Foundation (YIA, CDA)

NIH / NHLBI

THANK YOU FOR

YOUR ATTENTION

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