Katherine Walsh, MD Assistant Professor of Clinical Internal Medicine The Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute

1. Updates in Myeloproliferative Disorders,
including Chronic Myeloid Leukemia
Katherine Walsh, MD
No conflicts of interest to disclose
Off-label use: pegIFN, ruxolitinib in combination with azacitidine, investigational
agents

2. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
Objectives
 To discuss clinical updates in Philadelphia
chromosome negative myeloproliferative disorders
(MPDs).
 To discuss clinical updates in chronic myeloid
leukemia.

3. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
 Single agent studies
 Late breaking abstract: Pacritinib (PERSIST-2)
 Combination therapy studies
 Ruxolitinib plus additional agent
 Additional abstracts of interest
MPD Updates

4. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
RESULTS OF THE PERSIST-2 PHASE 3
STUDY OF PACRITINIB (PAC) VERSUS
BEST AVAILABLE THERAPY (BAT),
INCLUDING RUXOLITINIB (RUX), IN
PATIENTS WITH MYELOFIBROSIS (MF)
AND PLATELET COUNTS ≤100,000/ΜL
John Mascarenhas1, Ronald Hoffman1, Moshe Talpaz2, Aaron T. Gerds3, Brady
Stein4, Vikas Gupta5, Anita Szoke6, Mark Drummond7, Alexander Pristupa8, Tanya
Granston9, Robert Daly9, James P. Dean9, Suliman Al-Fayoumi9, Jennifer A.
Callahan9, Jack W. Singer9, Jason Gotlib10, Catriona Jamieson11, Claire Harrison12,
Ruben Mesa13, Srdan Verstovsek14
1Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; 2University of Michigan, Comprehensive
Cancer Center, Ann Arbor, MI, USA; 3Cleveland Clinic, Cleveland, OH, USA; 4Northwestern University, Feinberg School of
Medicine, Chicago, IL, USA; 5Princess Margaret Cancer Center, University of Toronto, Ontario, Canada; 6Albert Szent-Györgyi
Clinical Center, University of Szeged, Szeged, Hungary; 7Beatson West of Scotland Cancer Centre, Glasgow, UK; 8Ryazan’s
Clinical Hospital, Ryazan, Russia; 9CTI BioPharma Corp., Seattle, WA, USA; 10Stanford University Medical Center, Stanford, CA,
USA; 11University of California-San Diego, La Jolla, CA, USA; 12Guy's and St Thomas' NHS Foundation Trust, London UK;
13Mayo Clinic, Scottsdale, AZ, USA; 14MD Anderson Cancer Center, Houston, TX, USA.
Slides provided by presenting author Dr. Mascarenhas

5. Background
• MF is a life-threatening hematologic malignancy characterized by
splenomegaly and debilitating constitutional symptoms1-3
• ~1/4 of MF pts present with thrombocytopenia;4 platelets <50,000/µL associated with
reduced QoL,1 more severe symptom burden, and shorter overall survival5
• Approved JAK1/2 inhibitor RUX reduces splenomegaly and symptoms,
but is associated with dose-limiting cytopenias and not indicated for pts
with platelets <50,000/µL6,7
• PAC: oral kinase inhibitor with specificity for JAK2, FLT3, IRAK1, & CSF1R8
• PERSIST-1 trial: sustained spleen volume reduction (SVR) and symptom
control with PAC vs BAT (excluding JAK2 inhibitors) in pts with MF
regardless of baseline platelet count9
• PAC placed on full clinical hold by the US FDA (2/8/2016) due to
concerns over interim survival results, bleeding, and cardiovascular events
1. Tefferi A, et al. Blood. 2013;122:1395-1398. 2. Mesa et al. Cancer. 2007;109:68-76. 3. Geyer HL, et al. Blood. 2014;124:3529-3537. 4. Tefferi A, et al. Mayo Clinic Proc. 2012;87:25-33.
5. Alhuraiji A, et al. J Clin Oncol. 2016;34(suppl):abstract 7068. 6. Harrison C, et al. N Engl J Med. 2012;366:787-798. 7. Verstovsek S, et al. N Engl J Med. 2012;366:799-807.
8. Hart S, et al. Leukemia. 2011;25:1751-1759. 9. Mesa RA, et al. ASCO 2015. Abstract LBA7006.

6. Key Eligibility
Criteria
• Primary/
secondary MF
• Platelets
≤100,000/µL,
• Prior JAK2
inhibitors allowed 1:1:1
Randomization
(N=311)
BAT
(including RUX)
PAC
400 mg QD
PAC
200 mg BID
PERSIST-2 Phase 3 Study Design
• In PK simulations, PAC 200 mg BID was predicted to have higher Cmin and
lower Cmax than PAC 400 QD
• Crossover from BAT allowed after progression (any time) or at Wk 24
• Study Objectives:
• Primary: efficacy of pooled QD and BID PAC vs BAT
• Secondary: efficacy of QD PAC or BID PAC separately vs BAT
PK, pharmacokinetics; PPV, post-polycythemia; PET, post-essential thrombocythemia.
Co-Primary Endpoints
(Wk 24)
% of pts achieving
≥35% SVR
and
% of pts achieving
≥50% reduction in TSS*
Co-Primary Endpoints
(Wk 24)
% of pts achieving
≥35% SVR
and
% of pts achieving
≥50% reduction in TSS*
*TSS, total symptom score by MPN-SAF 2.0

7. Patient Demographics
(ITT Efficacy Population*)
Characteristic
PAC QD
n=75
PAC BID
n=74
BAT
n=72
Median age, yrs (range)
≥65 yrs, n (%)
69 (39-85)
53 (71)
67 (39-85)
46 (62)
69 (32-83)
51 (71)
Male, n (%) 38 (51) 48 (65) 39 (54)
ECOG PS, n (%)
0-1
2-3
57 (76)
17 (23)
65 (88)
8 (11)
54 (75)
15 (21)
MF diagnosis, n (%)
Primary
PPV
PET
46 (61)
16 (21)
13 (17)
55 (74)
14 (19)
5 (7)
43 (60)
16 (22)
13 (18)
DIPSS risk category, n (%)
Int-1
Int-2
High
13 (17)
40 (53)
22 (29)
14 (19)
38 (51)
22 (30)
13 (18)
37 (51)
22 (31)
JAK2V617F positive, n (%) 60 (80) 59 (80) 51 (71)
*Included all pts with randomization date that allowed them to contribute data for a wk 24 endpoint
(pts randomized prior to September 7, 2015; ≥ 22 wks prior to clinical hold)

8. Patient Demographics (Cont’d)
(ITT Efficacy Population)
Characteristic
PAC QD
n=75
PAC BID
n=74
BAT
n=72
Median spleen length by physical
exam, cm (range) 13 (3-33) 15 (5-32) 13 (2-34)
Platelet count <50,000/µL, n (%) 38 (51) 31 (42) 32 (44)
Hemoglobin <10 g/dL, n (%) 45 (60) 44 (59) 41 (57)
Peripheral blasts category, n (%)
0-<1%
≥1%
0-<5%
≥5%
Missing
41 (55)
30 (40)
62 (83)
9 (12)
4 (5)
38 (51)
30 (41)
61 (82)
7 (9)
6 (8)
36 (50)
31 (43)
60 (83)
7 (10)
5 (7)
White blood cell category, n (%)
>25 x 109/L
≤25 x 109/L
15 (20.0)
60 (80.0)
17 (23)
57 (77)
14 (19)
58 (81)
Received prior RUX, n (%) 31 (41.3) 31 (42) 33 (46)

9. Efficacy: Analysis by Arm
RUX (n=22)
Other (n=28)
RUX (n=22)
Other (n=29)
14.7%* 21.6%* 2.8%
17.3% 32.4%* 13.9%

10. Most Common TEAEs (≥10%)
Characteristic
PAC QD
n=104
PAC BID
n=106
BAT
n=98
Pts with ≥1 TEAE 104 (100) 100 (94) 87 (89)
Diarrhea 70 (67) 51 (48) 15 (15)
Nausea 39 (38) 34 (32) 11 (11)
Thrombocytopenia 34 (33) 36 (34) 23 (23)
Anemia 29 (28) 25 (24) 15 (15)
Vomiting 22 (21) 20 (19) 5 (5)
Fatigue 18 (17) 18 (17) 16 (16)
Peripheral edema 14 (13) 21 (20) 15 (15)
Dizziness 15 (14) 16 (15) 5 (5)
Abdominal pain 20 (19) 10 (9) 19 (19)
Pyrexia 11 (11) 16 (15) 3 (3)
Decreased appetite 13 (13) 13 (12) 11 (11)
Epistaxis 11 (11) 13 (12) 13 (13)
Constipation 15 (14) 8 (8) 6 (6)
Insomnia 12 (12) 10 (9) 4 (4)
Pruritus 10 (10) 11 (10) 6 (6)
Cough 11 (11) 9 (8) 10 (10)
Dyspnea 9 (9) 11 (10) 9 (9)
Upper respiratory tract infection 8 (8) 11 (10) 6 (6)
Characteristic
PAC QD
n=104
PAC BID
n=106
BAT
n=98
Pts with ≥1 TEAE 104 (100) 100 (94) 87 (89)
Diarrhea 70 (67) 51 (48) 15 (15)
Nausea 39 (38) 34 (32) 11 (11)
Thrombocytopenia 34 (33) 36 (34) 23 (23)
Anemia 29 (28) 25 (24) 15 (15)
Vomiting 22 (21) 20 (19) 5 (5)

11. Conclusions
Despite study truncation due to the clinical hold:
• PAC (QD+BID) was significantly more effective than BAT
(including RUX) for SVR (p=0.001) and trended toward
improved TSS (p=0.079)
• PAC BID appeared more effective than PAC QD versus BAT
for SVR and TSS
• SVR and TSS responses to PAC BID were consistent across
demographic and disease risk characteristics
• PAC BID appeared to have a better benefit/risk profile than
BAT, which included RUX

12. RUXOLITINIB IN COMBINATION WITH
5-AZACYTIDINE AS THERAPY FOR
PATIENTS WITH MYELOFIBROSIS
Naval Daver, Jorge Cortes, Naveen Pemmaraju, Elias
Jabbour, Prithviraj Bose, Linghsa Zhou, Sherry Pierce,
Stephanie Van Derbur, Gautam Borthakur, Zeev Estrov,
Guillermo Garcia-Manero, Hagop Kantarjian, Srdan
Verstovsek
Department of Leukemia, The University of Texas M.D.
Anderson Cancer Center, Houston, Texas
Slides provided by presenter Dr. Daver

13. • Ruxolitinib 15-20 mg PO BID (cycles 1-
3)
• Azacytidine 25 mg/m2 IV daily x 5 days
(starting cycle 4 day 1)
• Azacytidine could be increased to
50mg/m2 and 75 mg/m2
• Cycles repeated every 4-6 weeks
13
Rux + Aza in MF:
Design

14. Rux + Aza in MF:
Response Criteria IWG-MRT 2013
14
CI (clinical improvement) definitions:
• CI Spleen (palpation):
 Baseline >10 cm, decreases by ≥50%,
 Baseline 5-10 cm, becomes non-palpable
 Baseline <5 cm, not eligible
•CI Total symptom score (TSS): >50% reduction
in MPN-SAF
•CI Hb:
•Transfusion independent: > 20 g/dL improvement
•Transfusion dependent: becomes independent
All CI must be maintained > 12 weeks
Tefferi et al., Blood 2013

15. IWG-MRT 2013 response N (%)
Objective response 28 (72)
Partial Remission 2 (7)
CI spleen + TSS 7 (25)
CI TSS + Hb 2 (7)
CI spleen; CR cyto [1 PR Jak2] 2 (7)
CI TSS; CR cyto 1 (4)
CI spleen+TSS+PR Jak2/ PR Jak2 2 (7)
CI TSS only/ CI spleen only 8 (28)/ 4(14)
No IWG response 11 (28)
Rux + Aza in MF:
IWG-MRT Responses (N=39)
15

16. Rux + Aza in MF:
Conclusion
16
• Rux with Aza feasible and promising:
IWG response = 72%;
>50% spleen reduction at 24 wks = 48%;
Overall >50% spleen reduction = 79%.
• Well tolerated: only one patient off study due to
cytopenia
• Encouraging improvement in BM fibrosis, needs
sequential confirmation
• Patients being followed for hemoglobin, OS, JAK2
allele and fibrosis.

17. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
Additional Abstracts of Interest
17
 PV/ET
 PROUD-PV [Abstract 475]: Ropeginterferon α-2b
(longer-acting pegIFN non-inferior to HU
 MPD-RC 112 (PV/ET) [Abstract 478: pegIFN-α (PEG)
vs HU, similar efficacy but more SE [Abstract 479]
 Myelofibrosis
 Momelotinib [Abstract 1123]: JAK1/2 inhibitor
 Improved anemia (20% durable), but 50% toxicity
including peripheral neuropathy
 Ruxolitinib + PI3K inhibitor [Abstract 1125]:
 In patients with lost/sub-optimal response to ruxolitinib
 Sotatercept [Abstract 478]: BlocksTGF-ß
 Small sample size, 4 patients with anemia response

18. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
 TKI Discontinuation:
 Imatinib: EURO-SKI
 Nilotinib: Nilst, ENESTop
 Dasatinib: D-STOP
 Definitions:
 MR3 = <0.1% on IS (MMR)
 MR4 = <0.01% on IS
 MR4.5 = <0.0032% on IS
CML Updates:

19. After Stopping Imatinib Treatment of CML:
No Differences in Molecular Relapse-Free Survival
Between Patients with Prior 4.5 Log Reduction
(MR4.5) but Detectable and Patients with
Undetectable Disease in the EURO-SKI Trial
Markus Pfirrmann for all project partners
E-mail: pfi@ibe.med.uni-muenchen.de
San Diego, 5th December 2016
Slides provided by presenter Dr. Pfirrmann

20. Study outline of EURO-SKI
20
Follow‐up
RQ‐PCR RQ‐PCR
every 3rd month
Screening
phase
(confirmation
of MR4 in
central lab)
Stop TKIInformed
consent
Year 1 Year 2 Year 3
MR4
≥ 1 year
q4w q6w
≤ 6 weeks
Patients included between May 2012 and December 2014
TKI treatment
≥ 3 years
Relapse:
Loss of MMR
MMR: 3‐log reduction of BCR‐ABL1

21. Results presented by Richter et al., EHA meeting 2016
21
Molecular relapse-free survival
Molecular relapse-free survival, MRFS
Mol.relapse-freesurvival
Months MRFS, % 95%-C.I.
6 62 59-67
12 56 52-59
24 52 48-56
36 49 44-53
n=750 (of 868) patients
fulfilling inclusion
criteria
 What are prognostic factors for remaining in molecular relapse-
free survival 6 months after TKI-stop?
Results at 6 months for
all patients available
Months since discontinuation of TKI

22. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
Cessation of Tyrosine Kinase Inhibitors
Treatment in Chronic Myeloid Leukemia
Patients with Deep Molecular Response:
Results of the Euro-Ski Trial
 Francois-xavier Mahon et al,, Johan Richter, MD,
Joelle Guilhot, PhD, Henrik Hjorth-Hansen, MD, PhD,
Antonio Almeida, MD, PhD, Jeroen J.W.M. JWM
Janssen, MD, Jiri Mayer, Kimmo Porkka, MD, PhD,
Panayiotis Panayiotidis, MD, PhD, Ulla Stromberg, MD
PhD, Marc G Berger, MD, PhD, Professor, Joanna
Diamond, Hans Ehrencrona, MD, PhD, Veli Kairisto,
Katerina Machova Polakova, Martin C. Mueller, Prof.,
Satu Mustjoki, MD, PhD, Andreas Hochhaus, MD,
Markus Pfirrmann, PhD and Susanne Saussele, MD
22

23. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
EURO-SKI Results: Imatinib Subgroup
 821 patients enrolled on study
 448 treated with imatinib
 Predictors of sustained MMR at 6 months:
 Treatment duration with imatinib and MR4 duration
prior to the stop (p<0.001)
 Conclusion: Stopping TKI therapy appears feasible and
safe in this large cohort study.
23
Treatment >5.8 years ≤ 5.8 years
MMR at 6 months 65.5% 42.6%

24. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
 Norimitsu Kadowaki, MD, PhD, Tatsuya
Kawaguchi, MD, PhD, Junya Kuroda, MD, PhD,
Hirohisa Nakamae, MD, PhD, Itaru Matsumura, MD,
PhD, Toshihiro Miyamoto, MD, PhD, Jun Ishikawa,
MD, PhD, Koji Nagafuji, MD, PhD, Yutaka Imamura,
MD, PhD, Hirohito Yamazaki, Mototsugu Shimokawa,
PhD, Koichi Akashi, MD, PhD and Yuzuru Kanakura,
MD, PhD
Discontinuation of Nilotinib in Patients
with Chronic Myeloid Leukemia Who
Have Maintained Deep Molecular
Responses for at Least 2 Years: A
Multicenter Phase 2 Stop Nilotinib (Nilst)
Trial
24

25. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
 Consolidation
with 2 years of
nilotinib
 Primary
endpoint:
MR4.5 at 1 year
= 58.9%
 Longer duration
of therapy pre-
stop did not
correlate with
maintenance of
response
Nilst Trial: n=90 patients, MR4.5

26. 26
Treatment-Free Remission in
Patients With Chronic Myeloid Leukemia
in Chronic Phase According to Reasons
for Switching From Imatinib to Nilotinib:
Subgroup Analysis From ENESTop
Timothy P. Hughes, Carla Boquimpani, Naoto Takahashi, Noam Benyamini,
Nelma Cristina D. Clementino, Vasily Shuvaev, Sikander Ailawadhi,
Jeffrey H. Lipton, Anna G. Turkina, Beatriz Moiraghi, Franck E. Nicolini,
Jolanta Dengler, Tomasz Sacha, Dong-Wook Kim, Rafik Fellague-Chebra,
Sandip Acharya, Nancy Krunic, Yu Jin, François-Xavier Mahon
Slides provided by presenter Dr. Hughes

27. 27
ENESTop: Ongoing Single-Arm, Phase 2 Study
• Adults with CML-CP
• ≥ 3 years of TKI
therapy (first imatinib
for > 4 weeks, then
nilotinib for ≥ 2 years)
• No documented MR4.5
at time of switch to
nilotinib
• Achieved MR4.5 on
nilotinib
• Adults with CML-CP
• ≥ 3 years of TKI
therapy (first imatinib
for > 4 weeks, then
nilotinib for ≥ 2 years)
• No documented MR4.5
at time of switch to
nilotinib
• Achieved MR4.5 on
nilotinib
Nilotinib
consolidation
phase
(52 weeks)
Nilotinib
consolidation
phase
(52 weeks)
TFR phase
(up to 192 weeks after last
patient entered TFR phase)
TFR phase
(up to 192 weeks after last
patient entered TFR phase)
RQ-PCR every
12 weeks
EnrollEnroll No confirmeda loss of MR4.5
TFR-2 phase
(up to 192 weeks
after last patient
entered TFR phase)
TFR-2 phase
(up to 192 weeks
after last patient
entered TFR phase)
Nilotinib
treatment
reinitiation
phase
Nilotinib
treatment
reinitiation
phase
Nilotinib
continuation
phasec
(52 weeks)
Nilotinib
continuation
phasec
(52 weeks)
No confirmeda
loss of MR4.5
Criteria for reinitiating
nilotinib:
• Loss of MMR
or
• Confirmedb loss
of MR4
Confirmeda
loss of
MR4.5
1st year: RQ-PCR every 4 weeks
2nd year: RQ-PCR every 6 weeks
Thereafter: RQ-PCR every 12 weeks
MR4.5, BCR-ABL1IS ≤ 0.0032%; RQ-PCR, real-time quantitative polymerase chain reaction.
a Confirmed loss of MR4.5 was defined as BCR-ABL1IS > 0.0032%, confirmed in a second assessment within 4 weeks.
b Confirmed loss of MR4 was defined as BCR-ABL1IS > 0.01%, confirmed in a second assessment within 4 weeks.
c Patients with confirmed loss of MR4.5 during the continuation phase continued nilotinib treatment in the prolonged continuation phase until 192 weeks
after the last patient entered the TFR phase or until discontinuation due to unacceptable toxicity, disease progression, investigator discretion, or
withdrawal of consent.
 Primary endpoint: proportion of patients in TFR (no loss of MMR, no confirmed
loss of MR4, and no reinitiation of treatment) at 48 weeks after stopping nilotinib
Proportion of patients who entered the
TFR phase:
• Overall population: 126/163 (77%)
• Intolerance subgroup: 51/59 (86%)
• Resistance subgroup: 30/38 (79%)
• Physician preference subgroup: 45/66 (68%)

28. 28
Time to Loss of Response in the TFR Phase
by Reasons for Switch
 Kaplan-Meier–estimated median duration of TFR was not reached by
the data cutoff date
51:0 44:7 31:20 30:21 24:21 16:21 9:21 1:21
30:0 24:6 17:13 16:14 13:14 7:14 2:14 0:14
44:0 38:6 28:16 28:16 24:17 13:17 3:17 0:17
0:21
12 24 36 48 60 72 84 96
20
10
0
50
40
30
60
80
70
90
100
0
Time Since TFR, weeks
Intolerance
Resistance
Physician preference
Censored observations
Pts Evt Cen
51
30
44
21
14
17
30
16
27
PatientsWithoutLossofMMRor
ConfirmedLossofMR4,%
Intolerance
Resistance
Physician preference
At risk:Events

29. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
Discontinuation of Dasatinib after Deep
Molecular Response for over 2 Years in
Patients with Chronic Myelogenous
Leukemia and the Unique Profiles of
Lymphocyte Subsets for Successful
Discontinuation: A Prospective,
Multicenter Japanese Trial (D-STOP Trial)
Takashi Kumagai, MD, PhD, Chiaki Nakaseko, MD, Kaichi
Nishiwaki, M.D, PhD, Chikashi Yoshida, MD, PhD,
Kazuteru Ohashi, Naoki Takezako, MD, PhD, Hina Takano,
M.D, PhD, Yasuji Kouzai, MD, PhD, Tadashi Murase, MD,
PhD, Kosei Matsue, MD, PhD, Satoshi Morita, PhD, Prof,
Junichi Sakamoto, MD, PhD, Hisashi Wakita, MD, PhD,
Hisashi Sakamaki, MD, PhD and Koiti Inokuchi, MD, PhD,
Prof
29

30. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
 65 patients enrolled at
IS <0.01%
 Consolidation with
dasatinib for 2 years
 62.9% TFS at 12mos
feasible with relatively
high TFS
 Unique profile of
lymphocyte subsets
reported that may be
able to predict
successful
discontinuation
D-STOP results
At 12 months

31. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
TKI Discontinuation Criteria (NCCN, 1/2017)
 Chronic phase CML only
 Duration of treatment: At least 3 years
 Depth of response: stable MR4 (IS <0.01%) for at least 2
years
 On at least 4 tests, 3 months apart
 Depth of response recommended to remain off of TKI:
MR3 (IS <0.1%)
 Patients must have access to reliable PCR testing on the IS with
results available within 2 weeks while off of TKI
 Recommended monitoring while off of TKI:
 MONTHLY PCR testing for the first 6 months
 Bimonthly for months 7-24 if MMR sustained
 Quarterly for months 25 and beyond as long as MMR sustained
 If loss of MMR at any time, prompt resumption MONTHLY
testing for the first 6 months with resistance testing if not back in
MMR after resuming TKI by 6 months

32. The Ohio State University Comprehensive Cancer Center –
Arthur G. James Cancer Hospital and Richard J. Solove
Research Institute
MPD Summary
 Current therapy updates:
 TKI Discontinuation: NCCN guidelines released
January 2017
 Areas of ongoing and future investigation:
 PV/ET: pegIFN-α (PEG)
 Myelofibrosis: JAK2 inhibitors, combination of JAK2
inhibitors with novel agents, and development of
novel agents
 CML: Potential for second TKI discontinuation attempt
and novel agents (ABL-001, Abstract 625)
32