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Hematologic Malignancies: A Review of Key Clinical Studies

Ian W. Flinn, MD, PhD
Shaji K. Kumar, MD
Farhad Ravandi, MD
Released: September 23, 2020


Phase Ib Study of Magrolimab Plus Azacitidine in Patients With Myelodysplastic Syndromes or Acute Myeloid Leukemia

Farhad Ravandi, MD
We will now switch topics and discuss interesting new data from ASCO 2020 on leukemias. This study by Sallman and colleagues is very important because of the interest in checkpoint inhibitors in various malignancies and because checkpoint inhibitors such as PD-1 and PD-L1 inhibitors have shown some activity in hematologic malignancies. Magrolimab is an entirely new antibody, a first-in-class anti-CD47 macrophage immune checkpoint inhibitor that promotes tumor cell elimination through macrophage phagocytosis.[16,17] CD47 is a protein that prevents macrophage phagocytosis; thus, CD47 inhibition may allow activation of that pathway. This study examined the safety and efficacy of magrolimab plus azacitidine in patients with untreated myelodysplastic syndrome (MDS) and older unfit AML.

In the safety evaluation cohort of this multicenter phase Ib study, patients with untreated AML who were ineligible for induction cell transplant or untreated MDS (N = 68) received a 1-mg/kg priming dose of magrolimab followed by a dose ramp-up to 30 mg/kg by Week 2 plus 75 mg/m2 of azacitidine on Days 1-7. The safety evaluation phase was followed by an expansion phase with primary endpoints of safety and efficacy. The secondary endpoints included magrolimab pharmacokinetics, pharmacodynamics, and immunogenicity. Exploratory endpoints were CD47 receptor occupancy, immune activity markers, and molecular profiling.

The study enrolled 39 patients with MDS and 29 with AML (median age: 70 and 74 years, respectively). The patients with AML were not fit to receive intensive chemotherapy. All patients had to have intermediate or adverse risk cytogenetics to be enrolled; most of the patients with MDS were in the high or very high International Prognostic Scoring System (IPSS), revised, scoring category. Approximately 31% of MDS patients had therapy-related MDS, and 45% of the AML population carried the TP53 mutation.

Magrolimab Plus Azacitidine in Patients With MDS and AML: Response

Farhad Ravandi, MD
In 58 treated patients, ORR was 91% in patients with MDS (n = 33) and 64% in patients with AML (n = 25). The CR rate was similar for patients with MDS or AML (42% vs 40%). Red blood cell transfusion independence was achieved by 58% of the patients with MDS and 64% of the patients with AML. A cytogenetic response was seen in approximately 50% of patients with AML and 35% of patients with MDS. Interestingly, 50% of the patients with AML who had been assessed for MRD were MRD negative after treatment. The median duration of response was not reached for either cohort, but the median follow-up was short: 5.8 months for MDS and 9.4 months for AML.

Magrolimab Plus Azacitidine in Patients With MDS and AML: Response in Patients With TP53 Mutation

Farhad Ravandi, MD
There is strong interest in TP53‑mutated AML and MDS because other strategies have had only a limited response duration in this setting. Studies have suggested that hypomethylating agents can produce high responses, but these are generally also of limited duration.[18]

This study included patients with TP53‑mutated MDS (n = 12) and AML (n = 4), who responded well to the study regimen. Patients achieved a combined CR/CRi of 75% in both arms; CR alone occurred in 42% of patients with MDS and 50% of patients with AML TP53 mutant groups. The median duration of response was not reached for either TP53 cohort, and a 6-month OS was achieved in 100% of patients with AML and 91% of patients with MDS. Admittedly, the study involved a very small number of patients, but the data are intriguing.

Magrolimab Plus Azacitidine in Patients With MDS and AML: Safety

Farhad Ravandi, MD
The results of this study show that magrolimab is safe and can be added to azacitidine without a significant increase in toxicity and without an increased risk for infections, cytopenias, or immune‑related AEs, which we have encountered with other checkpoint inhibitors. No deaths occurred before Day 60 of follow-up. Only 1 patient (1.5%) discontinued treatment because of AEs.

Magrolimab Plus Azacitidine in Patients With MDS and AML: Conclusion

Farhad Ravandi, MD
This is an early report of the magrolimab plus azacitidine combination; larger randomized studies are ongoing. Magrolimab is a nontoxic addition to azacitidine and, perhaps in the future, to other hypomethylating agents. Because it does not appear to increase toxicity, the magrolimab plus azacitidine combination may become a standard of care in both high‑risk MDS and in elderly unfit AML, especially if it results in significant improvements in response, DoR, or survival.

Enasidenib Plus Azacitidine vs Azacitidine Monotherapy in mIDH2 Newly Diagnosed AML

Farhad Ravandi, MD
Another area of interest in AML treatment is the use of drugs that specifically target mutant pathways in AML. Mutations in the isocitrate dehydrogenase (IDH) enzymes result in the accumulation of 2‑hydroxyglutarate, which blocks important pathways in the epigenetic machinery of cells and results in leukemic transformation. IDH1 and IDH2 mutations have been reported in patients with AML—8% to 20% of patients with AML have IDH2 mutations, and the incidence increases with age.[19,20]

Enasidenib is an oral small-molecule inhibitor of mutated IDH2 that promotes myeloid cell differentiation and blocks 2-HG function. It has been approved by the FDA for use in the treatment of patients with IDH2-mutated R/R AML.[21-23] In previous studies, enasidenib monotherapy achieved a 30% response rate and a 20% CR.[24] Azacitidine has become a standard-of-care agent for older unfit patients with AML after showing reasonable but not dramatic activity in numerous studies.

This open‑label, randomized, multicenter phase I/II study enrolled patients with newly diagnosed AML who were ineligible for intensive chemotherapy. In the phase I portion, patients were grouped according to mIDH and then into 3 dose-finding cohorts: 500 mg ivosidenib (an IDH1 inhibitor plus azacytidine); 100 mg enasidenib plus azacitidine, and 200 mg enasidenib plus azacitidine, with this phase establishing safety.

In the current report from this study, investigators examined the addition of enasidenib 100 mg daily to azacitidine (n = 68) and compared it with azacitidine monotherapy (n = 33) in newly diagnosed, older, and unfit patients with AML with an IDH2 mutation. All patients had the IDH2 mutation; isoforms R140 and R172 were present in 75% and 24% of patients, respectively. The majority of patients (71% and 76% in each arm) had de novo AML rather than secondary AML. The primary endpoint was ORR; the key secondary endpoints were CR, safety, OS, and event-free survival (EFS).

Enasidenib Plus Azacitidine in Patients With Newly Diagnosed AML: Response

Farhad Ravandi, MD
The ORR was 71% with enasidenib plus azacitidine vs 42% with azacitidine alone (P = .0064). The CR was dramatically higher at 53% vs 12% respectively (P = .0001). Combined CRi/CR with incomplete platelet recovery (CRp) was 10% and 12%, respectively. The time to response was similar for both arms (1.9 vs 2.0 months), and time to achieve a CR was 5.5 months in the enasidenib arm vs 3.7 months with azacitidine alone. The DoR was double for the combination arm (24 months vs 12 months).

Enasidenib Plus Azacitidine in Patients With Newly Diagnosed AML: Safety

Farhad Ravandi, MD
Overall, there was no significant difference between the 2 arms for AEs commonly seen in this population, such as thrombocytopenia (62% vs 44%), nausea (69% vs 38%), anemia (53% vs 44%), and vomiting (49% vs 47%). IDH differentiation syndrome, associated with enasidenib, was seen in 18% of that patient cohort (all grades), with 10% (n = 7) having grade 3/4.[24]

Enasidenib Plus Azacitidine in Patients With Newly Diagnosed AML: OS and EFS

Farhad Ravandi, MD
The EFS is superior for the combination arm at 17.2 months vs 10.8 months with azacitidine alone (HR: 0.59; P = .1278).

Surprisingly, there is no difference in OS between arms (22.0 vs 22.3; HR: 0.99; P = .9686). However, 21% of patients in the azacitidine alone arm (n = 7) who progressed subsequently received enasidenib monotherapy, which could help to explain the OS anomaly.

Enasidenib Plus Azacitidine in Patients With Newly Diagnosed AML: mIDH2 VAF Suppression and 2-HG Reduction

Farhad Ravandi, MD
When considering the targeted IDH2 mutation, patients in the enasidenib plus azacitidine arm had a significantly greater reduction in variable allele frequency of mIDH2 (-83.4% vs -17.7%; P = .0008). The median maximal 2‑HG reduction with combination therapy was also significantly greater in the combination cohort vs azacitidine alone (-97.8% vs -54.3%; P = .0004).

Enasidenib Plus Azacitidine in Patients With Newly Diagnosed AML: Conclusion

Farhad Ravandi, MD
This study showed that greater and more significant responses can be achieved with azacitidine plus enasidenib combination therapy vs azacitidine alone in older patients with AML and IDH2 mutations who are unfit for intensive chemotherapy. A significant reduction in mIDH2 and 2-HG levels and significantly improved EFS was observed with combination therapy vs azacitidine alone. Although there was no difference in OS, keep in mind that the subsequent use of enasidenib in some patients who were randomized to azacitidine‑alone may have contributed to the overlapping OS.

AMG 330 BiTE in Patients With R/R AML: Update of First-in-Human Dose-Escalation Trial

Farhad Ravandi, MD
AMG 330 is a canonical bispecific T-cell engager (BiTE) molecule targeting CD3 and CD33. CD33 is on the surface of AML blasts and is a commonly used target for antibody drug development.[25-28] AMG 330 brings T-cells in close proximity to AML blasts by engaging the CD3 on the surface of T-cells and engaging the CD33 on the surface of AML blasts. This interaction results in T-cell activation and the killing of AML blasts. This study provides an update of the ongoing AMG 330 dose-finding study.

Patients with R/R AML were enrolled on this phase I dose escalation study, with the first 5 cohorts consisting of a single patient and subsequent cohorts in the classical 3+3 design. AMG 330 is a small-molecule drug that has to be administered by continuous intravenous infusion. The main toxicity of BiTE molecules is CRS; this can be mitigated, however, by various strategies (including the use of prophylactic dexamethasone), by developing a step-up dosing strategy, and through the use of tocilizumab (an anti–IL-6 antibody).

The first 5 cohorts established a dose of 10 µg/day as the initial dosing strategy. From cohort 6 onward, a dose step-up strategy of up to 480 µg was used. After this dose, a decision was made to have a 2-step dosing-up strategy. Thus, the subsequent cohorts went from 10 to 60 then up to 600; the last 2 cohorts had 2 step-up dosing steps, including 10 to 240, to 600, to 720, and then to 840. This step-up dosing strategy allows the delivery of much higher doses of AMG 330 to the patient while lowering the risk for CRS.

To date, 60 patients with R/R AML have been enrolled on this study: 62% have an adverse European LeukemiaNet risk classification, 50% have had ≥ 4 previous lines of therapy, and 45% have had a previous allogeneic stem cell transplant, all of which indicates a very heavily pretreated population. At the start of the study, every patient had previously had a grade ≥ 3 cytopenia, including 75% with thrombocytopenia, 58% with leukopenia, and 87% with neutropenia.

Phase I Study of AMG 330: Treatment-Related AEs

Farhad Ravandi, MD
As expected, the main AE encountered was CRS, which was seen in 67% of patients at all grades and in 15% of patients with grade ≥ 3. Elevated liver enzymes of grade ≥ 3 and rash of grade ≥ 3 were seen in 5% and 10% of patients, respectively. All other AEs encountered are commonly observed in patients with relapsed and refractory AML.

Various strategies were used to reduce CRS, including steroids before any step-up of the dosing level and tocilizumab at the first sign of significant CRS. A higher leukemic burden and higher effector:target cell ratio were associated with a higher incidence of CRS, and higher posttreatment levels of released cytokines such as IL-6 were associated with increased severity and frequency of CRS.

Phase I Study of AMG 330: Response

Farhad Ravandi, MD
Among 42 patients treated at a target dose ≥ 120 μg, there were 8 responders (19%) in this very heavily treated population, including 3 with CR, 4 with CRi, and 1 with morphological leukemia-free state, and the median response duration was approximately 40 days (range: 14-121). Some of the patients have had a significant response and, thus, were allowed to proceed to ASCT. There were more responders among patients with a lower (< 25%) leukemic burden at the time of treatment initiation, and there was no correlation between response and CD33 expression on leukemic blasts. Despite the fact that this was a very heavily treated population, 3 patients who had had ≥ 4 lines of previous therapy and even patients with adverse cytogenetics had a response. 

Phase I Study of AMG 330: Conclusions

Farhad Ravandi, MD
There is a lot of interest in bispecific antibodies, because they work by a different mechanism of action than conventional chemotherapy and are designed to induce the patient’s own immune system to attack leukemic cells. The CD19-directed CD3 T-cell engager, blinatumomab, is approved for patients with acute lymphoblastic leukemia (ALL). [29] Thus, we have hope for a similar agent in AML, because several of these bispecific antibodies, including AMG 330, are in development. We currently use continuous infusion dosing with blinatumomab in patients with ALL, but there are numerous molecules with a longer half-life that are being developed that could potentially be administered with a shorter infusion.

Another area of interest is the use of bispecific antibodies for the eradication of MRD. Based on a study showing an 80% MRD conversion rate, blinatumomab has been approved in patients with ALL to clear MRD. We hope that an agent such as AMG 330 will have similar efficacy in MRD eradication in AML. If more effective strategies produce higher responses in AML, but with persistent MRD, we can improve the DoR if we have an agent that has MRD clearance activity.

QUAZAR AML 001: Escalated Dosing Schedule for Early AML Relapse

Farhad Ravandi, MD
The QUAZAR AML‑001 study compared CC-486 with placebo for maintenance therapy in patients with AML. CC‑486 is an oral formulation of the hypomethylating agent azacytidine; it allows extended dosing of > 7 days/cycle, which may be important in terms of demethylation and increasing the response. The trial was a double‑blind, randomized phase III study in patients at least 55 years of age with AML in first CRi who had received previous induction therapy with or without consolidation and who were not considered eligible for allogeneic SCT during first remission. Patients had to be randomized within 4 months of achieving CR or CRi to receive either CC‑486 300 mg daily for 14 days in 28‑day cycles or placebo.

Overall, the use of CC‑486 was associated with significant improvement in OS (24.7 vs 14.8 months; HR: 0.69; P = .0009), and RFS (10.2 vs 4.8 months; HR: 0.65; 95% CI: 0.52-0.81; P = .0001). This is very important, because there has never been a study in AML that has shown improvement in survival using a maintenance strategy.[30]

There have been multiple studies of various agents for maintenance in the past. Some of these studies demonstrated improved RFS, but none has ever shown improvement in OS, mainly because of the small number of patients enrolled, drug toxicity, and a lack of adherence and compliance. The results of QUAZAR AML-001 showed that CC‑486 improved survival. In the presentation at ASCO 2020, the feasibility of using CC-486 in patients 75 years of age or older was examined.

This presentation focused on patients who received an escalating dosing schedule, in which they were randomized to CC-486 (n = 51) or placebo (n = 40) and monitored closely with bone marrow exams every 3 months to assess persistence of remission. Patients who had progression, either in peripheral blood or bone marrow, with increased blasts to > 5% but < 15%, were allowed to have an extended dosing of CC-486 or placebo. Median time to dose escalation was 9.2 months with CC-486 vs 6 months with placebo. There was a median of 2 escalated dosing cycles per arm, with > 3 in 43% of the CC-486 arm vs 18% of the placebo arm.

QUAZAR AML 001: Efficacy With Escalated Dosing Schedule for Early AML Relapse


Farhad Ravandi, MD
The escalating dosing strategy was associated with a better outcome in the CC-486 arm, with improvement in median OS over placebo of 22.8 vs 14.6 (HR: 0.66; P = .0729).

QUAZAR AML 001: AEs With First Onset During Escalated Dosing


Farhad Ravandi, MD
As expected, the incidence of AEs was higher with CC-486 because of its active agent. Febrile neutropenia and cytopenia occurred more frequently in the CC-486 arm; overall, however, the agent was very well tolerated, with the main AEs being gastrointestinal in nature (eg, diarrhea and nausea). The GI AEs were generally grade 1/2 and can be mitigated by the appropriate use of antiemetics and antidiarrheals.

QUAZAR AML 001: Older Patient Baseline Characteristics


Farhad Ravandi, MD
When we focus on patients 75 years of age or older (n = 105), we find that 50 received CC-486 and 55 received placebo. The majority of patients had de novo AML; this is very similar to the overall population in both arms of this study. In the CC-486 arm, 78% of all patients and 57% of the older patients received consolidation therapy: 47% of all patients and 43% of older patients with CC-486 had just 1 cycle of consolidation. Of note, this is an older population that has achieved CR. Many oncologists or practicing leukemia doctors only give 1 cycle of consolidation to these patients, mainly because of limited tolerability. MRD positivity at the time of randomization was higher in the placebo arm than in the CC-486 arm.

QUAZAR AML 001: CC-486 Treatment Duration and Survival Outcomes in Older Patients


Farhad Ravandi, MD
The median treatment duration in patients 75 years of age or older was 11.5 months in the CC-486 arm compared to 6 months in the placebo arm; this was consistent with the overall population. In this patient cohort, OS was significantly better in the CC‑486 arm compared to placebo (24.8 vs 9.9 months; HR: 0.48; P = .0281), and the RFS was significantly higher with CC-486, (10.2 vs 2.3 months; HR: 0.40; P = .0061).

An important point is that these survivals are from the time of randomization. Thus, one has to consider that the time from achieving a response to the initiation of therapy and randomization in this study could be up to 4 months. However, the survival results are significant.

QUAZAR AML 001: Safety With CC-486 in Older Patients


Farhad Ravandi, MD
As mentioned previously, there were more cytopenias in patients 75 years of age or older who received CC-486, with the exception of thrombocytopenia, which was seen at a surprisingly lower rate in patients who received CC-486 compared to placebo (11% vs 30%, respectively). More AEs were seen with CC-486 than with placebo, with the majority being grade 1/2 and consisting of GI issues. GI AEs could be mitigated with the appropriate use of antiemetics and antidiarrheals, which were allowed during this study but not mandatory. In practice, it is likely that the number of GI AEs could be significantly fewer with the use of prophylactic antiemetics.

QUAZAR AML 001: Health-Related Quality of Life

Farhad Ravandi, MD
Several health-related QoL measures were used in this study to compare the CC-486 and the placebo arms. This analysis showed that there were no significant differences between CC-486 and placebo in terms of QoL decline and that the clinically meaningful deterioration of QoL was low and similar between the 2 arms at most postbaseline assessments.

QUAZAR AML 001: Conclusions

Farhad Ravandi, MD
Several trials have studied the role of maintenance therapy in AML, but some of these studies used agents that were not well tolerated. For example, in very early studies, IL-2 and continuous dosing with cytotoxic chemotherapy were used as maintenance therapy in patients with AML. These were associated with significant deterioration in QoL, resulting in very limited adherence.

The current study is very important because it is the first in which a maintenance strategy was used effectively in AML and associated with improvement in OS. Of importance, this maintenance strategy has not been associated with deterioration of QoL, thus leading to improved patient adherence.

CC-486 has the potential to become the new standard of care in patients with AML, achieving a response and receiving consolidation in patients who are not eligible for ASCT and in patients in whom a maintenance strategy is desperately needed. The subset analyses showed that this strategy is feasible, tolerable, and highly effective in patients 75 years of age or older.

Would this strategy be a possible substitute for SCT in eligible patients, or should they still have an SCT rather than long‑term maintenance? I must emphasize that this strategy is not considered a substitute for SCT. The study did not examine this possibility; thus, one cannot make that conclusion. Again, the population that was enrolled on this study was considered by the enrolling physicians to be ineligible for ASCT in first remission.

The majority of patients who were enrolled on this study were at intermediate risk rather than adverse risk; even at an older age. Many physicians would consider an adverse-risk patient for SCT. The results of this study indicate the use of CC-486 in cases where there is no transplant option or if the patient declines having a transplant.

Ivosidenib Plus Venetoclax With or Without Azacitidine in IDH1-Mutated Hematologic Malignancies: Study Design

Farhad Ravandi, MD
This is a very interesting trial of targeted agents in patients with IDH1‑mutated AML, which is seen in 7% to 15% of patients who are typically older and have NPM1 mutations. Similar to IDH2 mutations, IDH1 mutations result in the accumulation of 2‑HG, which interferes with the normal function of the cellular epigenetic machinery, resulting in leukemogenesis.

Ivosidenib is a small-molecule inhibitor of mutant IDH that was approved as a single agent for initial therapy in very elderly unfit patients with IDH1‑mutated AML.[31,32] Azacitidine is also commonly used for older, unfit patients with AML. This study explored the efficacy and safety of combining ivosidenib with venetoclax with or without azacitidine. Azacitidine plus venetoclax[33] is now the FDA-approved standard of care in this population.[34]

This open‑label phase Ib study enrolled adults (N = 30) with IDH1 mutations with either advanced MDS or de novo or secondary AML or R/R AML. Patients had to have an ECOG PS of ≤ 2 and normal organ function adequate for enrollment. In the phase Ib dose escalation, the cohorts included ivosidenib 500 mg once daily plus venetoclax 400 mg once daily or 800 mg once daily, or ivosidenib plus venetoclax plus azacitidine for 7 days. In phase II, the recommended dose from previous cohorts was used, with primary endpoints of safety, tolerability, and response.

Ivosidenib Plus Venetoclax With or Without Azacitidine in IDH1-Mutated Hematologic Malignancies: Safety

Farhad Ravandi, MD
Overall, the treatment was well tolerated. There were no significant unexpected grade 3/4 AEs. Unfortunately, AEs such as pneumonia, febrile neutropenia, IDH differentiation syndrome, and abdominal pain are common in this population, particularly in the R/R setting. There were no deaths at Day 30 or Day 60. One patient had tumor lysis syndrome, which was managed with appropriate therapy.

Ivosidenib Plus Venetoclax With or Without Azacitidine in IDH1-Mutated Hematologic Malignancies: Overall Response

Farhad Ravandi, MD
Response was high for the treated patient population (n = 20); ORR was 90%, and the composite CR (CR + CRi + CR with incomplete hematologic recovery) was 80%. Composite CR by cohort was 67% for ivosidenib plus venetoclax 400, 100% for ivosidenib plus venetoclax 800, and 75% for ivosidenib plus venetoclax 400 plus azacitidine. This is a small number of patients, but the response rates are very high, with a very high MRD‑negative response achieved as well (50% for all cohorts).

Ivosidenib Plus Venetoclax With or Without Azacitidine in IDH1-Mutated Hematologic Malignancies: Disease Subgroup Response

Farhad Ravandi, MD
By disease subtype, a composite CR of 100% was achieved in 3 patients with de novo AML; 80% in 4 patients with secondary or therapy‑related AML; 63% in 5 patients with R/R AML; and 100% in 4 patients with MDS. A notable proportion of these patients had MRD negativity as well.

Ivosidenib Plus Venetoclax With or Without Azacitidine in IDH1-Mutated Hematologic Malignancies: Survival Outcomes

Farhad Ravandi, MD
Many of these responses have been durable, particularly in the cohort of previously untreated patients. Median OS was not reached for MDS, treatment-naive AML, or R/R AML. The median EFS for treatment-naive AML was not reached, either.

Ivosidenib Plus Venetoclax With or Without Azacitidine in IDH1-Mutated Hematologic Malignancies: Prognostic Factors

Farhad Ravandi, MD
Mechanisms of resistance with IDH inhibitors are well described. We know that RAS, RTK, and phosphatase pathway signaling mutations are associated with a higher likelihood of resistance and more adverse outcomes (eg, decreased DoR and median OS). It has also been established that MRD negativity is associated with improved survival. This study shows that MRD negativity, which was achieved in 50% of the 16 patients who achieved CR, is associated with significantly improved EFS and ongoing responses (median EFS was not reached vs a median 5 months for MRD-positive patients).

Ivosidenib Plus Venetoclax Plus Azacitidine in IDH1-Mutated Hematologic Malignancies: Conclusions

Farhad Ravandi, MD
We are now beginning to combine targeted agents in patients with AML to learn if we can improve the rate and depth of response, DoR, and survival using these combinations. This strategy has generated a great deal of interest because these agents are relatively nontoxic, generally allowing us to combine them without adding major toxicity. This approach may someday enable clinicians to treat older patients with AML without the use of any chemotherapy. This is somewhat akin to what we have done in acute promyelocytic leukemia, that is, using nonchemotherapy treatment regimens, we are producing very prolonged survival and potential cures, even in the older patient population.

Summary: ASCO Leukemias 2020

Farhad Ravandi, MD
The studies presented at ASCO 2020 demonstrate that the identification of various biologic pathways that lead to leukemogenesis allows us to identify and develop effective therapies. The role of the immune system in the clearance of leukemic cells is also being explored; consequently, the use of immune-modifying agents will play a role in future leukemia therapies. We are looking at the development of several immune-modifying strategies that could lead to the use of various combinations of chemotherapy, small-molecule targeted agents, and immune-based therapies to improve responses, eradicate minimal residual disease, and improve response duration and survival.

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