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Introduction. Approximately 40% of patients (pts) with newly diagnosed AML either fail to achieve complete remission with intensive induction therapy or experience disease recurrence after a short remission (CR1 6 months), the probability of response for PIF/ER pts is particularly poor (~12%) with median expected overall survival of ~3.5 month and no approved therapy for this specific population. We have recently shown that increased immune infiltration of the tumor microenvironment (TME) is associated with induction failure and poor prognosis; conversely, an infiltrated TME predisposes for immunotherapy response1. We provide an update of the first-in-human study of flotetuzumab (FLZ), an investigational CD123 x CD3 bispecific DART® molecule currently in clinical development for PIF/ER AML pts. Methods. In this phase of the study, PIF is defined as being refractory to induction with: ≥1 high-intensity cytarabine-based chemotherapy (CTx) cycles, or ≥2 but ≤4 Bcl-2 inhibitor-based combinations, or gemtuzumab ozogamicin only. ER is defined as relapse following CR1 < 6 months. Pts who receive up to one prior salvage attempt are included. Pts whose AML recurred following HSCT are excluded. The recommended Phase 2 dose (RP2D) of FLZ is 500 ng/kg/day administered as a continuous infusion in 28-day cycles following a step-up ('priming') lead-in dose during Cycle 1 Week 1. Disease status is assessed by modified IWG criteria. Duration of response is measured from initial response to relapse or death. Results. As of July 1, 2020, 38 PIF/ER (as defined above) AML patients have been treated at the RP2D (median age 63yrs [range 28-81]; 31.6% [12] pts female). Most pts (63.2%, 24/38) were PIF and the large majority (94.7%, 36/38) had non-favorable risk by ELN 2017 criteria (25 pts adverse, 11 pts intermediate); 34.2% (13/38) had secondary AML. For ER pts, median duration of CR1 was 2.9 months (range: 0.7-4.0 months). Cytokine release syndrome (CRS) was the most frequently reported treatment related adverse event (TRAE), with all pts experiencing mild-to-moderate (grade ≤ 2) CRS. No grade ≥ 3 CRS events have been reported in this cohort. Most CRS events (51.5%) occurred in the first week of treatment during step-up dosing. The incidence of CRS progressively decreased during dosing at RP2D (34.8% in week 2, 4.5% in week 3, and 6.1% in week 4), allowing outpatient treatment in most cases. Neurologic AEs have been infrequent, with the most prominent event being grade 1 or grade 2 headache in 23.7% (9/38) treated at the RP2D. Two pts experienced grade 3 confusion of short duration (1-2 days) that was fully reversible. Over half (57.9%) of pts had evidence of antileukemic activity (reduction in blast count) with a median decrease of 92.7% in BM blasts (Fig. 1). The overall complete response rate (CRR, Conclusion: FLZ demonstrated encouraging activity in pts with PIF/ER AML, a population with poor prognosis and high unmet medical need, with 42.1% achieving CRR and over half of those receiving a stem cell transplant. Treatment is tolerable with a minimum 8 day inpatient treatment. The study is currently enrolling patients [NCT02152956] 1 Vadakekolathu J, Minden MD, Hood T, Church SE, Reeder S, Altmann H et al. Immune landscapes predict chemotherapy resistance and immunotherapy response in acute myeloid leukemia. Sci Trans Med 2020. Disclosures Aldoss: abbvie: Consultancy, Research Funding; agios: Honoraria; kite: Consultancy; autolus limited: Consultancy; JAZZ: Honoraria, Speakers Bureau; Amgen: Consultancy; Agios: Consultancy. Uy:Genentech: Consultancy; Agios: Consultancy; Pfizer: Consultancy; Jazz Pharmaceuticals: Consultancy; Daiichi Sankyo: Consultancy; Astellas Pharma: Honoraria. Emadi:Amgen: Membership on an entity's Board of Directors or advisory committees; NewLink Genetics: Research Funding; Jazz Pharmaceuticals: Research Funding; Genentech: Membership on an entity's Board of Directors or advisory committees; KinaRx: Other: co-founder and scientific advisor; Servier: Membership on an entity's Board of Directors or advisory committees. Walter:Aptevo Therapeutics: Research Funding. Foster:Daiichi Sankyo: Consultancy; Bellicum Pharmaceuticals: Research Funding; Macrogenics: Consultancy, Research Funding. Arellano:Hanmi: Research Funding; Gilead Sciences, Inc: Consultancy, Membership on an entity's Board of Directors or advisory committees; Cephalon Oncology: Research Funding. Wieduwilt:Amgen: Research Funding; Macrogeneics: Research Funding; Leadiant: Research Funding; Merck: Research Funding; Shire: Research Funding; Daiichi Sankyo: Membership on an entity's Board of Directors or advisory committees. Michaelis:Jazz Pharmaceuticals: Research Funding. Stiff:Kite, a Gilead Company: Research Funding; Gamida Cell: Research Funding; Atara: Research Funding; Unum: Research Funding; Delta-Fly: Research Funding; Macrogenics: Research Funding; Amgen: Research Funding. Advani:Novartis: Consultancy, Other: advisory board; Pfizer: Honoraria, Research Funding; Takeda: Research Funding; OBI: Research Funding; Kite: Other: Advisory board/ honoraria; Amgen: Consultancy, Other: steering committee/ honoraria, Research Funding; Seattle Genetics: Other: Advisory board/ honoraria, Research Funding; Immunogen: Research Funding; Glycomimetics: Consultancy, Other: Steering committee/ honoraria, Research Funding; Macrogenics: Research Funding; Abbvie: Research Funding. Wermke:MacroGenics: Honoraria. Erba:AbbVie, Daiichi Sankyo, Forma, ImmunoGen, Jazz Pharmaceuticals, MacroGenics, Novartis, PTC: Research Funding; Glycomimetics: Other: member of Scientific Steering Committee; Celgene: Other: chair of the Scientific Steering Committee; Covance (AbbVie): Other: chair of the Independent Review Committee; AbbVie, Agios, Celgene, Incyte, Jazz Pharmaceuticals, and Novartis: Speakers Bureau; AbbVie, Agios, Amgen, Astellas, Celgene, Daiichi Sankyo, Glycomimetics, ImmunoGen, Incyte, Jazz Pharmaceuticals, MacroGenics, Novartis, and Pfizer: Consultancy. Topp:Amgen, Boehringer Ingelheim, KITE, Regeneron, Roche: Research Funding; Amgen, KITE, Novartis, Regeneron, Roche: Consultancy. Ravandi:Abbvie: Consultancy, Honoraria, Research Funding; Jazz Pharmaceuticals: Consultancy, Honoraria, Research Funding; Amgen: Consultancy, Honoraria, Research Funding; Xencor: Consultancy, Honoraria, Research Funding; BMS: Consultancy, Honoraria, Research Funding; Astellas: Consultancy, Honoraria, Research Funding; Macrogenics: Research Funding; Celgene: Consultancy, Honoraria; AstraZeneca: Consultancy, Honoraria; Orsenix: Consultancy, Honoraria, Research Funding. Muth:MacroGenics, Inc.: Current Employment, Current equity holder in publicly-traded company. Collins:IQVIA: Other: I have worked as a contractor for IQVIA in the past, within the past 24 months.; MacroGenics: Current equity holder in publicly-traded company, Other: I currently work as a contractor for MacroGenics. Guo:Macrogenics: Current Employment. Tran:MacroGenics: Current Employment. Kaminker:MacroGenics, Inc.: Current Employment, Current equity holder in publicly-traded company. Patel:MacroGenics: Current Employment. Bakkacha:MacroGenics: Current Employment. Jacobs:MacroGenics: Current Employment. Seiler:MacroGenics: Current Employment. Rutella:Kura Oncology: Research Funding; MacroGenics Inc.: Research Funding; NanoString Technologies Inc.: Research Funding. Bonvini:MacroGenics, Inc.: Current Employment, Current equity holder in publicly-traded company. Davidson-Moncada:Macrogenics: Current Employment. DiPersio:Magenta Therapeutics: Membership on an entity's Board of Directors or advisory committees.

Background: There is no standard of care treatment for Acute Myeloid Leukemia (AML) in relapse post-allogeneic hematopoietic stem cell transplant (post-HSCT), with overall 5-year survival about 5-10%. Venetoclax (Ven) is a novel BCL2 inhibitor approved by the FDA for treatment of newly diagnosed AML in combination with hypomethylating agents (HMA) or low dose cytarabine for patients unfit for intensive induction. However, data in relapsed/refractory AML are limited, especially in the post-HSCT setting. In this retrospective study, we reviewed outcomes of patients with AML relapse post-HSCT who received Ven in combination with HMA in a single center. Methods: Charts of 17 patients who had AML relapse post-HSCT treated with combination of Ven and HMA between November 2018 - March 2020 at the University of Kansas Medical Center were reviewed. We utilized descriptive statistics for baseline characteristics and outcomes, and Kaplan-Meier log-rank test for calculating overall survival. Results Seventeen patients received Ven+HMA for AML relapse post-HSCT in our center. At the time of SCT, patients were in first complete remission (CR) (n=15); second CR (n=1) and primary failure induction (1). Median age was 62 at time of relapse (31-71) years, and 8 patients were female (47%). 9 patients (53%) had adverse risk AML (ELN 2017) 8 of them were in CR1 and 1 with primary induction failure. Common mutations included DNMT3a, ASLX-1, TET2 (3); TP53 (2); IDH1/2 (2); NPM1/FLT3 (1); NPM1/IDH2 (1); NPM1 (1 transplanted in CR2); FLT3 (1). 2/17 had received Ven+HMA prior to SCT; 4 patients received HMA alone prior to SCT. 11 patients (65%) were naïve to either Ven or HMA prior to relapse. Median time to relapse was 181 (44-851) days post-HSCT. 9 (53%) patients received Azacitidine+Ven and 8 (47%) received Decitabine+Ven. HMA+Ven was the first line of therapy post-HSCT relapse in 14 patients. 2 had donor lymphocyte infusion (DLI) after either MEC or dacogen but relapsed prior to Ven+HMA. 1 had IDH (2) inhibitor. Patients received median of 2 (1-10) cycles of HMA+Ven. Six (35%) patients achieved complete remission/complete remission with incomplete hematologic recovery (CR/CRi), and 2/6 patients had negative measurable residual disease by multiparameter flow cytometry. Median overall survival was 361 days from relapse (Figure 1). 3/14 patients received subsequent DLI with Ven+HMA. Disease progression was the most common cause of death in 8/9 of patients who died during the follow up period. Most common side effects included neutropenic fever (n=8, 47%) and acute graft versus host disease (aGVHD) (n=5, 30%). 2/5 developed new aGVHD on HMA+Ven with no prior history of aGVHD. However, aGVHD was mainly grade I-II and responsive to therapy. Discussion HMA+Venetoclax demonstrates potential activity in patients with AML relapse post-HSCT with a CR/CRi rate of 35%, comparable to other salvage therapies. There were no unexpected side effect in this high-risk population. Larger studies are needed to confirm efficacy and toxicity in this setting. Disclosures McGuirk: Pluristem Ltd: Research Funding; Kite Pharmaceuticals: Consultancy, Honoraria, Research Funding, Speakers Bureau; Gamida Cell: Research Funding; Bellicum Pharmaceutical: Research Funding; Allo Vir: Consultancy, Honoraria, Research Funding; Juno Therapeutics: Consultancy, Honoraria, Research Funding; Astellas: Research Funding; Fresenius Biotech: Research Funding; Novartis: Research Funding. Lin:Aptevo: Research Funding; Abbvie: Research Funding; Bio-Path Holdings: Research Funding; Celgene: Research Funding; Gilead Sciences: Research Funding; Incyte: Research Funding; Jazz: Research Funding; Mateon Therapeutics: Research Funding; Ono Pharmaceutical: Research Funding; Pfizer: Research Funding; Prescient Therapeutics: Research Funding; Seattle Genetics: Research Funding; Tolero Pharmaceuticals: Research Funding; Trovagene: Research Funding; Genetech-Roche: Research Funding; Celyad: Research Funding; Astellas Pharma: Research Funding.

INTRODUCTION: Treatment outcome of pediatric acute myeloid leukemia (AML) patients has improved over the past few decades due to intensive chemotherapy. Primary induction failure (PIF), defined as failure to achieve complete remission after the second induction chemotherapy, occurs in around 10% of children with newly diagnosed AML. Effective treatment strategy for these patients is not established and their poor prognoses have been reported elsewhere. Here we investigated the clinical and biological features of pediatric AML patients with PIF who were registered in the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG) AML-05 Study (AML-05). METHODS: We conducted a retrospective survey of patients who were registered in the AML-05. We analyzed probabilities of overall survival (OS) according to gender, age at diagnosis, white blood cell count (WBC) at diagnosis, FAB classification, etc. Genetic analysis of primary leukemic blasts was performed. We screened fusion genes and gene mutations as follows: RUNX1-RUNX1T1, CBFB-MYH11, NUP98-NSD1, DEK-NUP214, MLL-PTD, WT1, NPM1, and MLL-rearrangements, gene mutations of KIT and FLT3-ITD. Furthermore, we evaluated the clinical and biological background of these PIF patients to define their prognostic factors statistically. RESULTS: Among the 443 patients registered in the AML-05 between November 2006 and December 2010, 43 patients (9.7%) had PIF. The observation period from the date of PIF was 5-78 months (median, 20 months). The age at diagnosis was 0.1-17 years (median, 6.1 years). There was no significant difference in gender (28 males vs15 females). The 3-year OS rate was 19.0% (95% confidence interval 1.0%-38.0%). This was extremely poor compared to the patients who achieved complete remission (CR): 66.7% for high-, 73.2% for intermediate-, and 92.6% for low-risk groups, respectively. Disease recurrence is the major cause of death (n=19, 46.3%). The mean WBC at diagnosis of PIF patients was 96 x 109/L: this is significantly higher than that of non-PIF patients (51 x 109/L, P CONCLUSIONS: The prognosis of pediatric AML patients with PIF was extremely poor. In our survey, unfavorable molecular biological background of leukemia was associated with PIF. It is necessary to explore more effective treatment strategies based on leukemia biology for these patients in the future. Disclosures No relevant conflicts of interest to declare.

Introduction: Prognosis of adult patients with Acute Lymphoblastic Leukemia (ALL) has improved in the last decades. Improvement of response rates with new innovative therapies in relapsed patients was associated with better outcome. In the present study we evaluate the impact of CR1 duration on long-term outcome of patients with relapsed disease. Methods: Patients with relapsed Philadelphia negative pre-B ALL initially treated at our institution between 2000 and 2014 were reviewed. Information regarding treatment, baseline characteristics, response to therapy and duration of remission was evaluated. Survival outcomes were analyzed in terms of response to induction chemotherapy and duration of CR1. Statistical analysis included Chi-squared for categorical variables, T-student for continuous variables and Kaplan-Meier for OS. Results: A total of 166 patients were analyzed. Patient characteristics are summarized in Table 1. Overall response rate to initial therapy was 94% (including 91% CR rate); 10 (6%) patients had primary induction failure. Median time to relapse was 25 months. Patients were grouped into three categories according to duration of CR1: 1) Patients with CR1 duration of less than 6 months, 2) CR1of 6-12 months, and 3) CR1 duration greater than 12 months. Among baseline characteristics, younger age was associated with a CR duration of more than 12 months (34y vs 44y and 46y, p=0.01). No significant differences were observed in terms of baseline hemoglobin, white blood cell count, platelet count, blasts, and LDH between these groups. Median survival after relapse was significantly longer in patients with a CR duration of more than 12 months compared to those with 6-12 months or less than 6 months remission duration (12 months vs 6 months vs 5 months respectively, p=0.04) (Figure 1A). Information regarding salvage therapy was available in 79 patients and is summarized in Table 1. Cytogenetic abnormalities at the time of relapse were available in 39 patients and predicted for survival. Presence of a diploid karyotype was associated with longer survival than patients with hypodiploid, hyperdiploid or complex karyotypes (17, 4, 8 and 2 months respectively, p Conclusions: Duration of CR1 in patients with pre-B ALL predicts survival after first relapse. Furthermore, Patients with diploid cytogenetics and CR1 of more than 12 months have the best outcome post frontline therapy failure. Table 1. Studied factor N (%) [range] Age 40 (16-86) Sex Male 96 (58) Female 70 (42) Treatment at Baseline HCVAD-R 69 (42) HCVAD 56 (34) Augmented BFM 41 (25) Treatment at Relapse HCVAD based 33 (42) Monoclonal antibodies 24 (30) FLAG-ida 5 (6) Investigational 11 (14) Asparaginase based therapy 6 (8) Mean blood counts at baseline Hemoglobin 8.9g/dL [3.6-15] Platelets 59 x109 /L [0-393] WBC 34 x109 /L [0.6-602] Karyotype at Relapse Diploid 18 (46) Hipodiploid 3 (8) Complex 12 (31) Hiperdiploid 6 (15) Baseline peripheral Blast % 40 [0-100] LDH (UI/dL) 2225 [172-28261] Bone Marrow Blast % 81 [0-100] Induction Failure 10 (6) Duration of CR1 12 months 91 (55) Figure 1. Figure 1. Disclosures Cortes: Pfizer: Consultancy, Research Funding; Teva: Research Funding; BMS: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; BerGenBio AS: Research Funding; Ariad: Consultancy, Research Funding; Astellas: Consultancy, Research Funding; Ambit: Consultancy, Research Funding; Arog: Research Funding; Celator: Research Funding; Jenssen: Consultancy. Pemmaraju:Stemline: Research Funding; Incyte: Consultancy, Honoraria; Novartis: Consultancy, Honoraria, Research Funding; LFB: Consultancy, Honoraria. Konopleva:Novartis: Research Funding; AbbVie: Research Funding; Stemline: Research Funding; Calithera: Research Funding; Threshold: Research Funding.

BACKGROUND: Despite excellent outcomes in pediatric ALL, 20-30% of patients relapse or become refractory to frontline therapies with subsequent CR2 rates of only 60%. For multiply relapsed patients, response rates remain around 40%, with OBJECTIVES: To determine the maximal tolerated dose and overall response rate of clofarabine in combination with mitoxantrone as reinduction therapy for refractory/relapsed acute leukemia. To determine the percent of minimal residual disease (MRD) following reinduction with mitoxantrone and clofarabine reinduction therapy.To further characterize the biology of childhood, adolescent and young adult refractory/relapsed acute leukemia. DESIGN: Prospective, multi-center, treatment-based, non-randomized, open label, uncontrolled, single group assignment, safety and efficacy study (phase I/II). Patients 0-30.99yr old with ALL, AML or NHL in 1st, 2nd or 3rd relapse OR primary induction failure were given 1 to 3 cycles of clofarabine (escalating doses 20, 30, 35 and 40mg/m2/day) Day 1-5, in combination with mitoxantrone 12mg/m2/day on Day 3-6. Dexrazoxane was given prior to Mitoxantrone. Dose escalation was planned every 3 patients pending dose limiting toxicities. CNS prophylaxis was achieved with intrathecal liposomal cytarabine. (Figure 1) Patients were allowed subsequent cycles pending response and anthracycline exposure. RESULTS: To date 15 patients have been enrolled on the safety portion of this study. Median Age is 16yrs (8months-23yrs); 9 ALL (3=Induction Failure, 4=Relapse1, 2=Relapse2), 5 AML (4=Induction Failure, 1=Relapse2), 1 NHL (=Progressive Disease). There have been 2 prolonged Grade III/IV toxicities at Dose Level 4 (Clofarabine 40mg/m2) (1 hepatic toxicity, 1 prolonged myelosuppression) hence we are currently enrolling at Dose Level 3 (Clofarabine 35mg/m2). Median time to neutrophil recovery is 24 days. Twelve of 14 (86%) evaluable leukemia patients achieved a CR after 1 cycle of therapy. Of these patients, 92% achieved MRD negativity ( CONCLUSION: The combination of clofarabine and mitoxantrone reinduction therapy for relapsed or refractory acute leukemia appears to be safe and well tolerated in children, adolescents and young adults with poor risk hematologic malignancies. The MTD or tolerable dose of this combination has yet to be reached. Hematopoietic recovery appears to be rapid and complete. Initial data from the first 15 patients enrolled is encouraging with an 86% CR rate in leukemic patients. Once the MTD or tolerable dose is reached, an extended multicenter Phase II Study will be initiated. Table 1. Treatment Schema DAY 1 2 3 4 5 6 7 8 21 CLOFARABINE ● ● ● ● ● DEXRAZOXANE ● ● ● ● MITOXANTRONE ● ● ● ● DEXAMETHASONE ● ● ● ● ● IT LIPOSOMAL ARAC ● FILGASTRIM (…continued until ANC > 1500/mm3 x 2 consecutive days) ● → → Disclosures No relevant conflicts of interest to declare.

Introduction Combination chemotherapy with a seven-day continuous infusion of cytarabine (100-200mg/m2/d) plus 3 days of an anthracycline (7+3 ) is considered standard of care for remission induction in newly diagnosed patients with acute myeloid leukemia (AML) However, the MRC AML 15 trial (Burnett et al. J Clin Oncol 2013, 31:3360) suggested that in younger AML patients, a combination regimen containing fludarabine plus intermediate dose cytarabine x 5 days with granulocyte colony-stimulating factor (GCSF) and idarubicin x 3 days (FLAG-Ida) may produce higher CR rates after one course and reduced relapse rates than a combination of cytarabine and daunorubicin given for 3+8 days. The schedule of cytarabine given during DA in the MRC AML 15 trial was not the same as the continuous infusion cytarabine given as standard of care for 3+7 regimens in the United States. We compared standard continuous infusion cytarabine (100mg-200mg/m2/d x 7 days) plus idarubicin (12 mg/m2 /d x 3 days) (AI) administered at our center to FLAG-Ida (fludarabine 25-30mg/m2/d followed 4 hours later by cytarabine (2g/m2/d) x 5 days with granulocyte colony-stimulating factor beginning day 1 until count recovery and idarubicin 10 mg/m2/d x 3 d with respect to safety and efficacy in the initial induction therapy of newly diagnosed AML Methods Patients with newly diagnosed AML who received remission induction therapy with FLAG-Ida or AI were identified from January 1 2008 through May 2014. Patients with M3 FAB subtype and those with relapsed or refractory AML were excluded. Supportive care measures were standardized and identical between the two groups. Primary endpoints included complete remission rate post induction therapy, overall survival (OS) and disease free survival (DFS). Remission status was categorized into complete remission (CR), incomplete remission (CRi), and primary induction failure (PIF). Secondary endpoints included non-relapse related mortality (NRM), time to neutrophil recovery >1000 and time to platelet recovery > 100K. CR, CRi and PIF were defined according to the International Working Group recommendations (Cheson B et al. J Clin Oncol 2003 Dec; 21 (24) 4624-49). NRM was defined as death by any cause through day 30 of induction therapy. OS was defined as time from start of therapy to death and DFS was time from diagnosis to relapse or non-relapse death. Subgroups analysis for the primary endpoints were completed based on age (≥60 and Results We identified 112 patients who received FLAG-Ida and 56 patients who received AI. Cytogenetic risk and previous antecedent hematologic disorder/secondary leukemia were similar between the two groups. FLAG-Ida achieved faster neutrophil recovery higher overall CR and CR+CRi rate with lower NRM (Table 2). In patients ≥60 years old, CR rates were 75% and 45% for FLAG-Ida vs. AI respectively (p=0.021). OS and DFS between the two regimens did not significantly differ in the subgroup analysis for age or cytogenetic risk group except that intermediate risk patients had better overall survival with FLAG-Ida (p=0.008, log rank test). In a multivariate logistic regression model on achievement of remission (CR+Cri), the use of AI had an odds ratio of 0.38 (p=0.012) compared to FLAG-Ida. In Cox analysis, AI vs FLAG-Ida was a factor of borderline statistical significance for NRM (HR 1.91, p=0.052) and overall survival (HR 1.62, p=0.062) Conclusions These data demonstrate faster hematopoietic recovery, superior remission (CR+CR1) and NRM rates for FLAG-Ida when compared to AI. Overall survival rates are confounded by subsequent therapies but also appear to be improved for patients in the intermediate risk group who received FLAG-Ida. Of particular interest was the improvement in CR rates for FLAG-Ida in patients ≥ 60 years of age. These data suggest that FLAG-Ida should be considered a valid option for the initial therapy of AML. Disclosures No relevant conflicts of interest to declare.

Introduction Early bone marrow (BM) evaluation (during aplasia or at “day 14” (D14)) in patients with AML undergoing conventional induction therapy has been adopted from clinical practice in pediatric acute lymphoblastic leukemia (ALL). While it has been shown that early persistence of AML correlates with decreased complete remission (CR) rates and overall survival (OS), unlike in ALL, there are no data to indicate that early initiation of re-induction therapy based on these findings will positively influence outcome. In fact, early re-induction, especially in older patients, may increase morbidity and mortality from prolonged cytopenias, infectious complications, and longer hospital stays. Moreover, it can be challenging to determine the nature of scattered blasts identified in a hypocellular BM at D14, as they may represent normal recovering marrow elements or malignant blasts. Even if malignant, the chemosensitivityof these cells will only be fully determined by later assessment of the BM at the time of expected count recovery (“day 28”). For these reasons, early re-induction therapy may not be advisable. In this retrospective study, we sought to evaluate the validity of D14 BM assessments as post-therapy prognostication to guide treatment decisions in AML. Methods We conducted a retrospective institutional study (2006-2014) of AML patients undergoing routine induction chemotherapy where diagnostic, interim (around D14) and recovery (D21-42) BM evaluations were available for review. Clinical information and pathology data were retrieved from our institutional database. Responses at D14 were categorized morphologically into three categories: optimal response (OR, blasts ≤5%), indeterminate response (IR, blasts 6-19%), and residual leukemia (RL, blasts ≥20% or a relative decrease in blast count from baseline of Results Evaluable patients (n=98) had a mean age of 51 years (20-73), and 45% were male. The median BM blast percentages at diagnosis, D14 and recovery were respectively 54.5%, 0% and 2.5% (Figure 1). There was a significantly greater absolute decrease in blast percentage from diagnosis to D14 in patients who recovered in CR compared to those who did not achieve CR (median: 53.5% vs 23.0%, P = 0.001). In patients that got early re-induction therapy for SOR at D14, the relative differential in baseline and D14 BM blasts was significantly lower compared to patients with D14 SOR who did not get re-induction therapy (median: 21.8% vs 77.8%, P=0.004) Ninety patients did not receive early re-induction therapy. Of these, 86 (95.6%) achieved CR and 4 patients (4.4%) recovered counts with residual leukemia. Fourteen (14.3%) patients were classified as SOR at D14. Of these, 6 (6.7%) did not receive re-induction therapy and 4 of these 6 patients (67%) achieved a CR. Eight patients received early re-induction therapy based on SOR at D14 (IR = 2, RL = 6); of these, 4 patients (50%) achieved CR at count recovery. Achieving an OR at D14 was predictive of achieving CR at recovery (sensitivity = 95.3%, PPV = 97.6%). However, not achieving an OR at D14 had low specificity (50%) and NPV (33.3%) for achieving CR (P = 0.021). Conclusions Our results indicate that a SOR at the D14 BM evaluation does not uniformly identify patients with primary induction failure (low NPV) and should not be used to dictate the timing of re-induction therapy. We confirmed the PPV of achieving an OR at D14 as previously reported, but we argue that no additional prognostic data is provided by an OR at D14, beyond what can already be predicted by pre-treatment variables (e.g., age and chromosomal abnormalities). We suggest that the D14 BM should be omitted from the routine evaluation of AML patients during induction therapy outside the context of a clinical trial. Figure 1 Figure 1. Progression and percentage of blasts at diagnosis, day 14 and recovery assessments (n = 98). Disclosures No relevant conflicts of interest to declare.

5-azacitidine (5AZA), a 5-methyltransferase inhibitor that demethylates and unsilences genes is a novel medication with epigenetic mechanism of action approved for therapy of myelodysplastic syndromes. There are few reports in the literature regarding use in acute non-lymphocytic leukemia (ANLL) some indicating efficacy and others lack of efficacy. Since January 3, 2010, we treated 6 patients in various stages of ANLL with 5AZA. Data is summarized in table.Age Cytogenetics Use Response Duration (Months) Survival (Months) 63 (male) 45,XY,add(5)(q13),-7,+11,add(16)(q12),-17,-18,+22 Induction Failure CR 8+ Alive 8+ 65 (male) 46,XY,t(16:21)(q24;q11.2),del(20)(q11.2) Induction Failure PR 8 Dead 9 93 (male) 46,XY Primary RX/Maintenance PR 12 Dead 13 68 (male) 46,XY/NPM1 Dysplasia 2o to ANLL induction PR 14 Alive 14+ 86 (male) 46,XY Maintenance CR 32+ Alive 32+ 72 (male) 46,XY/NPM1 RAEB-2/ANLL Primary RX/Maintenance PR 8 Dead 19 We treated 2 patients ages 63 and 65 with primary induction failure to standard 3+7 anthracycline/AraC, both with complex cytogenetics. One patient achieved hematological improvement following 1 cycle and complete remission at 3 months following 2 cycles of therapy. He continues to receive monthly 5AZA, is alive and in complete hematological remission (bone marrow not repeated) at 8+ months. The second patient achieved a partial remission at 1 month following 5AZA that remained stable on monthly 5AZA for 8 months at which time ANLL progressed resulting in death. We used 5AZA as induction and maintenance for a 93 year old with ANLL with normal cytogenetics. He achieved a partial then stable improvement with monthly 5AZA. At 12 months, ANLL progressed resulting in death. We treated a 68 year old with NPM1 positive normal cytogenetics ANLL who achieved remission with standard 3+7 therapy but at 6 months post induction developed secondary myelodysplasia. He achieved a stable partial response with monthly 5AZA for 14 months at which time ANLL relapsed. He is alive at the time of preparation of this abstract. We used 5AZA as maintenance for an 86 year old with ANLL with normal cytogenetics who achieved a complete remission with standard 3+7 therapy. This individual continues to receive 5AZA (monthly then every 6 weeks) and remains in complete remission 32+ months following diagnosis of ANLL. We treated a 72 year old with borderline RAEB-2/ANLL with NPM1 positive normal cytogenetics with 5AZA as primary induction therapy. He achieved a hematological response following 4 monthly cycles of 5AZA with normalization of platelets and decreased need for RBC support. ANLL relapsed at 8 months at which time he was treated with standard chemotherapy and lived an additional 11 months. This data indicates that 5AZA is useful for individuals with ANLL even with high risk cytogenetics with potential efficacy as primary therapy, for individuals with disease primary refractory to standard chemotherapy, and for maintenance of ANLL remission. Formal studies to more clearly define the role of 5AZA in various stages of ANLL are warranted. Disclosures: Off Label Use: 5-azacitidine for therapy of ANLL.

Abstract 3096 Relapsed or refractory AML is difficult to treat even with allogeneic BMT. In an attempt to reduce leukemia burden and limit toxicities from multiple re-induction attempts, we initiated a treatment strategy to offer allogeneic BMT prior to count recovery, within 3 to 4 weeks after re-induction. Among 156 consecutive AML patients referred to our BMT program between 01/2003 and 03/2008, 84 (54%) patients did not receive an allogeneic BMT due to: death (n=25, 30%), patient refusal (n=13, 16%), disease progression (n=13, 16%), autologous BMT (n=11, 13%) and other (n= 22, 26%). Seventy-two (46%) patients received an allogeneic BMT: 21 (29%) patients were prospectively identified with very high risk features (primary induction failure (PIF) or refractory relapse (RR)) and received re-induction with the intent-to-induce hypoplasia and transplant prior to count recovery. The remaining 51 patients received re-induction with the goal of inducing complete remission (CR) prior to BMT (the intent-to-induce remission group). Patient and BMT-related characteristics, as well as BMT outcomes are summarized in Table 1. Patients were prospectively accrued to myeloablative or reduced intensity BMT protocols depending on their age, KPS, co-morbidities, disease risk and the degree of HLA match. The intent-to-induce hypoplasia group had a lower 2-year PFS and OS (reflecting their very high risk disease characteristics). In subgroup analysis in patients with PIF or RR, there was no difference in 2-year PFS (15% vs. 22%, p=0.39) or 2-year OS (20% vs. 33%, p=0.32) between the intent-to-induce hypoplasia and the intent-to-induce remission groups. The overall and day 100 TRM was similar in both groups of patients with PIF or RR. Using this prospective strategy of identifying patients with very high risk disease with the intent to transplant them during hypoplasia after re-induction therapy, 46% of all the referred AML patients were able to undergo allogeneic BMT. This is higher than other published series where < 30% of patients proceeded to transplant where the goal of re-induction was to induce and achieve CR prior to transplant. Our data show that it is safe to transplant advanced AML patients early (within 3 to 4 weeks) after re-induction with acceptable mortality in patients with very high risk AML who otherwise might not be transplant candidates.Table.Patient Characteristics and OutcomesFactorIntent-to-induce remission (N=51)Intent-to-induce hypoplasia (N=21)PN(%)N(%)Patient and Disease CharacteristicsAge at BMT18-4016 (31)4 (19)NS41-6028 (55)13 (62)61+7 (14)4 (19)KPS at BMT≥9023 (45)1 (5)0.1 Disclosures: Hahn: Novartis: stock.

Abstract 2389 Autologous hematopoietic cell transplantation (autoHCT) is standard therapy for high-risk hematologic disorders and solid tumors. We assessed whether overall survival (OS) at Day 100, which represents early transplant-related mortality (TRM), and at one year, which represents disease-related mortality and later TRM, had changed over time. The study population was derived from patients undergoing 68,404 first autoHCTs between 1994–2005 in US and Canadian centers reported to the CIBMTR. Statistical significance was measured using Ptrend over 6 time cohorts to test whether the OS estimates were stable (slope = 0), increasing (slope>0) or decreasing (slope Table 1: Overall survival (95% CI) estimates over time. Autologous HCT 1994-5 1996-7 1998-9 2000-01 2002-3 2004-5 Ptrend NHL in CR2/Rel 1 sens N 890 1067 1041 1020 946 1116 NHL – non-Hodgkin lymphoma, HL – Hodgkin lymphoma, MM – myeloma, CR – complete remission, Rel – relapse, PIF – primary induction failure, sens – sensitive Disclosures: No relevant conflicts of interest to declare.

Abstract 4573 Patients with acute myeloid leukemia (AML) with FLT-3 mutations have an extremely high risk of relapse after conventional chemotherapy. The role of allogeneic stem cell transplantation (SCT) for this patient cohort has been discussed controversially in recent years. This retrospective analysis reports our cumulative experience in a cohort of 42 consecutive patients (age 17–70, median 51 years) allografted for FLT-3 positive AML in a single centre. In more than 80% a FLAMSA-RIC based conditioning regimen was used, in 5% BCNU/Melphalan/Fludarabine, and in 14% conventional radiation- or Busulfan- based regimens. Most patients received mobilized peripheral blood stem cells as graft and 10 patients had a sibling and 32 an unrelated donor (MUD), respectively. Half of the patients were allografted in complete remission and twenty with active, mostly refractory disease. With a median follow-up for surviving patients of nearly 2 years (range 64 – 1746 days) the Kaplan-Meyer procedure estimates a 48% probability of survival at 2 y after transplantation. Interestingly, there is no difference what so ever in survival if patients had an identical sibling donor or a MUD. Similarly, neither patient age below or above the median, nor the applied conditioning regimen did affect the outcome. The only significant variable for improved survival was being in complete remission at transplantation with a 2-year overall survival probability of 60% as compared to 30% for patients with active disease. Thirteen patients (31%) relapsed after allografting, which is substantially lower as to what is reported after conventional chemotherapy. Three of these patients could be salvaged by a second transplant, whereas 10 patients finally died from leukaemia. Non relapse mortality was 24% with 2 patients dying from acute GVHD, 7 from infections and 1 from suicide, despite being well physically. In conclusion, our data support the notion that allogeneic SCT is a highly effective treatment option for patients with AML and FLT-3 mutations and that, if the patient is eligible, it should be undertaken whenever possible in 1. complete remission. However, even patients with primary induction failure have a reasonable chance to be salvaged by allogeneic SCT. Disclosures: No relevant conflicts of interest to declare.

Abstract 2082 Poster Board II-59 Single agent arsenic trioxide (ATO) has proven efficacy in the management of newly diagnosed cases of acute promyelocytic leukemia (APL). To validate findings of an initial single center experience (Blood 2006:107; 2627) with this low cost, well tolerated, effective regimen, a multicenter study was undertaken in a resource constrained environment. Additionally, in an effort to improve on the earlier experience and study the role of duration of maintenance on reducing late relapses, patients were randomized to 6 vs. 12 months of ATO maintenance (ClinicalTrials.gov Identifier:NCT00517712). From July, 2004 to December, 2008, 182 patients were initially screened and enrolled based on morphological diagnosis of APL from 7 centers in India. Diagnosis was subsequently confirmed by molecular methods. Twenty seven cases were excluded from analysis (6 RT-PCR negative, 4 IC bleed at diagnosis, 5 septic/pneumonia at diagnosis, 9 withdrew consent prior to randomization and some were treated with other protocols, 1 withdrawn by investigator prior to randomization). Patients were treated with single agent ATO at standard doses (10mg/day for adults and 0.15mg/kg/day for pediatric patients) for up to 60 days in induction; this was followed by a 28 day consolidation after a 4 week break. Four weeks after completion of consolidation patients who were in molecular remission were randomized to 6 vs. 12 months of maintenance therapy with ATO administered for 10 days/month. Hydroxyurea was permitted for control of leucocytosis. Anthracyclines were permitted in induction for patients presenting with or WBC count rising >20×109/L in the first week, >50×109/L in the second week and for those who developed a differentiation syndrome. Of the 155 patients who could be evaluated 136 (87.7%) achieved hematological remission (CHR). One patient had primary induction failure and was removed from the study while the other 18 were induction deaths at a median of 17 days (range: 4 – 69). During induction, 52 (33.5%) patients received an anthracycline and 116 (75%) received hydroxyurea. A differentiation syndrome was documented in 25 (16%) cases and was fatal in one. Grade III/IV non hematological toxicity was seen in 26 (16.7%), which resolved in the majority after discontinuing ATO for a short period. One hundred and thirty six patients were randomized, 64 (47%) and 72 (53%) into a 6 and 12 month maintenance regimen respectively. A protocol change after randomization was done in 3 cases for persistent toxicity. Five (3.6%) patients did not complete the scheduled maintenance regimen due to poor compliance or was discontinued by the investigator. At a median follow up of 24 months, the 3-year Kaplan-Meir estimate of overall survival (OS), event free survival (EFS) and disease free survival (DFS) of the entire cohort was 76.87±4.33%, 71.57±4.64% and 80.69±4.77% respectively. Fourteen patients relapsed, the median time to relapse was 19.3 months (range: 9-51). The baseline characteristics of the two groups (6vs12 months) were not significantly different. Post randomization, the two groups were analyzed on an intention to treat basis. The OS, EFS and DFS of the two groups were not statistically significantly different. There was also no evidence that the group that received 12 months of maintenance had any increased incidence of toxicity. Single agent ATO based regimen as reported previously is well tolerated and results in durable remissions. Longer follow up is required to see if 12 months of maintenance therapy reduces risk of late relapses. Disclosures: No relevant conflicts of interest to declare.

Abstract 1209 Poster Board I-231 Background: The prognosis of patients with cytogenetically normal acute myeloid leukemia (CN-AML) ranges from relatively favorable to extremely poor. Recently, based on the presence or absence of well defined mutations, molecular subgroups have been identified, which allow an estimate of a patient's prognosis at the time of diagnosis. Allogeneic stem cell transplantation (SCT) is the only curative treatment for the majority of these patients. However, only limited data is available to describe the role of alloSCT in different molecular subgroups of CN-AML, particularly in advanced stages of the disease. Methods: We retrospectively analyzed the data on 247 patients with CN-AML, who uniformly had received the FLAMSA-RIC conditioning regimen for alloSCT in 14 European centers between 1996 and 2008. Results: Patients suffered from de novo AML (76%), sAML/MDS (21%), and tAML (4%). Median age was 52.1 (19-71) years. Donors were matched or mismatched family, and matched or mismatched unrelated donors in 30%, 2%, 50% and 18%, respectively. SCT was performed in untreated disease (6%), after primary induction failure (PIF, median time from diagnosis to transplantation 134 days; 23%), in first complete remission (CR1, 14%), and beyond CR1 (57%). Median follow-up of survivors was 19 months. Overall survival (OS) and leukemia-free-survival (LFS) of the entire cohort at 2 years from SCT was 51% and 47%, respectively. The disease stage at transplant was the most important variable for outcome (p=.001 for OS, Information on molecular markers was available in 183 patients (74%). As suggested by Schlenk et al. (NEJM 2008), analysis was based on two subgroups: 22 patients with isolated NPM1 mutation (NPM1mut), and 161 patients with other genotypes (FLT3 internal tandem duplication [FLT3-ITD], n=66; or wildtype FLT3/wildtype NMP1 [FLT3wt/NPM1wt], n=95). Patients with NPM1mut had a 4y OS/LFS of 75/63%. Results were not significantly different, when these patients were transplanted in PIF, CR1, or beyond CR1. Patients with other genotypes showed an OS/LFS of 51%/48% at 2y and of 40%/39% at 4y, without differences among patients with FLT-ITD and FLT3wt/NPM1wt. However, in this subgroup, outcome was highly dependent on the disease stage at SCT, with excellent results after transplantation in PIF (2y OS/LFS: 75%/74%) or in CR1 (2y OS and LFS: 76%), but inferior outcome after transplantation beyond CR1 (2y OS/LFS 38%/33%; p=.004 for OS and .001 for LFS). Conclusion: Allogeneic SCT following the FLAMSA-RIC conditioning produces excellent survival rates in patients with CN-AML, particularly when performed in CR1. Encouraging results in PIF support an early transplant, regardless of molecular subgroup, when CR is not reached after double induction therapy. In patients with an NPM1 mutation, transplantation in advanced disease achieved identical results as in early stage, which supports the strategy not to transplant these patients in CR1, but to delay alloSCT until relapse has occurred. In contrast, patients with FLT3-ITD or FLT3wt/NPM1wt achieved significantly worse results when transplanted beyond first relapse, arguing in favor of transplantation in CR1 for this molecular subgroup. Disclosures: Mayer: BMS: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; GSK: Consultancy; Fresenius: Consultancy; Roche: Research Funding; Pfizer: Research Funding.

ASCT is the standard therapy for relapsed HL. However, the majority of published studies suggesting benefit of ASCT for relapsed HL include relatively young patients (pts) with favorable prognostic features, and have relatively short follow-up. Moreover, very little data exists on the outcome of pts who experience progression of HL after ASCT. To determine the long-term outcome of ASCT in the modern, “ABVD-era”, and the impact of allogeneic transplantation in pts who fail ASCT, we reviewed all pts with HL who were treated with ASCT between 1990 and 2005 at the University of Rochester. 117 pts (44% female; 89% Caucasian) with documented HL were treated with ASCT for relapsed or refractory HL. At ASCT, median age was 34 years (range 19–66). 75% of these pts were treated initially with ABVD or MOPP-ABVD hybrid therapy. Histology was: NS (n=82), mixed cellularity (n=20), LP (n=6), LD (n=3), and classical NOS (n=6). 32% of pts had relapsed within 1 year of initial therapy, and 25% were refractory to therapy prior to ASCT. Conditioning regimens at ASCT were BEAC (n=80); BEAM (n=28); CBV (n=1); Cy/TBI (n=8). 49% of pts received XRT following ASCT. Median follow-up of entire cohort exceeded 5 years. At 5 years, overall survival (OS) for entire population was 50%, and event-free survival (EFS) was 38%. As expected, pts older than 45 yrs of age (n=21, p=0.06) and pts who relapsed within 1 year of initial therapy (p=0.0004) had an inferior OS after ASCT. In total, 49 pts have died; of these, 30 pts died of HL. 19 deaths occurred in remission: 9 were conditioning-related within the first 100 days of ASCT; 3 were from secondary malignancies (2 AML, 1 NHL), 1 from colitis, 1 from pulmonary fibrosis, and 5 with unknown cause. 9 of the deaths occurred more than 5 yrs after ASCT. 54 pts had progression of HL post ASCT; median survival for this group was 2.1 years after ASCT. 14 of these pts (26% of pts who failed ASCT) underwent allogeneic transplantation. 8 of these patients have died: 5 from progression of HL, 2 from pulmonary toxicity, and 1 from GVHD. Of the 5 remaining pts, 1 has progression of HL after allogeneic transplantation, and 3 have chronic GVHD. We conclude that ASCT remains a curative option for patients relapsing after ABVD, as there is a clear plateau on the relapse free survival curve after 5 years. Primary refractory disease and older age at ASCT dramatically affects outcome. In this modern era, deaths in remission after ASCT remain a significant problem due to both short-term and long-term toxicities of therapy. The risk of progression of HL persists until 5 years after ASCT, emphasizing the importance of prolonged follow-up. Although some pts who progress with HL after ASCT may live for years with a seemingly indolent form of HL, there is no plateau on the survival curve, and the majority of pts who progress after ASCT are not alive 2 years post ASCT. Allogeneic transplantation has not yet had a significant impact on OS for this group of pts. Novel approaches are clearly needed for the majority of pts who progress after ASCT, particularly older patients at ASCT and patients with primary induction failure.

Backgrounds: Adult acute lymphoblastic leukemia (ALL) has poor prognosis despite intensive chemotherapy. Allogeneic hematopoietic stem cell transplantation is an optimal therapeutic strategy in relapsed ALL patients. HLA-matched unrelated donation is difficult in some cases because of the rapid disease progression. Cord blood transplantation (CBT) excells other measures in its availability, render it particularly effective in urgent situations; however, the outcome of CBT for adult ALL cases has not yet been clarified. Patients/Methods: We reviewed medical records of 22 adult ALL patients who received CBT at Toranomon Hospital between January 2002 and June 2005. Median age of the patients was 54.5 (range 18–68). Disease status were CR1 (n=4), CR2 (n=3), RL1 (n=8), RL2 (n=1) and primary induction failure (n=6), respectively. 18 patients recieved fludarabine based regimen and the other received CY/TBI myeloablative regimen. Fludarabine based conditioning regimen was consisted of fludarabine (125 mg/m2), melphalan (80–140 mg/m2) and TBI (4–8Gy). GVHD prophylaxis was cyclosporine (n=12) or tacrolimus (n=10). Median total nucleated cell and CD34+ cell counts were 2.6×106 cells/kg (1.6–4.4) and 0.7×105 cells/kg (0.2–3.2), respectively. HLA disparity was 5/6 (n=1), 4/6 (n=20) and 3/6 (n=1). Results: The probability of disease free survival at 2 years was 59%. Overall survival curves of each conditioning regimen were depicted as below. Half of the relapsed/refractory ALL patients achieved complete remission and remained disease free after CBT. Discussion: Adult ALL patients without any suitable donor should be considered as a candidate for CBT. Figure Figure

Prognostic factors for AML at diagnosis include cytogenetics, FLT3 ITD, age, MDR status and white cell count at presentation. Several groups (Blood2000; 95:72; BJH1999; 107:69; Haematologica2004; 89:528) have reported that time to achievement of complete remission (CR) is an independent post-induction prognostic factor in AML. Furthermore, some investigators have classified patients who do not achieve CR with one cycle as primary induction failure. Between 1983 and 1993 1,959 patients were registered to 6 consecutive ECOG studies (E3483, PC486, E1490, E2491/INT0129, E3489 and E3993). These studies were for patients age 18–55 years (E3483, PC486 and E3489); age 56–70 years (E1490); age >56 years (E3993) and with no age limit (E2491/ INT0129). Of these 1,959 patients, 1261 achieved CR (64%) and were available for analysis. All patients received standard induction therapy, consisting of daunorubicin 60 mg/m2 (E3483, PC486 and E1490), or 45 mg/m2 (E2491/ INT0129) or idarubicin 12 mg/m2 (E3489), or a randomization between daunorubicin 45 mg/m2, idarubicin 12 mg/m2 or mitoxantrone 12 mg/m2 (E3993) - all for 3 days - together with cytarabine 100–200 mg/m2 by continuous infusion for 7 days. It should be noted that in the North American Intergroup APL study (E2491/ INT0129) patients who received ATRA in induction are excluded from this analysis. All patients were to receive a second cycle of identical induction therapy if the day 10–14 bone marrow demonstrated unequivocal residual leukemia. Identical study-specific post-remission therapy, including consolidation therapy and/or allogeneic or autologous bone marrow transplantation, was given to all patients who went into CR - irrespective if this was achieved after 1 or 2 cycles. This retrospective analysis compared patients who achieved CR after 1 cycle versus 2 cycles of induction therapy. The data were obtained from the ECOG database that recorded the number of days that patients received induction therapy (≤8 days vs >8 days). The table presents the data for disease-free survival (DFS) and overall survival (OS). These data are based on the Cox model, adjusting for other variables. Total Failed Median DFS/OS (mo) 5-year DFS/OS p-value DFS 1 cycle 406 321 10.2 24.4% 2 cycles 855 629 11.9 28.6% 0.07 OS 1 cycle 406 287 23.7 36.1% 2 cycles 855 583 24.1 35.7% 0.7 In this large cohort of patients, by multivariate analysis, age, WBC at diagnosis were significant factors for DFS and OS. However, the number of cycles given for induction or the time to achieve a CR in AML patients could not be demonstrated to have any independent prognostic significance. These data suggest that post-remission strategies in AML should not be influenced by the number of cycles required to achieve CR.