Azacitidine Treatment In Patients Research Articles

Long-term genetic and clinical remissions after cessation of azacitidine treatment in patients with VEXAS syndrome.

Long-term genetic and clinical remissions after cessation of azacitidine treatment in patients with VEXAS syndrome.

Azacitidine Treatment in Patients with Myelodysplastic Syndrome, Chronic Myelomonocytic Leukemia Type 2 and Acute Myeloid Leukemia According to their Cytogenetic Findings

Abstract Introduction: Azacitidine is one of the hypomethylating agents available for the treatment of elderly patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). It is also used as an appropriate treatment of chronic myelomonocytic leukemia (CMML) in the real life setting. As treatment of AML and CMML is not curative, and allogeneic stem cell transplantation (allo-SCT) remains traditionally the only option, significant clinical benefits by hypomethylating agents have been reported. According to the available data, 16% of subjects with MDS who received azacitidine had a complete or partial normalization of blood cell counts and bone marrow morphology, while two-thirds of patients who required blood transfusions no longer needed them. Nevertheless, it can also be hepatotoxic in patients with severe liver impairment and extensive liver tumors. Aim: to summarize the effect of azacitidine treatment in patients in the light of their general condition, blood count parameters, toxicity (general and hematologic), as well as the presence of cytogenetic aberrations. Materials and Methods: Twenty-seven patients of which 15 patients with MDS, 9 patients with CMML and 3 patients with AML received azacitidine treatment. The blood count levels and toxicity were followed for a period of twelve months. Results: 22.2% of our patients (6 of 27) of different hematologic diagnoses showed genetic aberrations in their DNA. All they showed quick disease progression and fatal outcome, four of them also developed hematologic toxicity. The remaining 77.8% had no cytogenetic findings. Of all the cohort, 19.05% developed toxicity during the course of the treatment, 38% – decreased leucocyte levels, 14.3% – decreased thrombocyte levels and 18.2% – decreased hemoglobin level. The erythrocyte levels were not substantially influenced by the treatment. The majority of the patients sustained stable levels of red blood cells, as well as of platelets and hemoglobin without remarkable changes between month 0 and month 6 of the treatment. Conclusion: Our results showed, that the main disadvantage of azacitidine treatment in our patients were progressive leucopenia (in 10/27 patients or 37% of cases) and toxicity (8/27 or 29.6% of cases).

Outcome After Azacitidine Treatment in Patients with High-Risk Myeolodysplastic Syndrome, Chronic Myelomonocytic Leukemia Type 2 and Acute Myeloid Leukemia – A Single Center Experience (Preliminary Data)

Abstract Introduction: Hypomethylating agents have become a standard therapy for certain myeloid malignancies. Aim: The aim of this preliminary study was to assess efficacy and safety of azacitidine in patients with myelodysplas tic syndromes (MDS), chronic myelomonocytic leukemia with 10-29% blasts (CMML-2) and acute myeloid leukemia (AML) treated in a single center. Material and Methods: Twenty-six (69% male and 31% female, median age 67.8 years) patients (MDS, = 15; CMML-2, n = 2; AML, n = 9) treated with azacytidine in the period April 2017 to October 2018 year were included in the study. Disease assessment was performed after the 3rd cycle, 6th cycle, and at progression. Results: The median number of administered cycles was 6 (1-16). Erythroid response was achieved in 46.7% after 3rd cycle and 66.7% after 6th cycle. Platelet response was reached in 72.7% after 3rd cycle and 40% after 6th cycle and neutrophil hematological improvement in 27.3% and 50%, respectively. Only one patient (8.3%) progressed after the 6th cycle, stable disease or better marrow response was achieved in the others. The median progression free survival (PFS) and overall survival (OS) were 7.9 and 10.7 months in the MDS group and 9.7 and 11.5 months in the AML group, respectively. None of the patients with CMML-2 progressed at the end of the study. The only found factor to correlate with shortened PFS and OS was IPSS high risk MDS. The most frequent grade ≥ 3 adverse events was neutropenia 38.5%, followed by anemia 15.4% and thrombocytopenia 11.5%. Conclusion: The therapy with azacitidine is an option for elderly patients with high-risk MDS, AML and CMML-2 that provides PFS and OS for approximately one year irrespective of age or nosological subgroup. These are preliminary data and larger patient cohort and longer follow-up period are needed for clinical conclusions.

Real-World Costs of Azacitidine Treatment in Patients With Higher-Risk Myelodysplastic Syndromes/Low Blast-Count Acute Myeloid Leukemia.

Azacitidine (AZA) is a standard of care for higher-risk myelodysplastic syndrome (MDS)/low blast-count acute myeloid leukemia (AML). Despite this, there is a paucity of data on the real-world health care resource utilization costs of AZA in this population. We linked the Ontario AZA MDS registry-higher-risk MDS/low blast-count AML-to population-based health system administrative databases. Patients were observed for 24 months after first AZA and censored at the earliest of 90 days after last AZA, date of death, time of AML induction/stem-cell transplantation, or March 31, 2016. Costs (2015 Canadian dollars) were expressed as standardized mean and median 28-day costs. Univariable quantile regression was used to explore the association of baseline patient and disease characteristics and median cost. Multivariable quantile regression was used to explore predictors of median costs. Among 877 patients in the registry, mean standardized 28-day cost per patient was $17,638 (median, $15,272; interquartile range [IQR], $11,869-$19,580) and $13,450 (median, $11,043; IQR, $7,981-$14,882) excluding the cost of AZA. Major nondrug drivers of cost were cancer clinic visits and inpatient care (mean standardized 28-day cost, $4,631; median, $1,558; IQR, $238-$4,961). Transfusion dependence at AZA initiation (P = .001) and greater comorbid disease burden (P = .009) were independently associated with increased cost. Our cohort of patients with uniformly higher-risk MDS/low blast-count AML treated with AZA demonstrates substantial costs of care above and beyond the cost of AZA alone. These results provide insight into the costs of AZA in the real world with implications for resource allocation.

PB2095 OUTCOME AFTER AZACITITINE TREATMENT IN PATIENTS WITH HIGH‐RISK MYEOLODYSPLASTIC SYNDROME, CHRONIC MYELOMONOCYTIC LEUKEMIA TYPE 2 AND ACUTE MYELOID LEUKEMIA–A SINGLE CENTER EXPERIENCE

Background:Hypomethylating agents have become a standard therapy for intermediate‐2 and high‐risk International Prognostic Scoring System (IPSS) myelodysplastic syndromes (MDS), chronic myelomonocytic leukemia with 10‐29% blasts (CMML‐2) and elderly patients with acute myeloid leukemia (AML).Aims:The aim of this preliminary study was to assess the efficacy and safety of azacitidine treatment in patients with MDS, CMML‐2 and AML by analyzing the therapeutic response, progression‐free survival (PFS) and overall survival (OS) for each group of treated patients.MethodsTwenty‐six (69% male and 31% female) patients treated for the period April 2017 to October 2018 year in the Clinic of Hematology at Military Medical Academy, Sofia were included in the study. Azacitidine was administered subcutaneously at a dose of 75 mg/m2 for 7 days. Disease assessment was performed after the 3rd cycle, 6th cycle, and at progression.Results:The median age was 67.8 years (58‐80 years old). Thirteen had MDS intermediate‐2 IPSS MDS, 2 had high‐risk IPSS MDS, 2 had CMML‐2 and 9 were with AML. Azacitidine was administered as a first‐line therapy at 17 (65.4%), and as the second line in 9 (34.6%) patients. The median number of administered cycles was 6 (1‐16). Thirteen patients completed 6 cycles of azacitidine (8 patients with MDS, 2 with CMML‐2 and 4 with AML), 8 MDS patients have not complete due to progression, 3 (2 MDS, 1 AML) because of death and 2 patients (1 MDS, 1 AML) were ongoing but not reached 6 cycles. Erythroid response was achieved in 46.7% (n = 7, 4 MDS, 3 AML) after 3rd cycle and 66.7% (n = 10, 3 MDS, 1 CMML II, 2 AML) after 6th cycle. Platelet response was reached in 72.7% (n = 8, 6 MDS, 1 CMML II, 1 AML) after 3rd cycle and 40% (n = 2, 1 CMML II, 1 AML) after 6th cycle. Neutrophil response in 27.3% (n = 3, 2MDS, 1 AML) and 50%(n = 2, 2 MDS, 1 AML) after 3rd and 6th cycle. Bone marrow complete response was achieved in 4 patients (33.3%) (2 MDS, 1 AML and 1 CMML‐2), partial response in 3 (25.0%) (2 MDS and 1 AML), stable disease in 4 (33.3%) (2 MDS, 1 AML and 1 CMML‐2) and progression in 1 patient with AML (8.3%) after 6th cycle. For one patient there is missing data for bone marrow blast count. The median PFS in the MDS group was 7.9 months and in the AML group 9.7 months. None of the patients with CMML‐2 progressed at the end of the study. The median OS was 10.7 months in MDS group and 11.5 months in AML group. The most frequent grade≥ 3 adverse events was neutropenia 38.5 (n = 10), followed by anemia 15.4% (n = 4) and thrombocytopenia 11.5% (n = 3). The only found factor to correlate with shortened PFS and OS was IPSS high risk MDS (IPSS intermediate‐2 vs high ‐ PFS: 1.05 months vs 7.9 months, P = 0,01; OS: 1.4 months vs 12.39 months, P = 0.01).Summary/Conclusion:The therapy with azacitidine is an option for elderly patients with high‐risk MDS, AML and CMML II that provides PFS and OS for approximately one year irrespective of age or nosological subgroup. These are preliminary data and larger patient cohort and a longer follow‐up period are needed for clinical conclusions.

Outcome after azacitidine treatment in patients with high-risk myelodysplastic syndrome and acute myeloid leukemia in the Clinic of Hematology at St. Marina University Hospital, Varna

Introduction: Hypomethylating agents have become a standard therapy for high-risk myelodysplastic syndromes (MDS) and elderly patients with acute myeloid leukemia (AML). Aim: The aim of the study was to assess the efficacy of azacitidine treatment in patients with MDS and AML followed for 18 months. Materials and Methods: Twenty-seven patients with MDS and AML treated in the Clinic of Hematology at St. Marina University Hospital, Varna were included in the study. Azacitidine was administered subcutaneously in at a dose of 75 mg/m 2 for 7 days. Disease assessment was performed on the 3 rd month, 6 th month, and at progression. Results: Twenty-seven patients were analyzed. Their median age was 71.5 years. Nine had refractory anemia with excess of blasts II (RAEB II), 5 had chronic myelomonocytic leukemia II (CMML II), 1 was with unclassifiable MDS (MDS-U), and 12 with AML. The median number of administered cycles was 6 (1-19). Eleven patients completed 6 cycles of azacitidine. Partial response was achieved in 9 patients (33%) (7 MDS and 2 AML), stable disease in 8 (29%) (5 MDS and 3 AML). Progressive disease was observed in 10 patients (37%). The response correlated with the type of the disease (p=0.03), cytogenetic risk (p=0.01), and survival (p=0.000). At 18 months, 60% of MDS patients were alive compared to 41.7% in the AML group. The median time to death in the AML patient group was 2.5 months. The mean overall survival was 10.4 months (12.6 months for MDS patients and 5.4 months for AML patients). Conclusion: The therapy with azacitidine is an option for elderly patients with high-risk MDS. In patients with AML a rapid progression is observed during the first two cycles with mortality rate of 58.3%.

A retrospective study of azacitidine treatment in patients with intermediate-2 or high risk myelodysplastic syndromes in a real-world clinical setting in Greece.

For patients with intermediate-2 or high risk [according to the International Prognostic Scoring System (IPSS)] myelodysplastic syndromes (MDS), azacitidine treatment offers hematologic improvement (HI) but also has the potential to modify the natural disease course. 'RETRO-AZA-MDS-001', a retrospective chart review study was conducted from February to November 2012 across 17 hematology hospital sites of Greece, aiming to evaluate the clinical efficacy and safety profile of azacitidine in IPSS intermediate-2/high risk adult MDS patients in routine care. A total of 88 patients (median age 74.7years), with a 6.6month median (range 1.0-49.5) azacitidine treatment duration were enrolled. The overall response rate [complete response (CR), marrow CR and partial response] was 37.7% (23/61), while stable disease with HI was achieved by 21.3% (13/61). The HI rate was 33.0% (29/88) and the AML transformation rate 6.8% (6/88). Of the transfusion-dependent patients, 7.3% (3/41) became transfusion-independent during azacitidine treatment. The incidence of non-serious and serious adverse events related to azacitidine was 50.0 and 42.0%, respectively. Patients not receiving prior ESA therapy were expected to be 7.6 times more likely to achieve a clinical response (p=0.012). The study corroborates the favorable risk-benefit profile of azacitidine for intermediate-2/high risk MDS patients in routine clinical practice.

Low serum vitamin D levels are associated with shorter survival after first-line azacitidine treatment in patients with myelodysplastic syndrome and secondary oligoblastic acute myeloid leukemia

Azacitidine (AZA) therapy has become the recommended first-line treatment for patients with high-risk myelodysplastic syndromes (MDS) and oligoblastic (<30% bone marrow blasts) acute myeloid leukemia (AML). However, improvement of the efficacy of AZA treatment remains a challenge. We retrospectively tested the hypothesis that VitD levels (25-hydroxyvitamin D3) prior to start of first-line AZA therapy are predictive of overall survival (OS) in patients diagnosed with MDS and secondary oligoblastic AML. Furthermore, the antiproliferative effects of AZA in combination with 25-hydroxyvitamin D3 and 1α,25-dihydroxyvitamin D3 were investigated invitro. A total of 58 patients treated at our center between 2006 and 2014 were analyzed. Serum levels of VitD were quantified using a standard, commercially available 25-hydroxyvitamin D3 chemiluminescent immunoassay. Effects on cell proliferation were assessed using tetrazolium-based MTT assays. Median serum VitD level prior to AZA treatment was 32.8nM (range 11.0-101.5nM). Patient, disease and treatment characteristics did not differ significantly between the low (≤32.8nM; n=29) and high (>32.8nM; n=29) VitD group. Estimated probability of 2-year OS in the low versus high VitD group was 14% versus 40% (P<0.05). In multivariable analysis with OS as endpoint, adverse cytogenetics (HR 2.66, P=0.03) and VitD (per 10nM decrease, HR 1.68, P=0.02) were independent predictors of worse survival. In-vitro treatment of myeloid cell lines with AZA in combination with VitD produced synergistic and additive antiproliferative effects. Addition of nanomolar VitD concentrations to AZA resulted in potentiation of AZA activity. Conversely, combination with the VitD antagonist TEI-9647 resulted in inhibition of AZA activity. Our study suggests that higher VitD levels were associated with a survival advantage following first-line AZA therapy. Enhanced cytotoxic effects upon combination treatment may contribute to the observed clinical effects. VitD repletion/supplementation during AZA treatment should be explored.

Low Vitamin D Levels Are Associated with Inferior Survival Following Azacitidine Treatment in Patients with Myelodysplastic Syndrome

▪Introduction: Azacitidine (AZA) therapy has become the recommended first-line treatment for patients with high-risk myelodysplastic syndromes (MDS) and oligoblastic acute myeloid leukemia (AML; bone marrow blasts <30%). However, only around 50% of patients achieve objective responses with AZA therapy and the vast majority of responding patients have disease progression within 2 years resulting in dismal survival rates.Vitamin D (VitD) is a central regulator of calcium and bone homeostasis and affects multiple signaling pathways controlling proliferation, apoptosis and differentiation. More than 30 years ago, VitD was demonstrated to induce in vitro differentiation of AML blast cells. Consequently, VitD alone or in combination with other differentiating agents has been used for treatment of MDS patients showing inconsistent and rather limited efficacy. We retrospectively tested the hypothesis that VitD levels prior to start of treatment are predictive of overall survival (OS) in newly diagnosed MDS and oligoblastic AML patients receiving upfront AZA therapy. In addition, the antiproliferative effects of AZA in combination with different VitD derivatives were investigated in vitro.Patients, materials and methods: A total of 58 patients treated at our center between 2006 and 2014 had serum samples available for assessment of VitD status. Serum samples were collected at a median of 18 days prior to start of AZA treatment and cryopreserved at -80°C. VitD status was assessed by measurement of circulating 25-hydroxyvitamin D levels applying a standard chemiluminescent immunoassay (DiaSorin Deutschland GmbH, Dietzenbach, Germany). Overall survival (OS) was estimated using the method of Kaplan and Meier. Survival times were measured from the date of AZA treatment start. Comparison of OS between the VitD groups was done using the logrank test and by cox regression adjusting for known confounders.For in vitro analyses, a tetrazolium based MTT assay was used for assessment of growth inhibition of two different AML cell lines (HL60 and MOLM13) after exposure to AZA alone or in combination with VitD (1alpha,25-dihydroxyvitamin D and 25-hydroxyvitamin D; both from Cayman Chemical, Ann Arbor, MI, USA) or the VitD antagonist TEI-9647 (kindly provided by Teijin Pharma Ltd., Tokyo, Japan). Drug interactions were analyzed using the median-effect method of Chou and Talalay and combination index (CI) values were calculated according to the classic isobologramm equation with CI<1, CI=1 or CI>1 corresponding to synergism, additivity or antagonism, respectively. In cases where no antiproliferative activity upon single-agent treatment was assessable (low-dose VitD and TEI-9647), an analysis in terms of sensitization (potentiation) or inhibition of AZA activity was performed instead.Results: Estimated median follow-up time was 14.2 months. Median serum VitD level prior to AZA treatment was 33 nM (range 11-102 nM). A total of 18 patients underwent allogeneic stem cell transplantation (alloSCT) following AZA therapy and follow-up was censored at the time of alloSCT. Patient, disease and treatment characteristics did not differ significantly between the low (≤33 nM; n=29) and high (>33 nM; n=29) VitD group. Estimated one-year survival was 72% (95% CI 54-90%) in the high VitD group, which was significantly longer as compared to the low VitD group (41%, 95% CI 20-62%, p<0.05; Figure 1). In multivariate analysis with OS as endpoint, VitD (per 10 nM decrease, HR 1.83 95% CI 1.06-3.16, p=0.03) and adverse cytogenetics (HR 2.58 95% CI 1.10-6.06, p=0.03) were independent predictors of shorter survival. In vitro treatment of HL60 and MOLM13 cells with AZA in combination with VitD produced synergistic and additive antiproliferative effects. Addition of nanomolar concentrations of VitD to AZA resulted in potentiation of AZA activity. Conversely, combination with TEI-9647 resulted in inhibition of AZA activity.Conclusions: Our study suggests that higher VitD levels were associated with a survival advantage following upfront AZA therapy. As compared to AZA monotherapy combination treatment with VitD resulted in enhanced cytotoxic effects in vitro. VitD repletion/supplementation during AZA treatment should therefore be explored. [Display omitted] DisclosuresLuft:Immundiagnostik AG: Research Funding.

Azacitidine in outpatient treatment - single center experience.

Aim of the studyAzacitidine is a hypomethylating agent which is used in the treatment of myelodysplastic syndromes, acute myeloid leukemia and chronic myelomonocytic leukemia. Because of good tolerance to the drug, azacitidine can be administered both during hospitalization and in an outpatient setting.The aim of our retrospective analysis was to assess the efficacy of azacitidine treatment in patients with a myelodysplastic syndrome and with acute myeloid leukemia who had received treatment in hospital and in an ambulatory care setting. Offsets in the course of azacitidine administration and discontinuations of treatment have a negative impact on patients’ response to the therapy.Material and methodsThe study included 31 patients. Sixteen patients received azacitidine in an ambulatory care setting, 15 patients within their hospitalization.ResultsA hematologic response was achieved in 48% of the patients. Forty-one percent of the cycles were delayed. In an outpatient setting, 62% of the cycles were administered systematically, while during hospitalization the patients received 54% of cycles on time. Administrative problems caused the delay of 26% of the cycles.ConclusionsAzacitidine has a high tolerance level and a high safety profile which allows for its use in an outpatient care setting. Outpatient administration of azacitidine is feasible and safe without compromising efficacy.

P-163 Efficacy and tolerablity of azacitidine treatment in patients with MDS, AML and CMML

P-163 Efficacy and tolerablity of azacitidine treatment in patients with MDS, AML and CMML

Outcome of azacitidine treatment in patients with therapy-related myeloid neoplasms with assessment of prognostic risk stratification models

Azacitidine's efficacy in therapy-related myeloid neoplasms (t-MN) has not been well-studied. In our retrospective review of 84 t-MN patients treated with azacitidine, median overall survival (OS) was 14.5 months and overall response rate was 43%, including 11% complete remission, 4% marrow complete remission, and 11% partial remission. In patients who underwent allogeneic transplant (25%), median OS was 19.2 versus 12.8 months (P=0.023) for those who did not. Response rates were comparable to those reported for de novo myelodysplastic syndrome. When we analyzed outcomes according to five scoring systems, only the Global MD Anderson Risk Model predicted survival with statistical significance.

Bone Marrow Hypocellularity Does Not Impair the Tolerability or Efficacy of Azacitidine (AZA) in Patients with Higher-Risk Myelodysplastic Syndromes Treated in the AZA-001 Study

AbstractAbstract 3808 Background:Approximately 10–15% of patients with myelodysplastic syndromes (MDS) have a hypocellular bone marrow (BM) at diagnosis. Some studies have suggested hypocellular MDS may have an adverse prognostic impact, but this is controversial. In the Phase 3 randomized AZA-001 study, AZA prolonged overall survival (OS) in patients with higher-risk MDS compared with conventional care regimens (CCR) (Lancet Oncol, 2009). However, the efficacy and tolerability of AZA in the subset of patients with hypocellular MDS has not been determined. Purpose:This post hoc analysis was conducted to determine whether the prolongation of OS observed with AZA compared with CCR in the AZA-001 study is influenced by baseline BM cellularity. We also sought to explore the tolerability of AZA treatment in patients with higher-risk MDS and hypocellular BM. Methods:Study design of AZA-001 is reported elsewhere (Lancet Oncol, 2009). Briefly, patients with higher-risk MDS (FAB: RAEB, RAEB-t, or CMML, and IPSS Int-2 or High risk disease) were randomized to AZA (75 mg/m2/d SC × 7d q 28d) or to CCR (supportive care, low-dose Ara-C [LDAC], or intensive chemotherapy [IC]). In the current analysis, patients were divided into 2 groups based on centrally reviewed baseline BM biopsy samples which confirmed the diagnosis of MDS (J. Bennett): a hypocellular (≤30%) group and a non-hypocellular (>30%) group. OS was assessed using Kaplan-Meier methods and treatments were compared by log-rank analysis. Results:Of 358 patients in AZA-001 (AZA n=179, CCR n=179), BM cellularity data were available for 299 patients (AZA n=154, CCR n=145). At baseline, 87% of patients (n=260) had non-hypocellular BM and 13% of patients (n=39) had hypocellular BM. Of patients with hypocellular BM in the CCR group (n=18), 7 patients (39%) received supportive care, 9 (50%) LDAC, and 2 (11%) IC. In general, baseline characteristics were similar between the hypocellular and non-hypocellular BM groups. Similarly, age, % BM blasts, cytogenetics, cytopenias, and transfusion dependence, were generally balanced across treatments within the 2 cellularity groups (Table). Median (range) duration of AZA treatment cycles in hypocellular patients was 35.5 (28–54) days and in non-hypocellular patients was 33.0 (15–75) days. Response (complete or partial response [CR+PR]) rates in hypocellular patients treated with AZA were 0% and with CCR were 5.6% (p=0.4615); and hematologic improvement (HI) rates were 52% and 41%, respectively (p=0.532). In non-hypocellular patients treated with AZA or CCR, rates of CR+PR were 7.5% and 0.8%, respectively (p=0.010); and HI rates were 48% and 28% (p=0.001), respectively. The improvement in OS in AZA-treated patients was more pronounced in the hypocellular group than the non-hypocellular group, whereas OS in CCR-treated patients was similar regardless of BM cellularity (Figure). Median OS was significantly prolonged with AZA vs. CCR in both the hypocellular and non-hypocellular groups. In patients with hypocellular BM, at 33 months median OS was not reached (NR; 95% CI: 19.2, NR) in the AZA arm vs. 16.9 months (95% CI: 11.1, 19.3) in the CCR arm (p=0.001). In patients with non-hypocellular BM, median OS in the AZA arm was 21.1 months (95% CI: 16.2, 34.7) vs. 15.3 months (95% CI: 9.3, 17.6) in the CCR arm (p=0.012). Safety and tolerability in the two BM cellularity groups were similar to that seen in the overall AZA-001 study (Lancet Oncol, 2009). Frequencies of grade 3–4 hematologic AEs in AZA-treated patients in the hypocellular and non-hypocellular groups were similar: anemia (9.5% vs 14.7%, respectively), febrile neutropenia (9.5% vs 11.6%), leukopenia (14.3% vs 13.2%), neutropenia (61.9% vs 60.5%), and thrombocytopenia (61.9% vs 58.1%). Conclusions:In this post hoc analysis, the prevalence of patients with hypocellular MDS was 13%, consistent with the reported prevalence in the general MDS population (Bennett, 2009). The survival advantage with AZA vs. CCR in both baseline BM cellularity groups observed in this analysis was consistent with the overall OS advantage with AZA shown in AZA-001. These findings suggest AZA is a safe and effective treatment option for patients with BM hypocellularity. [Display omitted] [Display omitted] Disclosures:Seymour:Celgene Corporation: Consultancy, Honoraria, Speakers Bureau, Travel support Other. Bennett:Celgene Corporation: Consultancy. List:Celgene Corporation: Consultancy. Mufti:Celgene Corporation: Consultancy, Research Funding, Speakers Bureau. Gore:Celgene Corporation: Consultancy, Research Funding. Fenaux:Celgene: Honoraria, Research Funding. Hetzer:Celgene Corporation: Employment, Equity Ownership. Songer:Celgene Corporation: Employment, Equity Ownership. Skikne:Celgene: Employment, Equity Ownership. Beach:Celgene Corporation: Employment, Equity Ownership.