Risk adapted therapeutic strategy in newly diagnosed acute myeloid leukemia: Refining the outcomes of ELN 2017 intermediate-risk patients

2021 ◽  
Vol 105 ◽  
pp. 106568
Author(s):  
Razan Mohty ◽  
Radwan Massoud ◽  
Zaher Chakhachiro ◽  
Rami Mahfouz ◽  
Samer Nassif ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Therapeutic Strategy ◽  
Intermediate Risk ◽  
Newly Diagnosed ◽  
Risk Patients ◽  
Acute Myeloid

Low Platelet Counts at Diagnosis Predict Better Survival for Patients with Intermediate-Risk Acute Myeloid Leukemia

2019 ◽  
Vol 143 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Yimin Zhang ◽  
Haihui Gu ◽  
Qi Chen ◽  
Ying Zhang ◽  
Hui Cheng ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Negative Impact ◽  
Disease Free Survival ◽  
Intermediate Risk ◽  
Hematopoietic Stem ◽  
Free Survival ◽  
Risk Patients ◽  
Immature Cells ◽  
Acute Myeloid

Background: Aggressive growth of primitive and immature cells in the bone marrow results in reductions in megakaryocyte and platelet (PLT) counts, leading to thrombocytopenia in acute myeloid leukemia (AML). However, not all AML patients show thrombocytopenia at the time of diagnosis, and the association of PLT count with patient survival is largely unknown. Methods: A retrospective study was performed to determine PLT counts at diagnosis in the peripheral blood in 291 newly diagnosed AML patients and assess the association of PLT counts with the overall survival (OS) and disease-free survival (DFS) of these patients. Results: Low PLT counts (≤40 × 109/L) were associated with better outcomes for the whole cohort (5-year OS, 55.1 ± 3.8 vs. 35.3 ± 3.5%, p < 0.001; 5-year DFS, 49.1 ± 3.8 vs. 25.7 ± 4.0%, p < 0.001) and intermediate-risk patients (5-year OS, 64.5 ± 5.4 vs. 41.0 ± 4.8%, p < 0.001; 5-year DFS, 60.8 ± 5.6 vs. 28.6 ± 5.6%, p < 0.001). Moreover, low PLT counts were related to deeper molecular remission. Low PLT counts correlated with better survival of intermediate-risk AML patients treated with chemotherapy only. Allogeneic hematopoietic stem cell transplantation attenuated the negative impact of high PLT counts on the survival of intermediate-risk patients. Furthermore, univariate and multivariate analyses demonstrated that PLT count at diagnosis was an independent prognostic factor for intermediate-risk AML. Conclusion: PLT count at diagnosis predicts survival for patients with intermediate-risk AML.

scholarly journals FLT3 ligand impedes the efficacy of FLT3 inhibitors in vitro and in vivo

Blood ◽  
2011 ◽  
Vol 117 (12) ◽  
pp. 3286-3293 ◽  
Author(s):  
Takashi Sato ◽  
Xiaochuan Yang ◽  
Steven Knapper ◽  
Paul White ◽  
B. Douglas Smith ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Therapeutic Strategy ◽  
Newly Diagnosed ◽  
Flt3 Ligand ◽  
Flt3 Inhibitor ◽  
Flt3 Inhibitors ◽  
Acute Myeloid

AbstractWe examined in vivo FLT3 inhibition in acute myeloid leukemia patients treated with chemotherapy followed by the FLT3 inhibitor lestaurtinib, comparing newly diagnosed acute myeloid leukemia patients with relapsed patients. Because we noted that in vivo FLT3 inhibition by lestaurtinib was less effective in the relapsed patients compared with the newly diagnosed patients, we investigated whether plasma FLT3 ligand (FL) levels could influence the efficacy of FLT3 inhibition in these patients. After intensive chemotherapy, FL levels rose to a mean of 488 pg/mL on day 15 of induction therapy for newly diagnosed patients, whereas they rose to a mean of 1148 pg/mL in the relapsed patients. FL levels rose even higher with successive courses of chemotherapy, to a mean of 3251 pg/mL after the fourth course. In vitro, exogenous FL at concentrations similar to those observed in patients mitigated FLT3 inhibition and cytotoxicity for each of 5 different FLT3 inhibitors (lestaurtinib, midostaurin, sorafenib, KW-2449, and AC220). The dramatic increase in FL level after chemotherapy represents a possible obstacle to inhibiting FLT3 in this clinical setting. These findings could have important implications regarding the design and outcome of trials of FLT3 inhibitors and furthermore suggest a rationale for targeting FL as a therapeutic strategy.

scholarly journals Addition of the Anti-CD33 Monoclonal Antibody Mylotarg to Fludarabine/High Dose Cytarabine - Based Induction Significantly Improves Outcome in Patient Affected By FLT3-ITD Positive Cytogenetically Normal Acute Myeloid Leukemia

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 1365-1365
Author(s):  
Paola Minetto ◽  
Anna Candoni ◽  
Fabio Guolo ◽  
Marino Clavio ◽  
Maria Elena Zannier ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Favorable Effect ◽  
High Dose ◽  
Intermediate Risk ◽  
Npm1 Mutation ◽  
Mutational Status ◽  
High Dose Cytarabine ◽  
Risk Patients ◽  
Acute Myeloid

Background: The addition of the anti-CD33 targeting antibody Mylotarg (MY) to conventional "3+7" induction has been shown to improve the outcome of patients affected by acute myeloid leukemia (AML) without adverse cytogenetic alterations. Early reports suggested that MY was particularly effective among low risk patients, such as core binding factor AML, particularly if included in a high dose cytarabine-based induction therapy. The role of MY for intermediate risk patients appears to be less clear. Cytogenetically defined intermediate risk patients may be further stratified considering two frequent molecular aberrations: FLT3 "internal tandem duplication" (FLT3-ITD) mutation, associated with poor prognosis and NPM1 mutation (NPM1-mut), associated with a good prognosis. The concomitant presence of NPM1-mutpartially overcomes the negative prognostic impact of FLT3-ITD, which is also modulated by FLT3-ITD/wild type allelic ratio. NPM1 and FLT3 mutational status assessment is strongly recommended for risk stratification at diagnosis by the last ELN 2017 guidelines. Aims: To investigate the efficacy of MY added to an intensive fludarabine, high dose cytarabine and Idarubicin-based induction regimen (FLAI) as frontline treatment for younger (&lt;65 years), cytogenetically normal AML patients according to NPM1 and FLT3-ITD mutational status. Methods:One-hundred and forty eight consecutive AML patients, treated in 3 Italian Hematology centersbetween 2008 and 2018and harboring at least one molecular alteration among NPM1-mut and FLT3-ITD, were included in the analysis. Thirty three patients carried isolated FLT3-ITD, 50patients showed concomitant FLT3-ITD and NPM1-mut and 65 isolated mutated NPM-1.Median age was 50 years(range: 18-65). All patients received FLAI induction (fludarabine 30 mg/sqm and ARA-C 2g/sqm on days1 to 5 plus idarubicin 10 mg/sqm on days 1-3-5), with or without low dose MY(3 mg/sqm, added in 42 patients), followed by a second induction without fludarabine and with idarubicin at the increased dose of 12 mg/sqm. Before 2017, patients with isolated FLT3-ITD mutation were scheduled for allogeneic stem cell transplantation (HSCT), if an HLA-matched sibling donor was available, whereas after 2017 only patients with high allelic burden isolated FLT3-ITD mutation received HSCT in first CR. The other patients received conventional high dose cytarabine consolidation for a total of 3 cycles. Results: Overall, 60-days mortality was 3%, and was not significantly influenced by receiving or not MY during induction. After one induction cycle, 126 patients achieved CR (85%) with no difference between patients receiving or not MY. After a median follow up of 70months, 3-year overall survival (OS) was 59.5% (median not reached). OS duration was significantly longer in NPM1 mutated patients (p &lt;0.05).Patients with isolated FLT3-ITD mutation had a significantly worse prognosis (3-year OS 38.3%, p&lt;0.05). The addiction of MY did not significantly improve outcome in the whole cohort but did show a significant positive effect on survival among FLT3-ITD patients (3-year OS 66.7% vs 46.6% for FLT3-ITD patients receiving or not MY, respectively, p&lt;0.03, Fig. 1). This effect was more evident among the 33 NPM1 negative/FLT3-ITD patients: in this subgroup, patients who received MY had an overall good outcome that was similar to patients with double mutation who received the same therapy(median OS not reached in both groups, p=n.s.). On the contrary, among patients who did not receive MY, NPM1 negative/FLT3-ITD positive patients had a poor outcome, significantly inferior to double positive patients receiving the same regimen(3-Year OS 39.8% and 57.3%, respectively, p&lt;0.05). The favorable effect of MY among FLT3-ITD patients was not influenced by FLT3-ITD allelic burden.Of note, the proportion of patients receiving HSCT in first CR, as expected, was higher among patients harboring isolated FLT3-ITD mutation, but there was no significant difference among patients receiving or not MY. Conclusions: Despite the potential bias due to the retrospective nature of the analysis, our data seem to indicate that Mylotarg, added to an intensive fludarabine/high dose cytarabine-based induction, provides a significant improvement in anti-leukemic efficacy in patients carrying FLT3-ITD mutation, especially if concomitant NPM1 mutation is not present. Disclosures Candoni: Gilead: Honoraria, Speakers Bureau; Celgene: Honoraria; Pfizer: Honoraria; Janssen: Honoraria; Merck SD: Honoraria, Speakers Bureau. Bocchia:Novartis: Honoraria; Incyte: Honoraria; BMS: Honoraria.

A Genome-Wide Map of Acquired Uniparental Disomy in Acute Myeloid Leukemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 996-996 ◽  
Author(s):  
Manu Gupta ◽  
Manoj Raghavan ◽  
Rosemary E. Gale ◽  
Claude Chelala ◽  
Christopher Allen ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Copy Number ◽  
Myeloid Leukemia ◽  
Uniparental Disomy ◽  
Normal Karyotype ◽  
Intermediate Risk ◽  
Snp Arrays ◽  
Risk Patients ◽  
Control Set ◽  
Acute Myeloid

Abstract The recent discovery of acquired uniparental disomy (aUPD) in acute myeloid leukemia (AML) has been linked to homozygosity for mutations in certain genes (Raghavan et al, Cancer Res. 2005, Fitzgibbon et al, Cancer Res. 2005). Although this phenomenon, which is undetectable by conventional cytogenetics, has been confirmed in subsequent small-scale studies, its extent and frequency remains uncertain. To determine the frequency and distribution of aUPD, DNA samples from 455 young adult AML patients entered in the UK Medical Research Council AML10 trial were analyzed using Mapping 10K 2.0 single nucleotide polymorphism (SNP) arrays (Affymetrix Inc.). Genomic DNA from blood samples of ten non-leukemic individuals was used as control to estimate the copy number values (control set I). We defined aUPD as 50 consecutive homozygous markers but allowed 2 heterozygous calls to accommodate contaminating normal tissue. Using this criterion a false positive rate of 3.3% was calculated from an available data of 90 independent controls (control set I). Overall, 120 regions of UPD were observed in 79 AML cases (17%), 87% of which involved at least one breakpoint, i.e. resulted from mitotic recombination, and 13% were whole chromosome aUPDs arising from chromosomal non-disjunction. They were the sole aberration, as detected by SNP arrays, in 61 samples (13%), and 84% of these had only a single region of aUPD. There was a non-random distribution across chromosomes; 13q (n=18 cases), 11p (n=8) and 11q (n=9) were the most frequently affected. Other chromosomes with regions of recurrent aUPD were 2p (n=7), 2q (n=6), 1p (n=5), 19q (n=4), 17q12–q21.2 (n=4), 21q (n=4), 9p (n=3), Xq (n=3), 6p (n=2), and 17p (n=2). Acquired UPDs were observed across all cytogenetic risk groups: in 25% of adverse risk patients, 11% of favorable risk, 19% of normal karyotype and 10% of the remaining intermediate risk patients. Samples with aUPD13q (5% of samples) belonged exclusively to the intermediate risk group. Chromosome 13 was the only chromosome to show recurrent whole chromosome aUPD. Fifteen samples with aUPD13q covered the region of the FLT3 gene at 13q12.2; all 15 had a FLT3-internal tandem duplication (ITD) and all cases with a high FLT3-ITD mutant level > 50% of total had 13q aUPD. Gains and losses were observed in 12% and 14% of the samples respectively. As expected, gains on chromosome 8 and losses on chromosomes 5 and 7 were common, confirming the general utility of this approach. No homozygous losses were observed. Comparison of arrays with cytogenetic analysis showed that additional information (aUPDs and/or copy number changes) was obtained in 23% of cases with a normal karyotype and 38% of cases without available cytogenetics. This study highlights the importance of aUPD in the development of AML and pinpoints regions that may contain novel mutational targets.

scholarly journals Use of Measurable Residual Disease to Evolve Transplant Policy in Acute Myeloid Leukemia: A 20-Year Monocentric Observation

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1083
Author(s):  
Francesco Buccisano ◽  
Raffaele Palmieri ◽  
Alfonso Piciocchi ◽  
Luca Maurillo ◽  
Maria Ilaria Del Principe ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Residual Disease ◽  
Low Risk ◽  
Risk Category ◽  
Intermediate Risk ◽  
Historical Cohort ◽  
Risk Patients ◽  
Measurable Residual Disease ◽  
Acute Myeloid

Measurable residual disease (MRD) is increasingly employed as a biomarker of quality of complete remission (CR) in intensively treated acute myeloid leukemia (AML) patients. We evaluated if a MRD-driven transplant policy improved outcome as compared to a policy solely relying on a familiar donor availability. High-risk patients (adverse karyotype, FLT3-ITD) received allogeneic hematopoietic cell transplant (alloHCT) whereas for intermediate and low risk ones (CBF-AML and NPM1-mutated), alloHCT or autologous SCT was delivered depending on the post-consolidation measurable residual disease (MRD) status, as assessed by flow cytometry. For comparison, we analyzed a matched historical cohort of patients in whom alloHCT was delivered based on the sole availability of a matched sibling donor. Ten-years overall and disease-free survival were longer in the MRD-driven cohort as compared to the historical cohort (47.7% vs. 28.7%, p = 0.012 and 42.0% vs. 19.5%, p = 0.0003). The favorable impact of this MRD-driven strategy was evident for the intermediate-risk category, particularly for MRD positive patients. In the low-risk category, the significantly lower CIR of the MRD-driven cohort did not translate into a survival advantage. In conclusion, a MRD-driven transplant allocation may play a better role than the one based on the simple donor availability. This approach determines a superior outcome of intermediate-risk patients whereat in low-risk ones a careful evaluation is needed for transplant allocation.

scholarly journals Response to Venetoclax and Hypomethylating Agents Among Prognostic Risk Groups and Genetic Subtypes of Acute Myeloid Leukemia

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 334-334 ◽  
Author(s):  
Ibrahim Aldoss ◽  
Dongyun Yang ◽  
Raju Pillai ◽  
James F Sanchez ◽  
Ahmed Aribi ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Somatic Mutations ◽  
De Novo ◽  
Recursive Partitioning ◽  
Response To Therapy ◽  
Intermediate Risk ◽  
Hypomethylating Agents ◽  
Newly Diagnosed ◽  
Acute Myeloid

Abstract The combination of venetoclax and hypomethylating agents (HMA) has demonstrated potent activity in acute myeloid leukemia (AML), both in newly diagnosed patients (pts) and those with relapsed/refractory (r/r) disease. We analyzed the association between response to therapy and leukemic somatic mutations, cytogenetics, and other pertinent patient- and leukemia-related features in a large series of newly diagnosed and r/r AML in adults treated with venetoclax in combination with HMA at City of Hope between October 2016 and May 2018. We identified 107 evaluable adults with AML treated with the combination of venetoclax and HMA. Sixty-one (57%) pts had r/r AML at the time of initiating treatment (median prior lines of therapy: 2; range: 1-10), while 46 (43%) were treated in the frontline setting. The median age of pts was 68 years (range: 19-86). AML was de novo in 57 (53%), therapy-related in 23 (21%) and secondary in 27 (25%) pts. Thirty-six (34%) pts had prior exposure to HMA, and 21 (20%) pts had relapsed following prior allogeneic hematopoietic cell transplantation (HCT). The majority of treated pts had unfavorable (52%) or intermediate-risk (39%) AML based on combined cytogenetics and molecular profiles. The most common detected somatic mutations (majority by next generation sequencing) were FLT3 (17%), followed by DNMT3A (15%), RAS and TET2 (each 14%), RUNX1 (13%), TP53 (12%), and IDH1/2 (11%). Most pts received decitabine in combination with venetoclax (N=97, 91%); only 10 (9%) pts received 5-azacitidine together with venetoclax. Complete remission (CR)/CR with incomplete hematologic recovery (CRi) was achieved in 57 (53%) pts after a median of 2 (range 1-4) cycles. For 36 pts who achieved CR/CRi and had available minimal residual disease (MRD) assessment by multicolor flow cytometry (MFC), 23 (64%) became MRD-. CR/CRi was higher in pts carrying favorable- or intermediate-risk AML compared to poor-risk AML (100% vs. 60% vs. 45%, P=0.029). CR/CRi was 48% in those with complex cytogenetics (N = 31), 45% in monosomal karyotype (N = 22), 36% in KMT2A gene rearrangement (N = 11), 74% in normal karyotype (N = 19), and 25% in inversion 3 (N =4). The CR/CRi rate was not significantly different between newly diagnosed or r/r AML (61% vs. 48%, P = 0.17), nor was there a difference associated with AML type (de novo vs. therapy-related vs. secondary, P= 0.26), patient age (> or ≤ 65 years) at time of therapy (P = 0.13), prior allogeneic HCT (P = 0.29), prior administration of HMA (P = 0.37) and the type or schedule (5- or 10-day decitabine) of HMA (P = 0.52). In multivariate analysis, only favorable- or intermediate-risk cytogenetics was associated with better CR/CRi (P = 0.036). CR/CRi was also comparable regardless of the presence or absence of various analyzed somatic AML mutations. However, in recursive partitioning analysis of detectable somatic mutations and response to therapy, the combined lack of RAS, TP53 and RUNX1 mutations was linked to an improved rate of CR/CRi. When AML cases were stratified into functional gene alteration subgroups (according to the TCGA data set), there was no significant difference in CR/CRi according to the presence or absence of certain functional genes/fusions. Median overall survival (OS) for all pts was 12.5 months and was 14.6 months for pts who achieved CR/CRi, in contrast to 4.6 months for non-responders (P <0.001). Only AML subtype (de novo vs. therapy-related vs. secondary) (P <0.001) and AML genetic risk (favorable/intermediate vs. high) (P = 0.042) independently impacted OS in multivariate analysis. None of the AML individual somatic mutations influenced OS for this cohort, however, in recursive partitioning analysis of detectable mutations, the presence of any of SRSF2, IDH1/2 or RUNX1 were associated with improved OS. Furthermore, the presence of myeloid transcription factor (P = 0.033) and spliceosome complex mutations (P = 0.004) predicted superior OS, whereas the presence of a chromatin modifying mutation predicted inferior OS (P = 0.004). Thirteen (23%) responders subsequently underwent allogeneic HCT. We report remarkable activity with venetoclax and HMA across various high-risk genetics and clinical features in AML patients. Prospective studies are warranted to compare this combination directly with chemotherapy in all AML subsets. This is particularly true for high risk AML where response to conventional chemotherapy is poor. Disclosures Ali: Incyte Corporation: Membership on an entity's Board of Directors or advisory committees. Salhotra:Kadmon Corporation, LLC: Consultancy. Khaled:Alexion: Consultancy, Speakers Bureau; Juno: Other: Travel Funding; Daiichi: Consultancy. Stein:Celgene: Speakers Bureau; Amgen Inc.: Speakers Bureau. Forman:Mustang Therapeutics: Other: Licensing Agreement, Patents & Royalties, Research Funding.

Outpatient Cytarabine Administration Is Safe and Effective For Consolidation In Acute Myeloid Leukemia

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5030-5030 ◽  
Author(s):  
Marci R. Allen ◽  
Omar S. Aljitawi ◽  
Jianghua He ◽  
Sunil Abhyankar ◽  
Siddhartha Ganguly ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Regression Analysis ◽  
Stem Cell ◽  
Myeloid Leukemia ◽  
Intermediate Risk ◽  
Significant Difference ◽  
Risk Patients ◽  
Number Of Cycles ◽  
Relapse Rates ◽  
Acute Myeloid

Abstract Introduction Although most patients with Acute Myeloid Leukemia (AML) achieve complete remission with induction chemotherapy, further consolidation with chemotherapy or stem cell transplantation (SCT) is recommended in order to prolong remission duration and prevent relapse. Since the 1990’s, high dose cytarabine has been a standard consolidation regimen, with a goal of 3-4 cycles every 28 days and dose adjustments for advanced age.  However, there is no data to define the optimal number of cycles or predict if delays in consolidation delivery alter its efficacy. Furthermore, it has not been demonstrated whether outpatient cytarabine is a safe and feasible alternative to repeated inpatient admissions.  Our institution has moved to outpatient administration of cytarabine consolidation for eligible patients (reside within 30 minutes of the hospital in private home or American Cancer Society Hope Lodge with full-time caregiver) in an attempt to reduce hospitalization days, cost, and improve patient quality of life by limiting inpatient days.  We hypothesized that outpatient administration of cytarabine consolidation is safe and effective without increased treatment delays or AML relapse and represents a potentially cost-saving approach in selected patients. Methods We performed a retrospective chart review of 50 consecutive adult AML patients treated with cytarabine consolidation at the University of Kansas from January 1, 2005, to October 1, 2012.  Data collected included AML prognostic category, age, inpatient/outpatient cytarabine consolidation, number of cycles, time between treatment cycles, reasons for any delays and duration of remission. Results The median age was 52 (ages 20-70).  42% of patients had favorable risk disease, while 20% were high risk and 36% were intermediate risk.  High risk patients who received cytarabine consolidation did so due to the lack of suitable stem cell donor or as a bridge while securing a donor for SCT.  Intermediate risk patients who received cytarabine consolidation had no matched sibling or unrelated donor or declined SCT in first complete remission.  At the time of this writing, 44% were in remission while 56% had relapsed, with a median duration of remission of 391 days (range 94-991 days).   Factors which determined whether patients were treated with cytarabine consolidation as an inpatient or outpatient included insurance coverage for outpatient cytarabine and availability of local housing/caregiver.  Patients who received inpatient versus outpatient cytarabine were older (median ages of 57 and 44 respectively, p<.01).  Inpatient cytarabine was given to 54% of patients, 77% of whom have relapsed.  In contrast, outpatient cytarabine was given to 46% of patients, with a significantly lower rate of relapse at 32% (p=0.002). Patients treated with outpatient consolidation more frequently had favorable or intermediate risk AML (92% vs 69% inpatient).  The difference in relapse rates remained significant on logistic regression analysis controlling for cytogenetic risk category (p=0.048), although the sample size is small.  Delays of more than 7 days between consolidation cycles occurred in 67% of all patients. The most common reasons for delay were infection and prolonged cytopenias. Using Cox regression analysis, there was no significant difference in rates of delayed consolidation cycles between patients treated inpatient or outpatient. There was no statistically significant difference seen in relapse rates whether or not delays in treatment occurred (p=0.13).  There were no recorded incidents of ambulatory pump failure.  Out of 71 cycles of outpatient cytarabine administered, there were 20 re-hospitalizations, and 20% of patients had re-hospitalization during at least one outpatient consolidation cycle. Conclusions The delivery of cytarabine consolidation in the outpatient setting appears safe with no increase in delays in chemotherapy delivery.  Although the statistically significant difference in relapse rate favors  outpatient cytarabine consolidation, this may reflect inherent AML biology as more patients had favorable risk AML. There was no evidence to suggest inferior outcomes with this approach.  This small retrospective sample demonstrates the feasibility of outpatient cytarabine consolidation, avoiding costly and inconvenient hospitalization without compromising the on-time delivery of chemotherapy or clinical outcome. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Update on Optimal Management of Acute Myeloid Leukemia

2013 ◽  
Vol 7 ◽  
pp. CMO.S8528 ◽  
Author(s):  
Fuad El Rassi ◽  
Martha Arellano
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Chromosomal Abnormalities ◽  
Intermediate Risk ◽  
Optimal Management ◽  
Therapeutic Approaches ◽  
Favorable Prognosis ◽  
Risk Patients ◽  
Immature Myeloid Cells ◽  
Acute Myeloid

Acute myeloid leukemia (AML) represents a malignant accumulation of immature myeloid cells in the marrow, presenting with impaired hematopoiesis and its attendant complications, including bleeding, infection, and organ infiltration. Chromosomal abnormalities remain the most powerful predictors of AML prognosis and help to identify a subgroup with favorable prognosis. However, the majority of AML patients who are not in the favorable category succumb to the disease. Therefore, better efforts to identify those patients who may benefit from more aggressive and investigational therapeutic approaches are needed. Newer molecular markers aim at better characterizing the large group of intermediate-risk patients and to identify newer targets for therapy. A group that has seen little improvement over the years is the older AML group, usually defined as age ≥ 60. Efforts to develop less intensive but equally efficacious therapy for this vulnerable population are underway.

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