scholarly journals Study of CD25 expression on leukemic cells: a prognostic factor in acute myeloid leukemia

2018 ◽  
Vol 49 (1) ◽  
pp. 20-27
Author(s):  
Amina H Hassab ◽  
Dalia A Nafea ◽  
Rania S Swelem ◽  
Basma M Ghazal
Keyword(s):  
Acute Myeloid Leukemia ◽  
Prognostic Factor ◽  
Myeloid Leukemia ◽  
University Hospital ◽  
Leukemic Cells ◽  
Response To Treatment ◽  
Molecular Characteristics ◽  
Newly Diagnosed ◽  
Cd25 Expression ◽  
Acute Myeloid

AbstractBackgroundAcute myeloid leukemia (AML) is a heterogeneous hematologic malignancy characterized by a clonal expansion of myeloid blasts. Treatment strategies of patients with AML are based on various prognostic factors, including age and performance status of the patient, as well as cytogenetic and molecular characteristics of the leukemic clone.Our aim was to study the expression of cluster of differentiation (CD)25 in adult Egyptian patients with newly diagnosed AML and to assess its prognostic relevance.MethodsThis study was conducted on 50 newly diagnosed AML patients at the Hematology Unit, Internal Medicine Department, Alexandria Main University Hospital. All patients were subjected to full history taking, thorough clinical examination, and laboratory investigations, including detection of CD25 expression on blast cells by flow cytometry. Conventional karyotyping was done on 11 patients at the time of diagnosis.ResultsIn our study group, 12 patients were positive for CD25 expression, and this positivity was associated with worse overall survival and shorter leukemia-free survival. On evaluating the response to treatment among CD25-positive AML patients with normal karyotype, they had lower complete remission rates and higher relapse and death rates.ConclusionsExpression of CD25 in AML patients at presentation can be considered a poor independent prognostic factor.

Clinical Activity, Pharmacokinetics, and Pharmacodynamics of Sorafenib In Pediatric Acute Myeloid Leukemia.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1073-1073
Author(s):  
Hiroto Inaba ◽  
Jeffrey E Rubnitz ◽  
Elaine Coustan-Smith ◽  
Lie Li ◽  
Brian D Furmanski ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Leukemic Cells ◽  
Clinical Activity ◽  
Newly Diagnosed ◽  
Pediatric Acute Myeloid Leukemia ◽  
Rtk Signaling ◽  
Acute Myeloid

Abstract Abstract 1073 Background: Aberrant receptor tyrosine kinase (RTK) signaling arising from genetic abnormalities, such as FLT3-internal tandem duplications (FLT3-ITD), is an important mechanism in the development and growth of acute myeloid leukemia (AML) and is often associated with a poor outcome. Hence, inhibition of RTK signaling is an attractive novel treatment option, particularly for disease that is resistant to conventional chemotherapy. We evaluated the clinical activity of the multikinase inhibitor sorafenib in children with de novo FLT3-ITD–positive AML or relapsed/refractory AML. Methods: Fourteen patients were treated. Six patients with newly diagnosed FLT3- ITD–positive AML (aged 9–16 years; median, 12 years) received 2 cycles of remission induction therapy and then started sorafenib (200 mg/m2 twice daily for 20 days) the day after completing induction II (low-dose cytarabine, daunorubicin, and etoposide). Nine patients (aged 6–17 years; median, 9 years) with relapsed AML (including one treated on the above regimen) received sorafenib alone (2 dose levels; 200 and 150 mg/m2) twice daily for the first week of therapy, concurrently with clofarabine and cytarabine on days 8–12, and then alone from days 13 to 28. Sorafenib pharmacokinetics were analyzed at steady-state on day 8 of sorafenib in patients with newly diagnosed AML and on day 7 in patients with relapsed AML. In patients with relapsed AML, the effect of sorafenib on signaling pathways in AML cells was assessed by flow cytometry. Results: All 6 newly diagnosed patients, including 2 whose AML was refractory to induction I, achieved a complete remission (CR) after induction II; 5 had negative minimal residual disease (MRD; <0.1% AML cells in bone marrow) after induction II. Both patients in this group who relapsed achieved second remissions, one with sorafenib alone and one on the relapse regimen described above. Of the 9 patients with relapsed AML, 6 (4 with FLT3-ITD) were treated with sorafenib 200 mg/m2. All 6 had a >50% decrease in blast percentage and/or bone marrow cellularity after 1 week of sorafenib. After concurrent sorafenib and chemotherapy, 5 of the 9 patients with relapsed AML achieved CR (2 had negative MRD) and 2 achieved a partial remission (PR; 5%-25% AML cells in bone marrow); all 4 patients with FLT3-ITD had a CR or PR. After sorafenib treatment, 6 patients underwent HSCT while 2 with FLT3-ITD who could not receive HSCT were treated with single-agent sorafenib and have maintained CR for up to 8 months. Hand-foot skin reaction (HFSR) or rash occurred in all patients and improved with cessation of sorafenib. Dose-limiting toxicity (DLT, grade 3 HFSR and/or rash) was observed in 3 of the 6 patients with relapsed AML treated with 200 mg/m2 of sorafenib; no DLT was observed at 150 mg/m2. The effect of sorafenib on downstream RTK signaling was tested in the leukemic cells of 4 patients: in most samples, phosphorylation of S6 ribosomal protein and 4E-BP1 was inhibited. The mean (± SD) steady-state concentration (Css) of sorafenib was 3.3 ± 1.2 mg/L in the newly diagnosed group and 6.5 ± 3.6 mg/L (200 mg/m2) and 7.3 ± 3.6 mg/L (150 mg/m2) in those with relapsed AML. In both groups, the mean conversion of sorafenib to sorafenib N-oxide was 27%-35% (approximately 3 times greater than previously reported), and mean sorafenib N-oxide Css was 1.0–3.2 mg/L (2.1-6.7 μM). In a 442-kinase screen, the inhibitory profiles of sorafenib N-oxide and sorafenib were similar, and FLT3-ITD phosphorylation was potently inhibited by both forms (sorafenib N-oxide Kd = 0.070 μM; sorafenib Kd = 0.094 μM). Sorafenib N-oxide inhibited the growth of an AML cell line with FLT3-ITD (IC50 = 0.026 μM) and 4 AML cell lines with wild-type FLT3 (IC50 = 3.9–13.3 μM) at approximately half the potency of sorafenib. Conclusion: In children with de novo FLT3-ITD and relapsed/refractory AML, sorafenib given alone or with chemotherapy induced dramatic responses and inhibited aberrant RTK signaling in leukemic cells. Sorafenib and its active metabolite (sorafenib N-oxide) likely contribute to both efficacy and toxicity. These results warrant the incorporation of sorafenib into future pediatric AML trials. Disclosures: Inaba: Bayer/Onyx: Research Funding. Off Label Use: Sorafenib and clofarabine: both used for treatment of pediatric acute myeloid leukemia.

scholarly journals Complete hematologic remissions induced by 2-chlorodeoxyadenosine in children with newly diagnosed acute myeloid leukemia

Blood ◽  
1994 ◽  
Vol 84 (4) ◽  
pp. 1237-1242 ◽  
Author(s):  
VM Santana ◽  
CA Hurwitz ◽  
RL Blakley ◽  
WR Crom ◽  
X Luo ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Plasma Concentrations ◽  
Leukemic Cells ◽  
Remission Induction ◽  
Significant Activity ◽  
Newly Diagnosed ◽  
Blast Cells ◽  
Acute Myeloid

Abstract The majority of children with acute myeloid leukemia (AML) who are treated exclusively with chemotherapy die of progressive disease. Improvement in outcome will likely require new active drugs capable of eradicating resistant blast cells early in the clinical course. We therefore assessed the cytoreductive potential of 2- chlorodeoxyadenosine (2-CdA), a halogenated purine analogue, in 22 consecutive children with newly diagnosed AML. The drug was administered as a single 120-hour continuous infusion (8.9 mg/m2 of body surface area per day) before the introduction of standard remission induction therapy. Six patients (27%) had complete hematologic remissions by a median of 21 days after treatment with the nucleoside (range, 14 to 33 days). Seven others had partial responses, yielding a total response rate of 59%. The drug also eliminated leukemic cells from cerebrospinal fluid in 4 of the 6 patients tested. Concentrations of 2-CdA in cerebrospinal fluid on day 5 after the initiation of treatment ranged from 12.4% to 38.0% (mean, 22.7%) of the steady-state plasma concentrations. Severe but reversible myelosuppression and thrombocytopenia developed in all patients. Analysis of factors that may have influenced the complete remission rate suggested a better outcome in patients with myeloblastic leukemia (M0-M2 subtypes in the revised French-American-British classification system). These results demonstrate clinically significant activity by 2- CdA against previously untreated AML in children, including leukemic blast cells in the central nervous system. Its use in combination chemotherapy may improve the outlook for patients with this often fatal hematologic cancer.

scholarly journals Interaction network of proteins associated with unfavorable prognosis in acute myeloid leukemia

2020 ◽  
Author(s):  
Juan Jose Rendon-Rodriguez ◽  
Luisa Fernanda Restrepo-Rodriguez ◽  
Sarah Rothlisberger
Keyword(s):  
Acute Myeloid Leukemia ◽  
Complete Remission ◽  
Myeloid Leukemia ◽  
Serum Proteins ◽  
Disease Free Survival ◽  
Leukemic Cells ◽  
Response To Treatment ◽  
Ppi Network ◽  
Hematopoietic Stem ◽  
Acute Myeloid

Acute myeloid leukemia (AML) is a malignant disorder of hematopoietic stem and progenitor cells, characterized by accumulation of immature blasts in the bone marrow and peripheral blood of affected patients. Standard induction therapy leads to complete remission in approximately 50% to 75% of patients. In spite of favorable primary response rates, only 20% to 30% of patients enjoy long-term disease free survival. Identifying proteins involved in prognosis is important for proposing biomarkers that can aid in the clinical management of the disease. The aim of this study was to construct a protein-protein interaction (PPI) network based on serum proteins associated with unfavorable prognosis of AML, and analyze the biological pathways underlying molecular complexes in the network. We identified 16 candidate serum proteins associated with unfavorable prognosis (in terms of poor response to treatment, poor overall survival, short complete remission, and relapse) in AML via a search in the literature: IL2RA, FTL, HSP90AA1, D2HGDH, PLAU, COL18A1, FGF19, SPP1, FGA, PF4, NME1, TNF, ANGPT2, B2M, CD274, LGALS3. The PPI network was constructed with Cytoscape using association networks from String and BioGRID, and Gene Ontology enrichment analysis using the ClueGo pluggin was performed. The central protein in the network was found to be PTPN11 which is involved in modulating the RAS-ERK, PI3K-AKT and JAK-STAT pathways, as well as in hematopoiesis, and in the regulation of apoptotic genes. Therefore, a dysregulation of this protein and/or of the proteins connected to it in the network leads to the defective activation of these signaling pathways and to a reduction in apoptosis. Together, this could cause an increase in the frequency of leukemic cells and a resistance to apoptosis in response to treatment.

Fludarabine Based Regimen (FLAI) Is an Effective Treatment for Induction of Multidrug Resistant Pgp-Positive Acute Myeloid Leukemia Patients.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1857-1857 ◽  
Author(s):  
Domenico Russo ◽  
Daniela Damiani ◽  
Michele Malagola ◽  
Antonio De Vivo ◽  
Mauro Fiacchini ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Multidrug Resistance ◽  
Myeloid Leukemia ◽  
Multidrug Resistant ◽  
Response To Treatment ◽  
Induction Treatment ◽  
Newly Diagnosed ◽  
Match Pair ◽  
Acute Myeloid

Abstract Induction treatment of acute myeloid leukemia (AML) is conventionally based on regimens containing cytarabine (Ara-C), one anthracycline and, sometimes, a third drug, such as etoposide. Primary P-glycoprotein (Pgp) overexpression is the most important mechanism of multidrug resistance (MDR) in AML cells and it is almost always associated with less response to treatment. To deal with this problem, in 1997, we started a treatment program with a regimen including Fludarabine (FLUDA) for the induction of newly diagnosed AML patients. FLUDA showed to be toxic against the MDR cells, in vitro, and able to enhance Ara-C cytotoxicity by increasing cell concentration of Ara-C 5′ triphosphate and inhibiting DNA repair. Between 1997 and 2004, 110 newly diagnosed AML patients aged less than 60 years were induced with FLAI (Fludarabine 25 mg/sqm/day days 1–5, Ara-C 2 gr/sqm/day days 1–5, Idarubicine 10 mg/sqm/day days 1, 3, 5) in the context of three consecutive prospective multicentric trials. At diagnosis, all the patients were assessed for the Pgp expression by an indirect immunofluorescence method with the anti-p170 monoclonal antibody MRK-16. The results were expressed as the mean fluorescence index (MFI) and patients with a MFI > 6 were setted as MDR+ve. We correlated the Pgp-expression, with the response to the induction. Interestingly, the Pgp+ve (MFI > 6) patients treated with FLAI entered CR as well as the Pgp-ve (MFI < 6). Twenty-four out of 39 Pgp+ve patients (61%) and 54 out of 71 Pgp-ve patients (76%) achieved a CR after a single induction course of FLAI (p= 0.1). This observation strongly supported the original hypothesis that fludarabine could play a favourable role against MDR+ve cells. In order to validate this finding we compared the results obtained in an hystorical group of 136 newly diagnosed AML patients younger than 60 years treated with a non-fludarabine containing regimen AI (Ara-C 200 mg/sqm/day c.i. days 1 - 7, Idarubicine 10 mg/sqm/day days 1, 3, 5). In the non-fludarabine group, 22 out of 69 Pgp+ve patients (32%) and 42 out of 67 Pgp-ve patients (63%) achieved a CR after one course of the induction therapy. This difference was stastically significant (p= 0.0006). Based on these observations, we decided to conduct a match pair study to confirm the superiority of FLAI for overcoming the primary multidrug resistance Pgp-mediated in AML.

Myelodysplastic syndrome is not merely “preleukemia”

Blood ◽  
2002 ◽  
Vol 100 (3) ◽  
pp. 791-798 ◽  
Author(s):  
Maher Albitar ◽  
Taghi Manshouri ◽  
Yu Shen ◽  
Diane Liu ◽  
Miloslav Beran ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Growth Factors ◽  
Myelodysplastic Syndrome ◽  
Cell Sorting ◽  
Early Phase ◽  
Myeloid Leukemia ◽  
Leukemic Cells ◽  
Newly Diagnosed ◽  
Therapeutic Approaches ◽  
Acute Myeloid

Abstract Myelodysplastic syndrome (MDS) is a disease characterized by ineffective hematopoiesis. There are significant biologic and clinical differences between MDS and acute myeloid leukemia (AML). We studied a cohort of 802 patients, 279 (35%) with newly diagnosed MDS and 523 (65%) with newly diagnosed AML, and compared clinical and biologic characteristics of the 2 groups. Complete clinical and cytogenetic data were available on all patients, and a subgroup of patients was studied for apoptosis, angiogenesis, proliferation, and growth factors. Our results demonstrate that MDS is a discrete entity that is different from AML and is characterized primarily by increased apoptosis in early and mature hematopoietic cells. Using cell sorting and loss of heterozygosity, we demonstrate that the leukemic cells from MDS patients are capable of differentiation into mature myeloid cells and monocytes. We also demonstrate that there is a significant overlap between AML and MDS when MDS is defined on the basis of an arbitrary percentage of blasts of 20% or 30%. These data suggest that despite similarities between AML and MDS in their responses to treatment and outcomes, MDS is biologically and clinically different from AML and should not be considered an early phase of AML. The data indicate that MDS must be better defined on the basis of its biology rather than the percentage of blasts; further, the data suggest that there is a need to develop therapeutic approaches that specifically address the biologic abnormalities of MDS.

scholarly journals Assessment of Minimal Residual Disease in Acute Myeloid Leukemia patient in Adult Egyptian Acute myeloid Leukemia Patients

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
M M Moussa ◽  
E A Abdelhady ◽  
N H Abdallah ◽  
I J Mahmoud
Keyword(s):  
Acute Myeloid Leukemia ◽  
Minimal Residual Disease ◽  
Myeloid Leukemia ◽  
Residual Disease ◽  
Statistical Significance ◽  
University Hospital ◽  
P Value ◽  
Newly Diagnosed ◽  
Minimal Residual ◽  
Acute Myeloid

Abstract Background The term minimal residual disease (MRD) is used to describe residual disease after suboptimal induction chemotherapy, but at the same time refers to the lowest levels of disease potentially compatible with cure or to molecularly defined relapse after long term remission. This study assesses the minimal residual disease in relation to the outcome in acute myeloid leukemia patients after 6 months of treatment of chemotherapy. Aim of the work The aim of this study is assessment of measurable minimal residual disease after treatment to identify acute myeloid leukemia patients who are at high risk of poor outcome. Patients and methods Minimal Residual Disease was measured using Flow cytometry in 30 newly diagnosed a 30 newly diagnosed acute myeloid leukemia (AML) patients. The patients were recruited from clinical hematology department at Ain shams university hospital over the period from May 2017 to November 2018. Results A total number of 30 acute myeloid leukemia patients were recruited from Ain Shams University hospital, hematology and Oncology Unit outpatient clinic, with age ranging from 18-60 years old (median age 40 years), 14 of them were males representing 46.6% of the total number and 16 were females representing 53.3% of the total number. There was no statistical significance between the age of the studied group and the MRD with P-value 0.147, the sex of the patients doesn’t contribute to the risk stratification with a P-value of 0.200. The number of cases with negative MRD after induction was 13 representing 43.3% of the total number, and was 12 patients after 6 months representing 70.5% of the remitted patients, considering that the cut out value of MRD is 0.1. There was a significant relationship between TLC and MRD, the higher the TLC the more positive the MRD. Positive MRD is associated with higher mortality rates, exhibiting a statistical significance with P-value of 0.005. Conclusion We concluded that assessment of minimal residual disease in AML is of great value in determination of prognosis of the disease and its outcome and it is of great value to determine the levels of minimal residual disease (MRD) during the course of therapy and to stratify patient to identify high risk patient and to plan the therapeutic program accordingly.

scholarly journals LYON-UNIVERSITY HOSPITAL EXPERIENCE WITH GEMTUZUMAB OZOGAMICIN THERAPY IN ACUTE MYELOID LEUKEMIA: A ‘REAL-LIFE’ STUDY

2020 ◽  
Vol 12 (1) ◽  
pp. e2020020 ◽  
Author(s):  
Xavier Thomas ◽  
Marica Laurino ◽  
Sandrine Loron ◽  
Marie-virginie Larcher ◽  
Gaëlle Fossard ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Real Life ◽  
Disease Free Survival ◽  
Gemtuzumab Ozogamicin ◽  
University Hospital ◽  
Newly Diagnosed ◽  
Hematopoietic Stem ◽  
Acute Myeloid ◽  
Refractory Aml

One-hundred and four adults with newly diagnosed or relapsed/refractory acute myeloid leukemia (AML) were treated with fractionated doses of gemtuzumab ozogamicin (GO) at one-single French center over a 10-year period. We attempted to define predictive factors for response and survival. The overall response rate was 70% (86% in newly diagnosed and 67% in relapsed/refractory AML). Disease-free survival (DFS) and overall survival at 3 years after GO treatment was 31% and 29%, respectively. Mortality during induction was 7%. Among remitters, allogeneic hematopoietic stem cell transplantation can be performed in 33 cases (45%). DFS at 3 years was 54%. Incidences of transplant-related mortality, grade ≥ 3 acute graft-versus-host (GvH) disease, and extensive chronic GvH disease were 15%, 12%, and 27%, respectively.No sinusoidal obstruction syndromes were reported among allografted patients as among the other patients in the studied cohort. GO-based chemotherapy is a viable option for treatment of newly diagnosed and relapsed/refractory AML patients, and is a feasible schedule as a bridge to allogeneic transplant.

scholarly journals Pracinostat plus azacitidine in older patients with newly diagnosed acute myeloid leukemia: results of a phase 2 study

2019 ◽  
Vol 3 (4) ◽  
pp. 508-518 ◽  
Author(s):  
Guillermo Garcia-Manero ◽  
Yasmin Abaza ◽  
Koichi Takahashi ◽  
Bruno C. Medeiros ◽  
Martha Arellano ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Older Patients ◽  
Myeloid Leukemia ◽  
Intensive Therapy ◽  
Single Agent ◽  
Response To Treatment ◽  
Phase 2 ◽  
Newly Diagnosed ◽  
Phase 2 Study ◽  
Acute Myeloid

Abstract Pracinostat, a potent oral pan-histone deacetylase inhibitor with modest single-agent activity in acute myeloid leukemia (AML), has shown synergistic antitumor activity when combined with azacitidine. This single-group, multicenter phase 2 study assessed the safety and efficacy of pracinostat combined with azacitidine in patients who were at least 65 years old with newly diagnosed AML and who were ineligible for standard induction chemotherapy. Patients received pracinostat 60 mg/d, 3 d/wk, for 3 consecutive weeks, plus azacitidine 75 mg/m2 daily for 7 days in a 28-day cycle. Primary endpoints were complete remission (CR), CR with incomplete count recovery (CRi), and morphologic leukemia-free state (MLFS) rates of the combination. Secondary endpoints included safety, progression-free survival (PFS), and overall survival (OS) of the regimen. Fifty patients (33 de novo, 12 secondary, and 5 therapy-related AML) were enrolled. Twenty-six patients (52%) achieved the primary endpoint of CR (42%), CRi (4%), and MLFS (6%). Median OS and PFS were 19.1 months (95% confidence interval [CI], 10-26.5 months) and 12.6 months (95% CI, 10-17.7 months), respectively, with a 1-year OS rate of 62%. Forty-three patients (86%) experienced at least 1 grade 3 or worse treatment-emergent adverse event with the combination, with infections (52%), thrombocytopenia (46%), and febrile neutropenia (44%) reported as the most common toxicities. The 30- and 60-day all-cause mortality rates were 2% and 10%, respectively. DNA sequencing revealed somatic mutations at baseline, and clearance rates correlated with response to treatment. Pracinostat plus azacitidine is a well-tolerated and active regimen in the frontline treatment of older patients with AML unfit for intensive therapy. A larger controlled trial is ongoing. This trial was registered at www.clinicaltrials.gov as #NCT01912274.

scholarly journals After Treatment Decrease of Bone Marrow Tregs and Outcome in Younger Patients with Newly Diagnosed Acute Myeloid Leukemia

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Mario Delia ◽  
Paola Carluccio ◽  
Anna Mestice ◽  
Roberta Frappampina ◽  
Francesco Albano ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Immune Response ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Leukemic Cells ◽  
Newly Diagnosed ◽  
Partial Responder ◽  
Younger Patients ◽  
Number Of Patients ◽  
Acute Myeloid

An emerging body of evidence demonstrates that defects in antileukemic effector cells in patients with acute myeloid leukemia (AML) can contribute to the development and/or persistence of the disease. In particular, immune suppressive regulatory T cells (Tregs) may contribute to this defective antileukemic immune response, being recruited by bone marrow leukemic cells to evade immune surveillance. We evaluated Tregs (CD4+/CD45RA-/CD25high/CD127low), performing multiparametric flow cytometry on freshly collected bone marrow aspirate (BMA), in addition to the usual molecular and cytogenetic work-up in newly diagnosed AML patients to look for any correlation between Tregs and the overall response rate (ORR). We studied 39 AML younger patients (<65 years), all treated with standard induction chemotherapy. ORR (complete remission (CR)+CR with incomplete hematologic recovery (CRi)) was documented in 21 out of 39 patients (54%); two partial responder patients were also recorded. Apart from the expected impact of the molecular-cytogenetic group ( p = 0.03 ) and the NPM mutation ( p = 0.05 ), diagnostic BMA Tregs did not show any correlation with ORR. However, although BMA Tregs did not differ in the study population after treatment, their counts significantly decreased in responder patients ( p = 0.039 ), while no difference was documented in nonresponder ones. This suggested that the removal of Treg cells is able to evoke and enhance anti-AML immune response. However, the role of BMA Tregs in mediating immune system-AML interactions in the diagnostic and posttreatment phase should be confirmed in a greater number of patients.

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