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Cacace, F.;  Iula, R.;  Novellis, D.D.;  Caprioli, V.;  D’amico, M.R.;  Simone, G.D.;  Cuccurullo, R.;  Wierda, W.G.;  Mahadeo, K.M.;  Menna, G.; et al. Pediatric Acute Myeloid Leukemia. Encyclopedia. Available online: https://encyclopedia.pub/entry/24580 (accessed on 20 December 2025).
Cacace F,  Iula R,  Novellis DD,  Caprioli V,  D’amico MR,  Simone GD, et al. Pediatric Acute Myeloid Leukemia. Encyclopedia. Available at: https://encyclopedia.pub/entry/24580. Accessed December 20, 2025.
Cacace, Fabiana, Rossella Iula, Danilo De Novellis, Valeria Caprioli, Maria Rosaria D’amico, Giuseppina De Simone, Rosanna Cuccurullo, William G. Wierda, Kris Michael Mahadeo, Giuseppe Menna, et al. "Pediatric Acute Myeloid Leukemia" Encyclopedia, https://encyclopedia.pub/entry/24580 (accessed December 20, 2025).
Cacace, F.,  Iula, R.,  Novellis, D.D.,  Caprioli, V.,  D’amico, M.R.,  Simone, G.D.,  Cuccurullo, R.,  Wierda, W.G.,  Mahadeo, K.M.,  Menna, G., & Tambaro, F.P. (2022, June 28). Pediatric Acute Myeloid Leukemia. In Encyclopedia. https://encyclopedia.pub/entry/24580
Cacace, Fabiana, et al. "Pediatric Acute Myeloid Leukemia." Encyclopedia. Web. 28 June, 2022.
Pediatric Acute Myeloid Leukemia
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This entry is adapted from the peer-reviewed paper 10.3390/biomedicines10061405

Pediatric acute myeloid leukemia is a clonal disorder characterized by malignant transformation of the hematopoietic stem cell. The incidence and the outcome remain inferior when compared to pediatric ALL, although prognosis has improved in the last decades, with 80% overall survival rate reported in some studies. The standard therapeutic approach is a combined cytarabine and anthracycline-based regimen followed by consolidation with allogeneic stem cell transplantation (allo-SCT) for high-risk AML and allo-SCT for non-high-risk patients only in second complete remission after relapse.

AML pediatric risk stratification

1. Introduction

Pediatric acute myeloid leukemia (AML) is a heterogeneous clonal disorder characterized by malignant transformation of the hematopoietic stem cell (HSC). Pediatric AML is less common than acute lymphoblastic leukemia (ALL); while ALL accounts for 80% of all pediatric acute leukemias, AML barely reaches 15–20%. Pediatric AML has a bimodal age distribution, with higher incidence in patients younger than 2 years and a second peak in adolescents up to 10 to 20 years old [1].
Pediatric AML is generally characterized by poorer prognosis compared to ALL although outcomes have improved in the recent years. The 3-year overall survival (OS) is 70% or even higher [2][3][4]. Notably, 30% of children with AML relapse after treatment with very poor OS. The AML BFM study group reported a 5-year OS of 45%± 4%, with fewer early deaths (8.1%vs.2.2%) [5][6].

2. Pathophysiology of Pediatric AML

While the majority of pediatric AML occurs de novo, there is an increased incidence of AML reported in certain hereditary disorders such as Fanconi anemia, Kostmann syndrome, Shwachman–Diamond syndrome, and Diamond–Blackfan anemia, which may be related to alterations of DNA repair or detoxification of reactive oxygen species genes to pathogenetic variants in telomere biology genes or ribosome function [7].Children with Down syndrome (DS) have an increased risk of developing AML, particularly the megakaryoblast (MK) subtype. Indeed, the most common genetic factor associated with the development of AML is trisomy 21 [8].Germ-line mutations were found in families with a high risk of AML, suggesting a familial predisposition [9].DS patients also harbor a GATA1 mutation that, as broadly established, can lead to the development of a transient myeloproliferative disease (TDM), which commonly resolves without any treatment. Residual cells may undergo apoptosis or acquire additional mutations leading to acute megakaryocytic leukemia (AMKL) with an average latency of 3 years. Nevertheless, these patients typically have less-aggressive disease, with a significantly longer disease-free survival (DFS) compared to other types of pediatric AML. This is possibly due the fact that DS-AMKL requires less intense therapy to achieve a cure compared to non-DS AMKL, showing that children with AML-DS are more responsive to chemotherapy [10][11].
AML is derived from a clonal proliferation and the abnormal differentiation of myeloid stem cells as a consequence of two sequential genetic events. This process is known as the two-hit model of leukemogenesis [12]. In AML, there are two different types of relevant mutations: class I mutations frequently result in uncontrolled proliferation and include receptor or cytoplasmatic–nuclear tyrosine kinase mutations such as FLT3, K/NRAS, TP53, and c-KIT, in 20–25%, 40%, 2%, and 12% cases, respectively, and do not affect differentiation. In contrast, class II mutations involve cellular differentiation arrest and/or self-renewal [13][14]. The most common type II cytogenetic abnormalities in children are t(8;21)(q22;q22), involving core-binding factor (CBF) β AML, as well as inv 16 or t(16;16), and t(15;17)(q22;q21) in acute promyelocytic leukemia (APL). Specific pediatric translocations rarely detected in adults include t(1;22)(p13;q13) and t(11;12)(p15;p13). The NPM1 and CEBPA, class II mutations, are observed in 5–10% and 4% of cases, respectively, and they are associated with a better prognosis [15][16]. Although attractive, this model represents an oversimplification of AML pathogenesis; many approaches revealed the presence of novel mutations and absence of tyrosine kinase lesions, particularly in normal-karyotype AML, reducing the relevance of the two-hit model [17].

3. Therapeutic Considerations: Past and Future

The WHO classification for hematological malignancies, revised in 2016, integrated genetic characteristics, such as karyotypes and molecular aberrations, with morphology, immunophenotype, and clinical presentation, but has limited application in children, since cytogenetic and genetic abnormalities are uncommon as compared to adult AML [18]. As such, pediatric AML is classified as “not-otherwise-specified” [19].
New discoveries in AML genetic alterations were applied to pediatric patients, improving risk stratification and therapeutic approaches. The TARGET project, an analysis of the molecular aberrations in pediatric AML, showed that the mutation rate is lower in pediatric than in adult AML, with different somatic aberrations including structural changes, aberrant DNA methylation, and specific pediatric mutations [20]. In particular, RAS, KIT, and FLT3 class I mutation types are the most common mutated genes while DNMT3, IDH1, and IDH2 gene mutations are rare [21].
Fusion genes specifically identified in pediatric AML and associated with a grim prognosis include CBFA2T3-GLS2 and NUP98-NSD1.CBFA2T3-GLS2 is a chimeric transcript derived from a cryptic inversion of the telomeric region of chromosome 16 and expressed especially in non-DS FAB M7 AML. This gene mutation is present in patients younger than 5 years old and is characterized by high bone marrow blast count and extra-medullary involvement [20]. In contrast, NUP98-NSD1 can be found in 3.8% cases of pediatric AML and is the most frequent NUP98 rearrangement. It is usually associated with other chromosomal abnormalities, particularly trisomy 8, and other genetic mutations, such as FLT3-ITD, WT1, and CEBPA, and appears to play a role in histone methylation and acetylation [22].
Diagnostic approaches in pediatric AML may be influenced by experience in adults [13]. Treatment decisions are based on risk stratification and further guided by the initial response to treatment [5][6][23]. Most international pediatric study groups (AIEOP/BFM/FRANCE/UK/COG/Japan) define risk classification according to genetic/molecular abnormalities and response to treatment by the measurement of residual disease by flow and morphology [24]. In particular, favorable prognostic factors include t(8;21)(q22;q22)/RUNX1-RUNX1T1, t(15;17)(q22;q21)/PML-RARA, NPM1-mutated AML, and CEBPA double mutation [6].AML with MLL translocations has variable outcomes, depending on the associated translocation and occurs more frequently in children compared to in adults [25]. Chromosome 3q and 5q abnormalities and monosomy karyotype and high blast count at diagnosis are predictors of poor outcome [6][26].
FLT3 mutation is also associated with dismal prognosis in adult AML [27] and remains controversial in pediatrics [28][29][30]. However, a large meta-analysis of 10 trials including 1661 patients with pediatric AML showed a shorter OS for FLT3-ITD mutated AML [31]. AIEOP-BFM AML 2020 proposed risk stratification in three groups (standard, intermediate, and high-risk AML); AML is high risk when minimal residual disease (MRD) is ≥1% after induction course 1 or ≥0.1% at induction 2 or blast count is ≥5% at induction 1 (only if flow results are not informative) with one of genetic/molecular aberration at diagnosis, as described in Table 1 [24].
Table 1. Characteristics of pediatric high-risk AML.
Genetic Risk Criteria Response to Treatment Criteria
Complex karyotype (≥3 aberrations including at least one structural aberration) MRD ≥ 1% after induction course 1 or ≥0.1% at induction 2 or blast count is ≥5% at induction 1
Monosomal karyotype, i.e., -7, -5/del(5q)
11q23/KMT2A rearrangements involving:
-
t(4;11)(q21;q23) KMT1A/AFF1
-
t(6;11)(q27;q23) KMT2A/AFDN
-
t(10;11)(p12;q23) KMT2A/MLLT10
-
t(9;11)(p21;q23) KMT2A/MLLT3 with other cytogeneticaberrations
t(16;21)(p11;q22) FUS/ERG
t(9;22)(q34;q11.2) BCR/ABL1
t(6;9)(p22;q34) DEK/NUP214
t(7;12)(q36;p13) MNX1/ETV6
Inv3(q21q26)/t(3;3)(q21;q26) RPN1/MECOM
12p abnormalities
FLT3-ITD with AR ≥0.5 not in combination with other recurrent abnormalities or NPM1 mutations
WT1 mutation and FLT3-ITD
inv(16)(p13q24) CBFA2T3/GLIS2
t(5;11)(q35;p15.5) NUP98/NSD1 and t(11;12)(p15;p13) NUP98/KDM5A
Pure erythroid leukemia

4. Novel Potential Therapies

Few changes were observed over the last forty years in the treatment algorithm of both pediatric and adult AML. The standard therapeutic approach is a combined cytarabine and anthracycline-based regimen followed by consolidation with allogeneic stem cell transplantation (allo-SCT) for high-risk AML and allo-SCT for non-high-risk patients only in second CR after relapse [32][33].In the last decade, several drugs such as epigenetic treatments, i.e., hypomethylating agents or histone-deacetylaseinhibitors, anti-CD33–ozogamicin conjugated monoclonal antibodies, and FLT3 and isocitrate dehydrogenase (IDH) inhibitors were used to treat pediatric and adult AML (Table 2).
Table 2. Target therapy for pediatric AML.
Therapeutic Mechanism Pediatric AML Approval Clinical Trials Adult AML Approval Comments
Hypomethylating Agents
Azacytidine Not approved NCT02450877
NCT01861002
NCT03164057		 Approved These agents are incorporated into DNA resulting in downregulation of oncogenes, reactivation of tumor suppressors, and increasing sensitivity to cytotoxic agents.
Decitabine Not approved NCT01177540 Approved
Histone Deacetylase Inhibitors
Panobinostat Not approved NCT02676323 Not approved HDAC inhibitors induce cell cycle arrest and apoptosis. In adult patients, panobinostat and vorinostat are approved in r/r multiple myeloma by the EMA and FDA and in advanced primary cutaneous T-cell lymphoma by the FDA, respectively.
Vorinostat Not approved NCT03263936 Not approved
Pinometostat Not approved NCT02141828
NCT03724084		 Not approved
Immunotherapy and Immune-MediatedChemotherapy
Gemtuzumabozogamicin (GO) Approved NCT00372593 Approved The FDA approved GO for
-
Newly diagnosed CD33-positive AML in adults.
-
r/r CD33-positive AML in adults and in pediatric patients 2 years and older.
The EMA approved GO for patients aged 15 years (AYA) and above who are newly diagnosed and have not tried other treatments. It is used in combination with daunorubicin and cytarabine.
CD123-targeting drugconjugate Not approved NCT02848248
NCT03386513		 Not approved These therapiesremain in the early phases of research.
Ipilimumab Not approved NCT00039091
NCT02890329
NCT00060372		 Not approved Immune check point inhibitors have shown a good clinical response in combination with other drugs.
These trials recruited patients up to 18 years old; NCT03825367 is for pediatric r/r AML.
Ipilimumab is approved in solid tumors andpembrolizumab and nivolumab in Hodgkin’s lymphoma and solid tumors by both FDA and EMA.
Pembrolizumab Not approved NCT03291353
NCT02996474
NCT02845297
NCT02768792
NCT02771197
NCT03286114
NCT02981914		 Not approved
Nivolumab Not approved NCT02397720
NCT02532231
NCT02275533
NCT02846376
NCT03825367		 Not approved
Car-T Cells
Anti-CD33 Not approved NCT03971799
NCT03927261
NCT03126864		 Not approved Early phase trials are planned including phase I/II trials in children and young adults.
Anti-CD123 Not approved NCT02159495
NCT04318678		 Not approved
Tyrosin Kinase Inhibitors
Dasatinib Not approved NCT03173612 Not approved Results from pediatric AML trials are ongoing. Dasatinib is approved in both adult and pediatric hematological malignancies.
Midostaurina Not approved NCT00866281
NCT03591510		 Approved It is approved in newly diagnosed FLT3+ AML adult patients.
Sorafenib Not approved NCT01518413
NCT00908167
NCT00665990
NCT01371981
NCT01445080		 Not approved Clinical trials are ongoing in both pediatric and adult patients.
Quizartinib Not approved NCT01411267 Not approved -
Listaurtinib Not approved NCT00469859
NCT00557193		 Not approved -
Gilteritinib Not approved NCT04240002
NCT04293562		 Approved It is approved in adult r/r AML with an FLT 3 mutation by the FDA and EMA.
Crenolanib Not approved NCT02270788 Not approved -
JAK Inhibitors/Ruxolitinib
Ruxolitinib Not approved NCT01251965
NCT02638428		 Not approved It is approved in adults for intermediate and high-risk myelofibrosis.
Proteasome/Ubiquitin/NEDD8 Inhibitor
Bortezomib Not approved NCT01371981 Not approved It is approved for multiple myeloma and non- Hodgkin lymphoma.
Pevonedistat Not approved NCT03813147 Not approved -
TP53/MDM2 Antagonists
TP53/MDM2 antagonists Not approved NCT03644716 Not approved -
BCL2 Inhibitors
Venetoclax Not approved NCT03236857
NCT03194932		 Approved Approved for CLL and AML in adults 75 years old or unfit.
IDH Inhibitors
Enasidenib Not approved NCT02813135 Approved Approved for the treatment of adult patients with r/r AML with IDH2 mutation.
Ivosidenib Not approved Not open Approved Approved in adult R/R AML IDH1-mutated (or first line in elderly patients with AML). NCT04195555 is currently ongoing to investigate ivosidenib in pediatric solid tumors and lymphomas with IDH1 mutations.
Menin Inhibitors        
Sndx-5613 Not approved NCT04065399 Not approved Multiple clinical trials are ongoing. Preliminary results in r/rNPM1mutant andKMT2ArAML have shown tolerable toxicity and promising clinical activity (see below in the text).
 

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Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Fabiana Cacace , Rossella Iula , Danilo De Novellis ,
Valeria Caprioli
,
Maria Rosaria D’Amico
,
Giuseppina De Simone
,
Rosanna Cuccurullo
,
William G. Wierda
,
Kris Michael Mahadeo
,
Giuseppe Menna
,
Francesco Paolo Tambaro
View Times: 718
Revisions: 2 times (View History)
Update Date: 29 Jun 2022
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