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Review
. 2021 Feb 13;13(4):777.
doi: 10.3390/cancers13040777.

Infant Acute Myeloid Leukemia: A Unique Clinical and Biological Entity

Charlotte Calvo  1 , Odile Fenneteau  2 , Guy Leverger  3 , Arnaud Petit  3 , André Baruchel  1 , Françoise Méchinaud  1
Affiliations
Review

Infant Acute Myeloid Leukemia: A Unique Clinical and Biological Entity

Charlotte Calvo et al. Cancers (Basel). .

Abstract

Infant acute myeloid leukemia (AML) is a rare subgroup of AML of children <2 years of age. It is as frequent as infant acute lymphoblastic leukemia (ALL) but not clearly distinguished by study groups. However, infant AML demonstrates peculiar clinical and biological characteristics, and its prognosis differs from AML in older children. Acute megakaryoblastic leukemia (AMKL) is very frequent in this age group and has raised growing interest. Thus, AMKL is a dominant topic in this review. Recent genomic sequencing has contributed to our understanding of infant AML. These data demonstrated striking features of infant AML: fusion genes are able to induce AML transformation without additional cooperation, and unlike AML in older age groups there is a paucity of associated mutations. Mice modeling of these fusions showed the essential role of ontogeny in the infant leukemia phenotype compared to older children and adults. Understanding leukemogenesis may help in developing new targeted treatments to improve outcomes that are often very poor in this age group. A specific diagnostic and therapeutic approach for this age group should be investigated.

Keywords: AML; acute myeloid leukemia; childhood; infant.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Bone marrow smears of acute megakaryoblastic leukemia (AMKL) patients, May–Grünwald–Giemsa staining, ×100. (A) Cytoplasmic blebs (black arrow) and binucleated cell. (B) Cell cluster giving a pseudo-solid tumor aspect of AMKL.
Figure 2
Figure 2
Molecular alterations in AMKL. Distribution of recurrent chromosome rearrangements and GATA1 mutations in pediatric non-Down syndrome (DS) AMKL [42,50].
See this image and copyright information in PMC

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