Genes 2025, 16(7), 798; https://doi.org/10.3390/genes16070798 (registering DOI) - 1 Jul 2025
Abstract
Acute myeloid leukemia (AML) accounts for only about 15–20% of pediatric leukemia and an overall incidence of 1.4 cases per 200,000 children under the age of 15 years. The majority of pediatric AML occurs de novo, often as the result of somatic first
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Acute myeloid leukemia (AML) accounts for only about 15–20% of pediatric leukemia and an overall incidence of 1.4 cases per 200,000 children under the age of 15 years. The majority of pediatric AML occurs de novo, often as the result of somatic first hits in utero. A minority of pediatric AML occurs in response to a predisposition syndrome, such as a bone marrow failure syndrome, or other inherited mutations and copy number changes. While the overall survival of pediatric patients with AML is approximately 70%, survival at the individual level is dependent on the abnormality detected either through cytogenomic analyses or sequencing for mutations in responsible genes. Indeed, de novo infant AML carries a more sobering prognosis than that of pediatric AML. This review describes many of the common genomic abnormalities associated with pediatric AML and characterizes their detection from a laboratory assessment perspective. Pediatric AML is primarily a disease of gene rearrangements rather than of gene mutations, and, as such, clinical cytogenetics takes a primary role.
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(This article belongs to the Section Molecular Genetics and Genomics)
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