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Acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) are two majorformsof leukemia developed from myeloid cells (MCs). To understand why AML andCML occurin children, we analyzed the causes and the mechanism of celltransformation of a MC. I. Forthe MCs in marrow cavity, repeatedbone-remodeling during bone-growth may be a source ofcell injuries. II. As atype of blood cell, a MC may have higher survivability from DNAchanges andrequire obtaining fewer cancerous properties for cell transformation than atissuecell. III. Point DNA mutations (PDMs) and chromosome changes (CCs) arethe two majortypes of DNA changes. CCs have three subtypes by effects on acell: great effect CCs(GECCs), mild-effect CCs (MECCs), and intermediate-effectCCs (IECCs). A GECC affectsone or more genes and can alone trigger celltransformation. PDMs/MECCs are mostly mildand can accumulate in cells. Some ofthe PDMs/MECCs contribute to cell transformation. AnIECC affects one or moregenes and participates in cell transformation. IV. Based on II andIII, wehypothesize that a MC may have two pathways on transformation: a slow andanaccelerated. Slow pathway is driven by accumulation of PDMs/MECCs.Accelerated pathwayis driven by accumulation of PDMs/MECCs/IECC(s). Atransformation via slow pathwayoccurs at old age; whereas that via acceleratedpathway occurs at any age. Thus, CML andpediatric AML may develop viaaccelerated pathway, and adult AML may develop via bothpathways. In conclusion,pediatric AML and CML may develop as a result of transformationof a MC viaaccelerated pathway; and repeated bone-remodeling for bone-growth may beatrigger for the transformation of a MC in a child.

Development of pediatric myeloid leukemia may be related to the repeatedbone-remodeling during bone-growth