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