Background: Acute lymphoblastic leukemia (ALL) predominates in early childhood, whereas acute myeloid leukemia (AML) becomes increasingly represented during adolescence. Although this developmental shift is consistently observed, its biological drivers remain unclear. Puberty represents a major endocrine transition that influences immune and hematopoietic regulation. We evaluated whether age-specific subtype patterns support a hormonally mediated shift in leukemogenic lineage susceptibility . Methods: All pediatric leukemia cases (0–19 years) recorded in a national registry were pooled (n = 2,829). Cases were stratified into age groups (0–4, 5–9, 10–14, 15–19 years) and classified by lineage subtype. Subtype proportions were calculated within age strata. Logistic regression assessed odds of AML relative to ALL using ages 0–4 years as reference. Age × sex interaction was evaluated using chi-square testing. Results: Early childhood (0–4 years) accounted for 39.0% of cases, with lymphoid leukemia comprising 71.2%. AML proportion increased progressively from 13.8% in ages 0–4 to 20.7% in 10–14 years and peaked at 34.2% in adolescents. The AML:ALL ratio rose from 0.19 to 0.69 across developmental stages. Adolescents demonstrated 3.65-fold higher odds of AML compared with children aged 0–4 years (95% CI 2.70–4.93; p < 0.001). A significant age × sex interaction wasidentified (? ² = 192.86; p = 1.53 × 10? ²? ). Conclusions: The marked adolescent expansion of AML temporally aligns with pubertal endocrine transition, supporting a developmental endocrine–immune framework for lineagespecific leukemogenesis.