TO THE EDITOR:

Precursor B-cell acute lymphoblastic leukemia (B-ALL), a frequent malignancy in children, is characterized by recurrent primary numerical or structural alterations that provide specific molecular markers of the developing malignant clone. The most common alterations, accounting for >50% of all cases, are high hyperdiploidy (51-67 chromosomes) and the chromosomal translocation t(12;21) that generates the ETV6-RUNX1 (synonymous with TEL-AML1) fusion gene. Studies that use monozygotic twins concordant for leukemia, retrospective analyses of archived neonatal blood spots, and molecular screening of umbilical cord blood (UCB) have demonstrated that these subtypes of B-ALL frequently emerge before birth during fetal hematopoiesis.1,3-5  Both alterations are only mildly oncogenic and require secondary mutations for disease onset. This requirement partially explains the long latency of these leukemias, which emerge after birth at age 2 to 5 years (range, 1-15 years). Rarer B-ALL...

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