Phenomenon of evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia

An analysis of chromosomal abnormalities in bone-marrow cells was performed in 116 children with diagnoses of acute myeloid leukemia (AML). The frequency of the evolution of clonal chromosomal abnormalities in AML constituted 42.3%. Quantitative abnormalities of chromosomes 8, 9, and 21, as well as the secondary structural abnormalities in the chromosomal regions 12p12, 9p22, 9q22, 9q34, 11q14–23, and 6q2, were the most abundant. Quantitative abnormalities were registered in 26.7% cases. The basic mechanism of evolution of the leukemic clone contained trisomy, deletions, and monosomy. The frequency of evolution was seven times higher in the age group of up to 2 years and twofold higher in the age group of up to 5 years. The high frequency of evolution at t(15;17)(q22;q22) was established, while its absence was revealed at inv(16)(p13q22). Patients with clonal evolution were characterized by the increased frequency of relapses and earlier death before reaching remission, which might be explained by the severe initial state of those patients. The conception of abnormalities in the evolution of the clone was proposed to occur at certain stages as follows: (1) appearance of balanced rearrangements; (2) trisomy occurrence; (3) loss of chromosomal material. The occurrence of an unbalanced genome during evolution possesses advantages in the clonal proliferate activity and may be related to its response to chemotherapy. An identity in abnormal chromosomal structure was revealed as a result of the comparison of karyotypes during diagnostics and during relapse, which could be evidence of the initial induction of some types of evolution of chromosomal abnormalities in leukemic cells in AML children by the chemical agents.