Clinical features, cytogenetics and outcome in acute lymphoblastic and myeloid leukaemia of infancy: report from the MRC Childhood Leukaemia working party

Abstract

The clinical features, cytogenetics and response to treatment have been examined in 180 infants (aged Ͻ1 year) with acute leukaemia; 118 with acute lymphoblastic leukaemia (ALL) and 62 with acute myeloid leukaemia (AML). Comparison of clinical features showed no difference in age or sex distribution between infants with ALL and AML but infants with ALL tended to have higher leucocyte counts at presentation. Cytogenetic abnormalities involving 11q23 were found in 66% of ALL and 35% of AML cases, the commonest, t(4;11) being found only in ALL. The other recognised 11q23 translocations were found in both types of leukaemia. Few patients had the common cytogenetic abnormalities associated with ALL in older children and few with AML had good risk abnormalities. Four year eventfree survival 60% cf 30% (P = 0.001) and survival 65% cf 41% (P = 0.007) were significantly better in AML than ALL. These results were due to a lower risk of relapse 27% cf 62% at four years. Superior event-free survival was also seen in the subgroup of patients with 11q23 abnormalities and AML (55% cf 23%). The reasons for superior response in AML are unknown but may be related to the intensity of treatment, lineage of the leukaemia or other as yet unidentified factors. Leukemia (2002) 16, 776-784.

Mature B-cell acute lymphoblastic leukemia with t(9;11) translocation: a distinct subset of B-cell acute lymphoblastic leukemia

“…[7][8] However, the t(9;11) translocation, although the most common 11q23 chromosomal abnormality associated with de novo AML with monocytic differentiation (FAB M4 and M5) and DNA-topoisomerase inhibitor therapyrelated AML, is only rarely seen in precursor B-ALL. [10][11][12]26,27 Although the exact fusion gene in our cases was not determined, studies of the t(9;11) translocation in AML most commonly results in a fusion of the MLL and AF9 genes. 26 Additional studies have suggested that the resultant MLL/AF9 fusion gene is involved in myeloproliferation 13 and leukemogenesis.…”

“…Infantile B-ALL, generally a precursor B-ALL, has a poor prognosis and is frequently associated with rearrangement of the MLL gene [10][11][12] through different genetic aberrations involving chromosome 11q23. Reciprocal translocations are most common and the following are most common in decreasing order of frequency: t(4;11)(q21;q23), t(11;19)(q23;p13.3) and t(9;11)(p21-22;q23).…”

“…Reciprocal translocations are most common and the following are most common in decreasing order of frequency: t(4;11)(q21;q23), t(11;19)(q23;p13.3) and t(9;11)(p21-22;q23). [10][11][12] MLL gene rearrangements are seen in both B-ALL and T-cell ALL, and in acute myelogenous leukemia (AML), especially DNAtopoisomerase inhibitor therapy-related AML. 13,14 Infantile B-ALL with MLL gene rearrangements or MLL þ precursor B-ALL has typically a CD10À, CD20À, CD34 þ , TdT þ, and HLA-DR þ pro-B-cell immunophenotype.…”

Prognostic impact of t(9;11) in childhood acute myeloid leukemia (AML)

“…6 Thus, it is conceivable that the type of hematopoietic cells targeted by MLL rearrangements influences the drug sensitivity of transformed blasts. According to recent evidence on childhood ALL with 11q23 alterations, 7,8 it is possible that leukemic cells with MLL rearrangement involve early progenitor cells that are more likely to exhibit drug resistance than are cells from patients older than 1 year or, in case of AML with FAB M5, harboring the same genetic change.…”

Clinical features, molecular diagnosis, and treatment outcome of infants with leukemia in Taiwan

“…The clinical and biological features of infant leukemia are different from those of childhood leukemia. Infants with this disease more frequently have hyperleukocytosis, massive hepatosplenomegaly, and central nervous system (CNS) involvement [2][3][4]. Infant ALL usually presents with CD10-negative precursor-B immunophenotype, and the blast cells often express myeloid-associated antigens [2,3,5].…”