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CH Pui, DL Williams, DK Kalwinsky, AT Look, SL Melvin, RK Dodge, G Rivera, SB Murphy and GV Dahl
Leukemic cells from 89 (24%) of 369 children with newly diagnosed acute
lymphoblastic leukemia (ALL) were found to have a pre-B immunophenotype. By
comparison with blasts having the common ALL phenotype, the pre-B cells
were more likely to have a DNA index less than 1.16 (P = 0.02), a
pseudodiploid karyotype (P less than 0.001), and a chromosomal
translocation (P = 0.001). Increased serum lactic dehydrogenase levels (P =
0.001) were also characteristic of pre-B ALL; otherwise, the clinical and
laboratory features of the two groups were similar. A nonrandom chromosomal
translocation, t(1;19)(q23;p13.3), was identified in blast cells from 16
(23%) of the 70 patients with pre-B ALL and adequate chromosome banding
studies; different translocations were found in 11 of the remaining
patients. The presence of any chromosomal translocation in the pre-B group
was significantly related to a higher leukocyte count, an increased level
of serum lactic dehydrogenase, an increased percentage of S-phase cells,
black race, and a blast cell DNA index less than 1.16. Four presenting
features were found to confer an increased risk of treatment failure among
pre-B patients: pseudodiploidy, chromosomal translocation, black race, and
higher serum lactic dehydrogenase level. In a multivariate analysis,
pseudodiploidy emerged as the strongest factor for predicting relapse in
pre-B ALL. The frequent association of chromosomal abnormalities of known
adverse prognostic significance and high serum lactic dehydrogenase levels
with pre-B-cell ALL explains, at least in part, the poor treatment outcome
reported for children with this subtype of leukemia.
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| Copyright © 1986 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||