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Molecular rearrangements on chromosome 11q23 predominate in infant acute
lymphoblastic leukemia and are associated with specific biologic variables
and poor outcome
CS Chen, PH Sorensen, PH Domer, GH Reaman, SJ Korsmeyer, NA Heerema, GD Hammond and JH Kersey
Department of Laboratory Medicine/Pathology, University of Minnesota,
Minneapolis.
Acute lymphoblastic leukemia (ALL) in infants generally shows distinctive
biologic features and has a poor prognosis. Cytogenetic studies indicate
that many infant leukemias have chromosome 11q23 translocations. Because of
these findings and the distinct clinical features of infant leukemia, we
investigated 30 cases of infant ALL for molecular defects of 11q23.
Fourteen cases had cytogenetic abnormalities of 11q23, and all of them
showed 11q23 rearrangements at the molecular level. An additional seven
cases also had 11q23 molecular rearrangements, including one with normal
cytogenetic analysis. Molecular abnormalities of 11q23 were significantly
correlated with adverse prognostic factors, including age under 6 months,
hyperleukocytosis, CD10- phenotype, and early treatment failure. Molecular
analysis identified a group of infants with germline 11q23 that had a very
good treatment outcome with a projected event-free survival of 80% at
median follow-up of 46 months compared to 15% in infants with rearranged
11q23 (P < .001). These findings suggest that a high proportion (70%) of
infants with ALL have 11q23 rearrangements and that these rearrangements
are not always detectable by cytogenetic analysis. The presence of germline
11q23 DNA may identify a subgroup of infant ALL patients with a good
outcome using current therapy and a different etiology for their ALL.
Volume 81,
Issue 9,
pp. 2386-2393,
05/01/1993
Copyright © 1993 by The American Society of Hematology

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