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Breakpoint clustering in t(4;11)(q21;q23) acute leukemia
CS Chen, PS Medberry, DC Arthur and JH Kersey
Department of Laboratory Medicine/Pathology, University of Minnesota,
Minneapolis.
Chromosome 11 band q23 is commonly involved in nonrandom chromosomal
translocations in hematopoietic malignancies, especially in infant acute
leukemias. By using pulsed-field gel electrophoresis (PFGE) with
restriction endonuclease digests of DNA from both a leukemia cell line
(RS4;11) bearing the t(4;11)(q21;q23) and from human/hamster hybrid cells,
we have been able to construct a detailed restriction map of the chromosome
11q23 region and have localized the t(4;11) chromosome 11 breakpoint to a
region located approximately 200 to 230 kb telomeric to the CD3 gamma
region and approximately 580 kb centromeric to the PBGD gene. PFGE analyses
of DNA from clinical leukemia specimens and cell lines indicated a tight
clustering of breakpoints in all eight t(4;11) acute leukemias studied.
These data strongly suggest that discrete genetic loci are interrupted on
both chromosomes 4 and 11 in a manner likely to be critically involved in
the pathogenesis of t(4;11) acute leukemias. To our knowledge, these
results represent the first evidence of breakpoint clustering in t(4;11)
acute leukemias. In contrast to t(4;11), other 11q23 abnormalities studied
to date have frequently shown evidence for alternative breakpoint sites in
11q23.
Volume 78,
Issue 10,
pp. 2498-2504,
11/15/1991
Copyright © 1991 by The American Society of Hematology
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