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Loss of heterozygosity in the chromosomal region 12p12-13 is very common in
childhood acute lymphoblastic leukemia and permits the precise localization
of a tumor-suppressor gene distinct from p27KIP1
H Cave, B Gerard, E Martin, C Guidal, I Devaux, J Weissenbach, J Elion, E Vilmer and B Grandchamp
Laboratoire de Biochimie Genetique, Hopital Robert Debre, Paris, France.
Abnormalities of the short arm of chromosome 12 are relatively common in
hematologic malignancies and deletions of the region. 12p12-13 are found in
approximately 5% of the patients with acute lymphoblastic leukemia (ALL).
As a potent inhibitor of cyclin-dependent kinases, p27KIP1 prevents the
progression of the cell cycle and the gene encoding p27KIP1 represents a
potential tumor-suppressor gene. Its recent assignment to the chromosomal
region (12p12.3) prompted us to study the p27KIP1 gene in a series of 61
children with ALL. Microsatellite polymorphic markers flanking the p27KIP1
gene were analyzed to detect losses of heterozygosity (LOH). Eleven
patients displayed LOH for at least one of the markers. The deleted are
encompassed the p27KIP1 gene locus in 10 cases, but inactivation of the
remaining allele by deletion, translocation, or mutation was never
observed. In addition, in 1 patient, the p27KIP1 gene was situated outside
of the region of LOH. Thus, p27KIP1 does not seem to be the target gene of
12p12-13 alterations. However, this study indicates that 12p12-13
alterations at the molecular level, which are present in about 27% of the
children with B-lineage ALL, are much more common than had previously been
reported by usual chromosome analysis. Moreover, LOH mapping allowed us to
better define the location of a putative tumor- suppressor gene implicated
in these malignancies and should therefore help in identifying this gene.
Volume 86,
Issue 10,
pp. 3869-3875,
11/15/1995
Copyright © 1995 by The American Society of Hematology
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