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p15ink4B and p16ink4 gene inactivation in acute lymphocytic leukemia
O Rasool, M Heyman, LB Brandter, Y Liu, D Grander, S Soderhall and S Einhorn
Radiumhemmet, Karolinska Hospital, Stockholm, Sweden.
Malignant cells from 52 children with acute lymphocytic leukemia (ALL) were
investigated for inactivation of the p15ink4B and p16ink4 genes and other
genetic alterations on chromosome 9p21. Homozygous deletions of the
p15ink4B and/or the p16ink4 genes were detected in 16 cases and a further 9
cases showed evidence of allelic loss either by hemizygous deletion or loss
of heterozygosity (LOH) for 9p21 markers. Most cases had loss of both
genes, but 5 patients had lost only p16ink4 and 2 cases had homozygous loss
of p15ink4B only. Sequence analysis of all exons of p15ink4B and p16ink4
was performed in patients with hemizygous deletions or LOH for 9p21
markers. A frame shift mutation of p16ink4 exon 1 was shown in 1 case,
whereas all other clones carried the wild- type sequence of p15ink4B and
p16ink4 in the remaining allele. The data suggest that both the p15ink4B
and p16ink4 genes can be inactivated in ALL. The existence of a hitherto
undefined tumor-suppressor gene on chromosome 9p cannot be ruled out.
Volume 85,
Issue 12,
pp. 3431-3436,
06/15/1995
Copyright © 1995 by The American Society of Hematology
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