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Genomic Alterations of the p19ARF Encoding Exons in
T-Cell Acute Lymphoblastic Leukemia
Betty Gardie,
Jean-Michel Cayuela,
Sophie Martini, and
François Sigaux
From the Laboratory of Molecular Hematology, INSERM U462, Centre
Hayem, Hopital Saint Louis, Paris, France.
We have previously shown that the disruption/deletion of the MTS
(MTS1-MTS2) locus due to illegitimate V(D)J
recombinase activity is a genetic event characteristic of T-cell acute
lymphoblastic leukemia (T-ALL). Inactivation of the
p16INK4a tumor suppressor protein, encoded by MTS1,
is thought to be the major functional consequence of these chromosomal
rearrangements. The two other cell cycle inhibitors encoded by genes
identified in the locus (p19ARF by MTS1 and
p15INK4b by MTS2), also represent possible
candidates for inactivating events. By analyzing p16INK4a
expression in three cases in which an identical 36-kb deletion had
deleted MTS2 and disrupted the p19ARF, but spared
the p16INK4a MTS1 encoding exons, we have excluded
p16INK4a and pinpointed p19ARF and/or
p15INK4b as the functional target(s) of this rearrangement.
Moreover, by the study of the MTS genomic configuration of 149 rearranged alleles from a large series of T-ALL cases, we have shown
that p19ARF encoding exons were always disrupted or
deleted, whereas p16INK4a and p15INK4b encoding
exons were spared in four and 21 cases, respectively. These results
suggest that p19ARF may be targeted by the genetic events
that occur in the MTS locus in the majority of T-ALLs.
Blood, Vol. 91 No. 3 (February 1), 1998:
pp. 1016-1020
© 1998 by The American Society of Hematology.
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