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17p Deletion in Acute Myeloid Leukemia and Myelodysplastic
Syndrome. Analysis of Breakpoints and Deleted Segments by Fluorescence
In Situ
Valérie Soenen,
Claude Preudhomme,
Christophe Roumier,
Agnès Daudignon,
Jean Luc Laï, and
Pierre Fenaux
From the Laboratoire d'Hématologie, Service de
Cytogénétique, and Service des Maladies du Sang, Centre
Hospitalier Universitaire, Lille; Inserm U124 Institut de Recherche sur
le Cancer, Lille; and Département
d'Hématologie-Cytogénétique, CH Valenciennes,
France.
Recently, we and other groups reported in acute myeloid leukemia
(AML) and myelodysplastic syndrome (MDS) a strong correlation between
cytogenetic rearrangements leading to 17p deletion, a typical form of
dysgranulopoiesis combining pseudo-Pelger-Huët hypolobulation and
small vacuoles in neutrophils, and p53 mutation. To gain further
insight into this "17p-syndrome," we studied 17 cases of AML and
MDS with 17p deletion by whole chromosome painting (WCP) and
fluorescence in situ hybridization (FISH) with probes spanning the 17p
arm, including a p53 gene probe. Cytogenetically, 15 patients had
unbalanced translocation between chromosome 17 and another chromosome
(chromosome 5 in nine cases and unidentified chromosome -add 17p- in
three cases), one patient had monosomy 17, and one had i(17q). All
rearrangements appeared to result in 17p deletion. Sixteen patients had
additional cytogenetic rearrangements. WCP analysis confirmed the
cytogenetic interpretation in all cases and identified one of the cases
of add 17p as a t(17;22). WCP also identified chromosome 17 material on
a marker or ring chromosome in two cases of t(5;17). FISH analysis with
17p markers made in 16 cases showed no deletion of the 17p markers
studied in the last two patients, who had no typical dysgranulopoiesis;
p53 mutation analysis in one of them was negative. In the 14 other
cases, FISH showed a 17p deletion of variable extent but that always
included deletion of the p53 gene. All 14 patients had typical
dysgranulopoiesis, and all but one had p53 mutation and/or
overexpression. These findings reinforce the morphologic, cytogenetic,
and molecular correlation found in the 17p- syndrome and suggest a
pathogenetic role for inactivation of tumor suppressor gene(s) located
in 17p, especially the p53 gene.
Blood, Vol. 91 No. 3 (February 1), 1998:
pp. 1008-1015
© 1998 by The American Society of Hematology.
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