AML1 amplification in a case of childhood acute lymphoblastic leukemia.
We report an 8-year-old girl with B-cell acute lymphoblastic leukemia (ALL). The blast cell karyotype at diagnosis included a marker chromosome revealed by fluorescence in situ hybridization to be a derivative of chromosome 21. A high level amplification of the AML1 gene was identified, but it disappeared upon complete remission. This rare but recurrent abnormality warrants research of B-cell ALL, especially when a marker chromosome is present in the blast cell karyotype.
Morel
Frédéric
F
Laboratoire de Cytogénétique, Faculté de Médecine, Université de Bretagne Occidentale, 22 Avenue Camille Desmoulins, F-29285 Brest cedex, France.
Herry
Angèle
A
Le Bris
Marie-Josée
MJ
Douet-Guilbert
Nathalie
N
Le Calvez
Geneviève
G
Marion
Véronique
V
Berthou
Christian
C
De Braekeeler
Marc
M
D002648:Child; D002869:Chromosome Aberrations; D002872:Chromosome Deletion; D002891:Chromosomes, Human, Pair 21 / Q000235:genetics*; D050676:Core Binding Factor Alpha 2 Subunit; D004268:DNA-Binding Proteins / Q000235:genetics*; D005260:Female; D005784:Gene Amplification; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics*; D011518:Proto-Oncogene Proteins; D014157:Transcription Factors / Q000235:genetics*
D050676:Core Binding Factor Alpha 2 Subunit; D004268:DNA-Binding Proteins; D011518:Proto-Oncogene Proteins; C493728:RUNX1 protein, human; D014157:Transcription Factors