Detection of ATM gene deletion/duplication by multiplex ligation-dependant probe amplification in childhood lymphoid malignancies: a report from the Children's Oncology Group.
ATM gene alterations have been described in various lymphoproliferative malignancies suggesting that ATM contributes to lymphomagenesis. Using multiplex ligation-dependant probe amplification (MLPA), we screened 61 childhood lymphoid malignancies for ATM genomic deletion/duplication. Five samples were found to have a complete deletion or duplication. All the three deletions were found in B-precursor ALL (15%), two were submicroscopic, not detected by standard cytogenetic studies. These observations indicate that as in adult ALL, complete ATM submicroscopic deletion is frequent in childhood B-precursor ALL. As previously hypothesized, these results suggest that ATM may act as a tumor suppressor gene in the pathogenesis of childhood B-precursor ALL.
Gumy-Pause
Fabienne
F
Department of Pediatrics, Unit of Hemato-Oncology, University Hospital of Geneva, Switzerland. Fabienne.GumyPause@medecine.unige.ch
Ozsahin
Hulya
H
Khoshbeen-Boudal
Mary
M
Betts
David R
DR
Maillet
Philippe
P
Sappino
André-Pascal
AP
D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000235:genetics*; D002648:Child; D004268:DNA-Binding Proteins / Q000235:genetics*; D005784:Gene Amplification; D017353:Gene Deletion; D018628:Gene Dosage; D020440:Gene Duplication; D006801:Humans; D008223:Lymphoma / Q000235:genetics*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D025521:Tumor Suppressor Proteins / Q000235:genetics*; D015016:Yohimbine
D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D025521:Tumor Suppressor Proteins; D015016:Yohimbine; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases