Detection of ATM gene deletion/duplication by multiplex ligation-dependant probe amplification in childhood lymphoid malignancies: a report from the Children's Oncology Group

Leuk Res. 2008 Aug;32(8):1207-13. doi: 10.1016/j.leukres.2007.12.012. Epub 2008 Feb 7.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins / genetics*
  • Child
  • DNA-Binding Proteins / genetics*
  • Gene Amplification
  • Gene Deletion*
  • Gene Dosage
  • Gene Duplication*
  • Humans
  • Lymphoma / genetics*
  • Protein Serine-Threonine Kinases / genetics*
  • Tumor Suppressor Proteins / genetics*
  • Yohimbine

Substances

  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Tumor Suppressor Proteins
  • Yohimbine
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein Serine-Threonine Kinases