No evidence for a major role of heterozygous deletion 657del5 within the NBS1 gene in the pathogenesis of non-Hodgkin's lymphoma of childhood and adolescence

Br J Haematol. 2000 Apr;109(1):117-20. doi: 10.1046/j.1365-2141.2000.01973.x.

Abstract

Nijmegen breakage syndrome (NBS) is an autosomal recessive DNA repair disorder with a high predisposition for lymphoid malignancies. The majority of NBS patients carry a homozygous founder mutation (657del5) within the NBS1 gene. The observation of a high incidence of cancer in close relatives of NBS patients suggests a potential pathogenetic role of NBS1 mutations in heterozygotes as well. We assessed the frequency of the 657del5 mutation in 109 paediatric patients with non-Hodgkin's lymphoma (NHL). None of the patients analysed carried a NBS1 allele with the 657del5 mutation, suggesting that this mutation does not play a major role in the pathogenesis of NHL of childhood and adolescence.

MeSH terms

  • Adolescent
  • Cell Cycle Proteins / genetics*
  • Child
  • Child, Preschool
  • Chromosome Breakage
  • Chromosomes, Human, Pair 14
  • Chromosomes, Human, Pair 7
  • Chromosomes, Human, Pair 8*
  • DNA Mutational Analysis
  • Female
  • Gene Deletion*
  • Genetic Predisposition to Disease
  • Heterozygote
  • Humans
  • Lymphoma, Non-Hodgkin / genetics*
  • Male
  • Nuclear Proteins*

Substances

  • Cell Cycle Proteins
  • NBN protein, human
  • Nuclear Proteins