High levels of allele loss at the FHIT and ATM genes in non-comedo ductal carcinoma in situ and grade I tubular invasive breast cancers

Cancer Res. 1996 Dec 1;56(23):5484-9.

Abstract

Fifty-four grade 1 tubular breast cancers and nine non-comedo ductal carcinoma in situ samples have been analyzed for loss of heterozygosity using a series of microsatellite markers. Markers mapping to regions of the genome for which loss of heterozygosity has been documented previously in higher-grade breast cancers were selected for this analysis. Even within this group of good prognostic early breast cancers, genetic events are very common. The highest levels of loss were observed for D3S1300, which maps within an intron of the recently identified FHIT gene. High levels of loss were also observed within the ATM gene. These findings indicate that allele loss at FHIT and ATM may be an important early event in the development of sporadic breast cancer.

Publication types

  • Comparative Study

MeSH terms

  • Acid Anhydride Hydrolases*
  • Adenocarcinoma / genetics*
  • Adenocarcinoma / pathology
  • Alleles
  • Ataxia Telangiectasia Mutated Proteins
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology
  • Carcinoma in Situ / genetics*
  • Carcinoma in Situ / pathology
  • Carcinoma, Ductal, Breast / genetics*
  • Carcinoma, Ductal, Breast / pathology
  • Cell Cycle Proteins
  • Cell Transformation, Neoplastic / genetics
  • Chromosomes, Human / genetics
  • DNA, Neoplasm / genetics
  • DNA-Binding Proteins
  • Female
  • Gene Deletion*
  • Heterozygote
  • Humans
  • Microsatellite Repeats
  • Neoplasm Invasiveness
  • Neoplasm Proteins / genetics*
  • Polymerase Chain Reaction
  • Protein Serine-Threonine Kinases*
  • Proteins / genetics*
  • Sensitivity and Specificity
  • Tumor Suppressor Proteins

Substances

  • Cell Cycle Proteins
  • DNA, Neoplasm
  • DNA-Binding Proteins
  • Neoplasm Proteins
  • Proteins
  • Tumor Suppressor Proteins
  • fragile histidine triad protein
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein Serine-Threonine Kinases
  • Acid Anhydride Hydrolases