Acceleration of chromosomal instability of BRCA1-associated hereditary breast cancers by p53 abnormality

Breast J. 2002 Mar-Apr;8(2):77-80. doi: 10.1046/j.1524-4741.2002.08201.x.

Abstract

Chromosomal instability (CIN) of BRCA1-associated hereditary breast cancers was studied by fluorescence in situ hybridization of chromosomes 1, 11, and 17. CIN values (the percentage of cells with a nonmodal chromosome) were obtained for each of three chromosomes, and their average was finally used as the CIN value of the sample. BRCA1-associated tumors showed a significantly (p = 0.0089) higher CIN value than normal breast tissues (24.3 +/- 4.3, n = 7, vs. 9.2 +/- 1.1, n = 6, mean +/- SE). In addition, BRCA1-associated tumors with positive p53 immunostaining showed a significantly (p = 0.0018) higher CIN value than those with negative p53 immunostaining (35.7 +/- 3.5, n = 3, vs. 15.8 +/- 1.3, n = 4). These results demonstrate that a loss of BRCA1 function results in the growth of breast cancers with CIN, and this phenotype is further accelerated by p53 abnormality.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Breast Neoplasms / chemistry
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology*
  • Chromosome Aberrations*
  • Chromosomes, Human, Pair 1 / genetics
  • Chromosomes, Human, Pair 11 / genetics
  • Chromosomes, Human, Pair 17 / genetics
  • Female
  • Genes, BRCA1*
  • Genes, p53*
  • Genetic Predisposition to Disease
  • Genetic Testing
  • Germ-Line Mutation
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization, Fluorescence
  • Middle Aged
  • Receptor, ErbB-2 / analysis
  • Tumor Suppressor Protein p53 / analysis*

Substances

  • Tumor Suppressor Protein p53
  • Receptor, ErbB-2