Methylation is less abundant in BRCA1-associated compared with sporadic breast cancer

Ann Oncol. 2008 Nov;19(11):1870-4. doi: 10.1093/annonc/mdn409. Epub 2008 Jul 22.

Abstract

Background: Promoter methylation is a common epigenetic mechanism to silence tumor suppressor genes during breast cancer development. We investigated whether BRCA1-associated breast tumors show cancer-predictive methylation patterns similar to those found in sporadic tumors.

Patients and methods: Quantitative multiplex methylation-specific PCR of 11 genes involved in breast carcinogenesis (RARB, RASSF1, TWIST1, CCND2, ESR1, SCGB3A1, BRCA1, BRCA2, CDKN2A, APC, CDH1) was carried out on 32 BRCA1-associated and 46 sporadic breast carcinomas and on normal breast tissue from seven BRCA1 mutation carriers and 13 non-carriers.

Results: The extent of cumulative methylation increased with age (P < 0.001). The median cumulative methylation index (CMI) of all studied genes was significantly higher in tumors (89) than in normal tissue (13, P < 0.001). The median CMI was significantly lower in BRCA1-associated (59) than in sporadic breast tumors (122, P = 0.001), in estrogen receptor (ER)-negative tumors (73) than in ER-positive tumors (122, P = 0.005) and in lymph node-negative (77) compared with lymph node-positive tumors (137, P = 0.007). In subgroup analysis, the effect of a BRCA1 germline mutation on methylation proved to be independent of ER status, lymph node status and age.

Conclusions: These data indicate that BRCA1-associated breast cancers show less promoter methylation compared with sporadic breast carcinomas indicating a difference in disease etiology.

Publication types

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

MeSH terms

  • Adult
  • Age Factors
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology
  • DNA Methylation*
  • DNA, Neoplasm / genetics
  • Female
  • Genes, BRCA1*
  • Genetic Markers
  • Germ-Line Mutation
  • Humans
  • Lymphatic Metastasis
  • Middle Aged
  • Polymerase Chain Reaction
  • Promoter Regions, Genetic
  • Receptors, Estrogen / genetics

Substances

  • DNA, Neoplasm
  • Genetic Markers
  • Receptors, Estrogen