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Prenatal BRCA1 epimutations contribute significantly to triple-negative breast cancer development.

Oleksii NikolaienkoHans P EikesdalElisabet OgnedalBjørnar GiljeSteinar LundgrenEgil S BlixHelge EspelidJürgen GeislerStephanie GeislerEmilius A M JanssenSynnøve YndestadLaura MinsaasBeryl LeirvaagReidun LillestølStian KnappskogPer Eystein Lønning
Published in: Genome medicine (2023)
Our findings suggest prenatal BRCA1 epimutations might be the underlying cause of around 20% of TNBC and low-ER expression breast cancers. Such constitutional mosaic BRCA1 methylation likely arise through gender-related mechanisms in utero, independent of Mendelian inheritance.
Keyphrases
  • pregnant women
  • breast cancer risk
  • poor prognosis
  • mitochondrial dna
  • dna methylation
  • genome wide
  • estrogen receptor
  • gene expression
  • young adults
  • copy number
  • childhood cancer