Molecular and epigenetic profiles of BRCA1-like hormone-receptor-positive breast tumors identified with development and application of a copy-number-based classifier.

Journal: Breast cancer research : BCR
PMID: 30683142

Abstract

BACKGROUND: BRCA1-mutated cancers exhibit deficient homologous recombination (HR) DNA repair, resulting in extensive copy number alterations and genome instability. HR deficiency can also arise in tumors without a BRCA1 mutation. Compared with other breast tumors, HR-deficient, BRCA1-like tumors exhibit worse prognosis but selective chemotherapeutic sensitivity. Presently, patients with triple negative breast cancer (TNBC) who do not respond to hormone endocrine-targeting therapy are given cytotoxic chemotherapy. However, more recent evidence showed a similar genomic profile between BRCA1-deficient TNBCs and hormone-receptor-positive tumors. Characterization of the somatic alterations of BRCA1-like hormone-receptor-positive breast tumors as a group, which is currently lacking, can potentially help develop biomarkers for identifying additional patients who might respond to chemotherapy.

Authors

  • Youdinghuan Chen
    Department of Epidemiology, Lebanon, USA.
  • Yue Wang
    Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
  • Lucas A Salas
    Department of Epidemiology, Lebanon, USA.
  • Todd W Miller
    Department of Molecular and Systems Biology, Lebanon, USA.
  • Kenneth Mark
    Department of Molecular and Systems Biology, Lebanon, USA.
  • Jonathan D Marotti
    Department of Pathology and Laboratory Medicine, Lebanon, USA.
  • Arminja N Kettenbach
    Department of Molecular and Systems Biology, Lebanon, USA.
  • Chao Cheng
    Department of Molecular and Systems Biology, Lebanon, USA. Chao.Cheng@bcm.edu.
  • Brock C Christensen
    Department of Epidemiology, Lebanon, USA. Brock.C.Christensen@dartmouth.edu.

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