Updates in the treatment of basal/triple-negative breast cancer

Curr Opin Obstet Gynecol. 2013 Feb;25(1):40-8. doi: 10.1097/GCO.0b013e32835c1633.


Purpose of review: Triple-negative breast cancer (TNBC) is clinically characterized by the lack of expression of the estrogen receptor/progesterone receptor and the human epidermal growth factor receptor 2. It is highly heterogeneous and exhibits considerable overlap with basal-like and BRCA-related breast cancers. Constituting 15-20% of breast cancers, TNBC exhibits an aggressive phenotype with a poor prognosis. This review summarizes recent progress and studies in TNBC and discusses some of the ongoing clinical trials and emerging therapies for the treatment of TNBC.

Recent findings: Conventional cytotoxic chemotherapy and DNA damaging agents continue to be the mainstay for treatment of this disease. The use of targeted agents such as bevacizumab, epidermal growth factor receptor and polyadenosine diphosphate-ribose polymerase inhibitors have led to conflicting results. However, recent research has prompted evaluation of additional drugs targeting multiple signaling pathways and epigenetic modifications for the treatment of this disease.

Summary: TNBC remains a challenging disease to treat with recent trials having demonstrated only modest improvements in outcomes. Increased understanding of the heterogeneity of this complex subtype may help tailor therapies to specific patient subgroups.

Publication types

  • Review

MeSH terms

  • Angiogenesis Inhibitors / therapeutic use
  • Breast Neoplasms / classification
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / metabolism
  • Cytotoxins / therapeutic use
  • DNA Damage / drug effects
  • ErbB Receptors / antagonists & inhibitors
  • ErbB Receptors / therapeutic use
  • Female
  • Humans
  • Receptor, ErbB-2 / metabolism
  • Receptors, Estrogen / metabolism
  • Receptors, Progesterone / metabolism


  • Angiogenesis Inhibitors
  • Cytotoxins
  • Receptors, Estrogen
  • Receptors, Progesterone
  • ErbB Receptors
  • Receptor, ErbB-2