Characteristics of triple-negative breast cancer

J Cancer Res Clin Oncol. 2011 Feb;137(2):183-92. doi: 10.1007/s00432-010-0957-x. Epub 2010 Nov 11.

Abstract

Background: Triple-negative breast cancers (TNBC) neither express hormone receptors, nor overexpress HER2. They are associated with poor prognosis, as defined by low five-year survival and high recurrence rates after adjuvant therapy. Overall, TNBC share striking similarities with basal-like breast cancers (BBC), so a number of studies considered them being the same. The purpose of this review is to summarise the latest findings on TNBC concerning its relation and delineation to BBC, discuss the developmental pathways involved and address clinical implications for this complex type of breast cancer.

Methods: The recent literature from PubMed and Medline databases was reviewed.

Results: Not all TNBC are of the intrinsic BBC subtype (nonbasal (NB)-TNBC), nor are all BBC triple-negative (non-triple-negative (NTN)-BBC). There is increasing evidence that a triple-negative, basal-like breast cancer (TNBBC) subtype develops mainly through a BRCA1-related pathway. Somatic mutations that contribute to NTN-BBC and NB-TNBC development are possibly not related to this pathway, but may occur randomly due to increased genomic instability in these tumours. Several therapeutic options exist for TNBBC, which exhibited promising results in recent clinical trials. Cytotoxic therapies, e.g. combined treatment with anthracyclines or taxanes, achieved good tumour regression rates in the neo-adjuvant setting, but also showed considerable recurrence during the first 5 years after therapy. Targeted therapy options involve PARP1 and EGFR inhibition, although both approaches still need further investigation.

Conclusions: TNBC and BBC are not the same disease entity. The TNBBC subtype shows the largest homogeneity in terms of tumour development, prognosis and clinical intervention options.

Publication types

  • Review

MeSH terms

  • Anthracyclines / administration & dosage
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use*
  • Biomarkers, Tumor / metabolism*
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / mortality
  • Breast Neoplasms / pathology
  • Clinical Trials as Topic
  • ErbB Receptors / antagonists & inhibitors
  • Female
  • Gene Expression Regulation, Neoplastic
  • Genes, BRCA1*
  • Genomic Instability
  • Humans
  • Molecular Targeted Therapy / methods*
  • Mutation*
  • Neoadjuvant Therapy / methods
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Prognosis
  • Receptor, ErbB-2 / metabolism
  • Receptors, Estrogen / metabolism
  • Receptors, Progesterone / metabolism
  • Taxoids / administration & dosage
  • Treatment Outcome

Substances

  • Anthracyclines
  • Biomarkers, Tumor
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Receptors, Estrogen
  • Receptors, Progesterone
  • Taxoids
  • PARP1 protein, human
  • Poly (ADP-Ribose) Polymerase-1
  • ErbB Receptors
  • Receptor, ErbB-2