Characteristics of triple-negative breast cancer.
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.
Division of Medical Oncology, Department of Internal Medicine, GROW School for Oncology and Developmental Biology, Maastricht University Medical Centre, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands.
Tim C
TC
de Ruijter
Jürgen
J
Veeck
Joep P J
JP
de Hoon
Manon
M
van Engeland
Vivianne C
VC
Tjan-Heijnen
D018943:Anthracyclines / Q000008:administration & dosage; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000378:metabolism*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000235:genetics* / Q000378:metabolism / Q000401:mortality / Q000473:pathology; D002986:Clinical Trials as Topic; D066246:ErbB Receptors / Q000037:antagonists & inhibitors; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D019398:Genes, BRCA1; D042822:Genomic Instability; D006801:Humans; D058990:Molecular Targeted Therapy / Q000379:methods*; D009154:Mutation; D020360:Neoadjuvant Therapy / Q000379:methods; D000071137:Poly (ADP-Ribose) Polymerase-1; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D011379:Prognosis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D043823:Taxoids / Q000008:administration & dosage; D016896:Treatment Outcome
D018943:Anthracyclines; D014408:Biomarkers, Tumor; D066246:ErbB Receptors; D000071137:Poly (ADP-Ribose) Polymerase-1; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D043823:Taxoids; C499320:PARP1 protein, human