BACKGROUND: Triple-negative breast cancers (TNBC) do not represent a single 
disease subgroup and are often aggressive breast cancers with poor prognoses. 
Unlike estrogen/progesterone receptor and HER2 (human epidermal growth factor 
receptor 2) breast cancers, which are responsive to targeted treatments, there 
is no effective targeted therapy for TNBC, although approximately 50% of 
patients respond to conventional chemotherapies, including taxanes, 
anthracyclines, cyclophosphamide, and platinum salts.
CONTENT: Genomic studies have helped clarify some of the possible disease 
groupings that make up TNBC. We discuss the findings, including copy 
number-transcriptome analysis, whole genome sequencing, and exome sequencing, in 
terms of the biological properties and phenotypes that make up the constellation 
of TNBC. The relationships between subgroups defined by transcriptome and genome 
analysis are discussed.
SUMMARY: TNBC is not a uniform molecular or disease entity but a constellation 
of variably well-defined biological properties whose relationship to each other 
is not understood. There is good support for the existence of a basal expression 
subtype, p53 mutated, high-genomic instability subtype of TNBC. This should be 
considered a distinct TNBC subtype. Other subtypes with variable degrees of 
supporting evidence exist within the nonbasal/p53wt (wild-type p53) TNBC, 
including a group of TNBC with PI3K (phosphoinositide 3-kinase) pathway 
activation that have better overall prognosis than the basal TNBC. Consistent 
molecular phenotyping of TNBC by whole genome sequencing, transcriptomics, and 
functional studies with patient-derived tumor xenograft models will be essential 
components in clinical and biological studies as means of resolving this 
heterogeneity.