Table 1.

Molecular subtypes of triple-negative breast cancer by Lehmann et al.^[17]

TNBC subtype	Gene Ontologies	Differential gene expression	Therapeutic targets/drugs
Basal-like 1	Cell cycle pathway DNA damage response (ATR/BRCA pathway)	DNA damage response genes	Cisplatin PARP inhibitor
Basal-like 2	Growth factor signaling pathway Glycolysis/ Gluconeogenesis	Myoepithelial markers	Cisplatin PARP inhibitor
Immunomodulatory	Immune cell signaling pathway Cytokine signaling Antigen processing and presentation Signaling through core immune signal transduction pathways	Immune signal transduction Immune cell-surface antigens Cytokine signaling Complement cascade Chemokine receptors ligands Antigen presentation	Immune checkpoint inhibitors
Mesenchymal-like	Cell motility ECM receptor interaction Cell differentiation pathways	TGF-β, EMT-associated, growth factors signaling pathway components	PI3K/mTOR inhibitor Src inhibitor
Mesenchymal stem-like	Cell motility Cell differentiation pathways Growth factor signaling pathways	Enriched MSC-specific markers Low expression of claudins 3, 4, 7	PI3K/mTOR inhibitor Src inhibitor
Luminal androgen receptor	Hormonally regulated pathways	AR and downstream AR targets and coactivators	AR antagonist PI3K/mTOR inhibitor

AR: Androgen receptor; ATR: ATM and Rad3-related; ECM: extracellular matrix; EMT: epithelial mesenchymal transition; MSC: mesenchymal stem cell; PARP: poly ADP ribose polymerase; TGF-β: transforming growth factor beta; TNBC: triple-negative breast cancer.