Table 1.

Genomic TNBC subtypes and potential therapeutic targets

Subtypes	Genetic abnormalities	Potential therapeutic target
BL1	Cell cycle gene expression DNA repair gene (ATR–BRCA pathway) Proliferation genes	PARP inhibitors Genotoxic agents
BL2	Growth factor signaling pathways (EGFR, MET, NGF, Wnt/β-catenin, IGF-1R) Glycolysis, gluconeogenesis Expression of myoepithelial markers	mTOR inhibitors Growth-factor inhibitors
Immunomodulatory	Immune cell processes (CTLA4, IL12, IL7 pathways, antigen processing/presentation) Gene signature for medullary BC (rare TNBC with a favorable prognosis)	PD1/PDL1 inhibitors
Mesenchymal-like	Cell motility Cell differentiation Growth factor signaling EMT	mTOR inhibitors EMT-and CSC-targeted treatment
Mesenchymal stem-like	Similar to M+ Low proliferation Angiogenesis genes	PI3K inhibitors Antiangiogenic therapy Src antagonist
Luminal androgen receptor	Androgen receptor gene Luminal gene expression pattern Molecular apocrine subtype	Antiandrogen therapy

Note: Data from Lehmann et al.²⁵

Abbreviations: BC, breast cancer; BL, basal-like; CSC, cancer stem cells; DNA, deoxyribonucleic acid; EGFR, epidermal growth factor receptor; EMT, epithelial-mesenchymal-transition; IGF-1R, insulin-like growth factor I receptor; IL, interleukin; IM, immunomodulatory; LAR, luminal androgen receptor; M, mesenchymal-like; MET, hepatocyte growth factor; mTOR, mammalian target of rapamycin; MSL, mesenchymal stem-like; NGF, nerve growth factor; PARP, poly ADP ribose polymerase; PD1, programmed cell death 1; PDL1, programmed death-ligand 1; PI3K, phosphatidylinositol 3-kinase; TNBC, triple negative breast cancer.