Table 1.

Breast cancer classification based on molecular profiling

Molecular class	Chemotherapy response	Target therapy	Resistant factors	Overcome resistant therapy
Luminal A	Low	TAM, fulvestrant, aromatase inhibitor	ER amplification, mutation, methylation, phosphorylation, acetylation, Mutation PI3K/mTOR, FGFR1/2 amplification, KRAS and P53 mutation, CYP2D6 mutation	ARN-810, fulvestrant alone or in combination with CDK4/6 inhibitor (palbociclib), Combination of alpelisib and letrozole, the PI3K inhibitor, epigenetic drugs such as vidaza or decitabine along with histone deacetylase inhibitors such as vorinostat or romidepsin
Luminal B	Intermediate	TAM, Fulvestrant, Aromatase inhibitors	Mutations of PIK3CA, the gain of CCND1 and CDK4, moderate PTEN reduction, Up-regulation and autocrine activation of HER2	Alone or in combination mTOR, AKT, or MEK inhibitors with fulvestrant The combination between lapatinib or trastuzumab and aromatase inhibitors (letrozole, anastrozole, exemestane)
HER2-positive	High	HER2 and kinase inhibitor: lapatinib, pertuzumab, trastuzumab and adotratuzomab emtansine, immune cell activation(Ertumaxomab)	Mutations of PIK3CA, RAS, Src, NF-KB and PTEN, truncated isoforms of HER2, stable HER2 homodimers formation, overexpression of EGFR and HER-3	PI3K/AKT/mTOR inhibitor, Lapatinib, Tyrosine kinase inhibitors
Basal-like	High	PARP1 inhibitor(olaparib and iniparib), cisplatin	Mutation in TP53	PI3K/AKT/mTOR inhibitor
Claudin-low	Intermediate/low