Table 1 Molecular typing of breast cancer
Molecular typing (Molecular subtype) | Molecular characteristics | Possible treatment strategies | Cell line names represented | ||||
|---|---|---|---|---|---|---|---|
HER2 | ER | PgR | Ki67 | Other molecular features | |||
HER2 positive | Positive | – | – | Whatever | / | Anti-Her2 treatment | SK-BR-3, AU-565, MDA-MB-453 |
Luminal A | – | Positive | Positive and high expression of | Low expression | / | Endocrine therapy | MCF-7, T47D, SUM185 |
Luminal B (HER2 negative) | – | Positive | Low expression or - | High expression | / | Endocrine therapy combined with chemotherapy | / |
Luminal B (HER2 positive) | Positive | Positive | Whatever | Whatever | / | Anti-Her2 treatment with endocrine therapy combined | BT-474, ZR-75-1 |
Triple-negative | – | – | – | Whatever | / | Chemotherapy based comprehensive treatment | MDA-MB-468, SUM190, BT549, MDA-MB-231, Hs578T, SUM1315, BT483,MCF-12A, HBL101, HS598T (Appropriate cell lines were selected based on different populations and genetic circumstances) |
Triple-negative (BL1) | / | / | / | / | Highly expressed cell cycle and DNA damage response genes | Platinum based chemotherapeutics, PARP inhibitors | |
Triple-negative (BL2) | / | / | / | / | Increased activity of growth factor pathways and PI3K pathway | mTOR inhibitors, growth factor inhibitors | |
Triple-negative (IM) | / | / | / | / | Highly expressed immune-related genes | Immune checkpoint inhibitors | |
Triple-negative (LAR) | / | / | / | / | AR signaling pathway activation; enrichment of PIK3CA mutations | Antiandrogens, PI3K inhibitors | |
Triple-negative (M) | / | / | / | / | EMT characteristics; growth factor pathway activation | mTOR inhibitors, growth factor inhibitors | |
Triple-negative (MSL) | / | / | / | / | EMT characteristics; growth factors and PI3K pathway activation | mTOR inhibitors, PI3K inhibitors, growth factor inhibitors | |