Table 1.
Class, specific pathways, and agents actually involved in the treatment and prevention of ER-breast cancer.
| Class | Targets | Drugs or agents |
|---|---|---|
| Nuclear receptors | Retinoid acid receptor RXR | Fenretinide (4-HPR) 9 cis-retinoic acid (Targretin) |
| VDR | VIT D3 analogues | |
| PPARγ | Troglitazone, rosiglitazone, pioglitazone | |
|
| ||
| Membrane receptors and signal transduction | HMG-CoA | Statins |
| Tyrosine kinase | Gefitinib (Iressa) | |
| HER-1, HER-2 | Trastuzumab (Herceptin), lapatinib, gefitinib, erlotinib | |
| IGF-R, IGF-1, IGFBP3 | Metformin | |
|
| ||
| Anti-inflammatory and antioxidant | COX-2 | celecoxib, rofecoxib, NSAIDs |
|
| ||
| Angiogenesis | VEGF | Bevacizumab |
|
| ||
| DNA modulation | BRCA1-BRCA2 | PARP inhibitors |
4-HPR: N-(4-hydroxyphenyl) retinamide; COX: cyclooxygenase; ER: oestrogen receptor; HMGCoA: 3 hydroxy-3 methylglutaryl coenzyme A; NSAIDs: nonsteroidal anti-inflammatory drugs; PARP: poly (ADP-ribose) polymerases; PPAR: peroxisome proliferator-activated receptor; RXr: retinoid X receptors, VDR: vitamin D receptor.