Possible individualized investigational approaches to the treatment of metastatic or recurrent clear cell ovarian cancer.
| Molecular subgroup | Target | Possible agent(s) | Additional comments |
| ARID1A mutant tumors | DDR pathway | ATR inhibitors | (±PARP inhibitors) |
| Histone deacetylase | HDAC inhibitors | ||
| Zeste homolog 2 | EZH2 inhibitor | ||
| PI3K/AKT/mTOR activated | PI3K/AKT/mTOR pathway | PI3K/mTOR/TORC inhibitors | |
| MAPK pathway activated | MAPK pathway | RAS/RAF/MEK inhibitors | Inhibitor choice mutation-dependent |
| Mismatch repair deficient | PD1/PD-L1 | PD1/PD-L1 inhibitors | May require to be part of basket study |
| Mesenchymal-type gene expression profile | Angiogenic pathways | VEGF monoclonal antibodies and VEGFR tyrosine kinase inhibitors |
ATR, ataxia telangiectasia and Rad3-related protein; DDR, DNA damage response; EZH2, Zeste homolog 2; HDAC, histone deacetylase; MAPK, mitogen-activated protein kinase; mTOR, mammalian target of rapamycin; PARP, poly-ADP ribose polymerase; PD1, programmed cell death protein 1; PD-L1, programmed death ligand 1; TORC, mammalian target of rapamycin complex; VEGF, vascular endothelial growth factor; VEGFR, vascular endothelial growth factor receptor.