Table 1.
Description of ESCAT Tiers and List of Glioma-Relevant Targets
| ESMO Scale for Clinical Actionability of Molecular Targets (ESCAT) | |
|---|---|
| Tier | Short description of tiers |
| I | Alteration-drug match is associated with improved clinical outcomes in a specific tumor type in randomized (IA), nonrandomized (IB) or clinical trials across tumor types (IC). |
| II | Alteration-drug match is associated with antitumor activity in a specific tumor type but with unknown magnitude. Evidence of clinical benefit from retrospective studies (IIA), or higher response rates in prospective trials without survival data (IIB). |
| III | Alteration-drug match is associated with clinical meaningful evidence but from other tumor types. Limited evidence for specific tumor types or broadly across tumor types (IIIA). Similar molecular alteration as a tier I target but without supportive clinical data (IIIB). |
| IV | Alteration-drug match is associated with supportive preclinical data. In vivo or in vitro data available (IVA). Only supportive in silico data (IVB). |
| V | Alteration-drug match is associated with objective responses, but no improved outcomes. |
| X | Lack of supportive evidence |
| List of Glioma-Relevant Targets According to EANO | |
| Gene | Alteration type |
| ALK | Fusions, mutations |
| BRAF | V600E mutations, KIAA1549:BRAF fusions |
| CDK4/6 | Amplifications |
| EGFR | Mutations in the intracellular domain |
| FGFR | FGFR3 (fusions, mutations), FGFR1 mutations (N546K, K656E) |
| HRD | Homologous recombination deficiency |
| MDM2/4 | Amplifications, fusions, mutations |
| MET | Exon 14 skipping, fusions, amplifications |
| MMR | De novo and treatment-induced mismatch repair deficiency |
| NF1 | Loss-of-function alterations |
| NTRK1-3 | Fusions |
| PDGFRA | Amplifications, fusions, mutations |
| POLE | De novo and treatment-induced POLE alterations |
| ROS1 | Fusions |
| TMB-high | De novo and treatment-induced TMB-high |
| TSC1/2 | Mutations |