Table 1.
Summary of key clinical studies identifying MET amplification as a mechanism of resistance in oncogene-driven NSCLC
| Molecular subset of NSCLC | Number of lung cancer samples + Type | Prior targeted therapy | Incidence of MET amplification | Method of MET amplification testing | Reference |
|---|---|---|---|---|---|
| EGFR | Following second-line osimertinib: range 10%-22% | ||||
| 83 Plasma |
19% (14/83) | NGS | 52 | ||
| 32 Tumor tissue |
22% (7/32) | FISH | 8 | ||
| 42 Tumor tissue |
14% (6/42) | FISH and/or NGS | 54 | ||
| 41 Tumor tissue |
10% (4/41) | NGS and FISH | 53 | ||
| EGFR | Following first-line osimertinib: range 7%-15% | ||||
| 91 Plasma |
15% (14/91) | NGS | 55 | ||
| 27 Tumor tissue |
7.4% (2/27) | NGS | 51 | ||
| ALK | Post-treatment tissue (n = 101) or | Crizotinib, or next-generation ALK inhibitors (e.g. lorlatinib) | 11 (13%) | FISH and/or NGS | 77 |
| Plasma (n = 106) | |||||
| RET | 23 | Selpercatinib or pralsetinib | 15% | FISH or NGS | 82 |
| ROS1 | 17 | Lorlatinib | 6% | NGS and FISH | 85 |
| KRAS | 10 Tumor tissue and/or plasma |
Adagrasib | 20% | NGS | 95 |
NGS, next-generation sequencing; NSCLC, non-small-cell lung cancer.