Table 1.
Genomic alterations of lung cancer.
| Type of alteration | Frequency (%) | FDA approved therapy | |
|---|---|---|---|
| EGFR | Mutation | 10–35 | Yes |
| KRAS | Mutation | 25–30 | No |
| FGFR-1 | Amplification | 20 | No |
| ALK | Rearrangement | 5–7 | Yes |
| MET | Amplification | 2–4 | Yes, but for a different mutation |
| ROS1 | Rearrangement | 1 | Yes, but for a different mutation |
| RET | Rearrangement | 1 | Yes, but only for other cancers |
| BRAF | Mutation | 1–3 | Yes |
EGFR, epidermal growth factor receptor; KRAS, Kristen RAt Sarcoma; FGFR-1, fibroblast growth factor receptor-1; ALK, anaplastic lymphoma kinase; MET, hepatocyte growth factor receptor. ALK, MET, ROS1, and RET are proto-oncogenes that arise from chromosomal rearrangements that generate a fusion gene, resulting in the constitutive activation of kinase domain.