Table 1.
Lung adenocarcinoma and squamous cell carcinoma mutations, incidence, downstream effects, and targeted therapies
| Genetic alterations | Incidence (%) | Downstream effect | Targeted therapya | Sources |
|---|---|---|---|---|
| Adenocarcinomas | ||||
| EGFR (mut) | ~15 | ↑ Proliferation, survival, angiogenesis, and metastasis | Gefitinib, erlotinib, afatinib, AZD9291, AZD8931 | [10, 11] |
| EML4-ALK (fus) | 2–7 | ↑Proliferation, survival, and migration | Crizotinib, ceritinib, alectinib | [11, 79, 80] |
| KRAS (mut) | ~30 | ↑ Chemoresistance, proliferation, and survival | N/A | [10] |
| MET (amp) | 3–5 | ↑ Cell survival, proliferation, and metastasis | Tivantinib, crizotinib cabozantinib, ornatuzumab | [11, 13, 24, 81] |
| ROS1 (fus) | 1–2 | ↑ Survival | Foretinib & crizotinib | [13, 24] |
| RET (fus) | 1–2 | ↑Proliferation | Carbozantinib, vandetanib, ponatinib | [11] |
| BRAF (mut) | 5–10 | ↑ Resistance to EGFR inhibitors, proliferation, and survival | Debrafenib, sorafenib | [10, 24] |
| TP53 (mut) | 46 | ↑ Growth, ↓ apoptosis | N/A | [10, 11] |
| Squamous cell carcinomas | ||||
| FGFR1 (amp) | 16–25 | ↑ Proliferation, survival, and chemoresistance; ↓ patient prognosis | Nintendanib, ponatinib, AZD4547, dovitinib | [9, 11, 12, 82] |
| PIK3CA (mut) | 8–18 | ↑ Proliferation and survival | Buparlisib, PX-866, BYL719, GDC-0941 or inhibitors for AKT: AZD5363, MK-2206 | [9, 11, 13, 24, 82] |
| DDR2 (mut) | 4 | ↑ Cell migration, invasion, proliferation, and survival | Dasatinib | [9, 13] |
| MET (amp) | 3 | ↑ Cell survival, proliferation, and metastasis | Tivantinib, crizotinib cabozantinib, onartuzumab | [12, 24, 81] |
| SOX2 | 21 | ↑ Proliferation | N/A | [9] |
| PTEN (mut & del) | 15–29 | ↑PI3K signaling, proliferation, and survival | PI3K inhibitors: buparlisib, PX-866, BYL719, GDC-0941 or inhibitors for AKT: AZD5363, MK-2206 | [9, 11, 24, 82] |
| TP53 (mut) | 81 | ↑ Growth, ↓ apoptosis | N/A | [9, 11, 12] |
| CDKN2A (del) | 51 | ↑ Growth | N/A | [9] |