Table 1.
Gene | Most Common Variants | Prevalence | Age | Gender | Smoking | Histology | Prognostic Significance |
---|---|---|---|---|---|---|---|
EGFR | Mutations in exons 19 and 21 | 10–16% in Western populations, 40–50% in Asians. | Younger patients | Females | Never smokers | Adenocarcinoma | Response to specific TKIs, T790M predictor of resistance |
ALK | EML4-ALK variants | 1–10% of NSCLC | Younger patients | Females? Not clear | Never smokers | Adenocarcinoma | Aggressive tumors, response to specific TKIs |
ROS1 | CD74-ROS1 variants | 0.9–2.6% of NSCLC | Younger patients | Females | Never smokers | Adenocarcinoma | Less aggressive tumors, response to specific TKIs |
KRAS | Mutations in codons 12 and 13 | 30–40% of NSCLC, more common in Caucasians | Older ages | Males? Not clear |
Smokers | Adenocarcinoma | Poor prognosis or response to TKIs? Not clear |
BRAF | Mutations in exon 15 | 2–4% of NSCLC | No predilection | V600E in females and others in males | Smokers | Adenocarcinoma | Aggressive tumors and poor prognosis? Not clear. Response to BRAF inhibitors. |
MET | Mutations in exon 14, amplification | Mutations in 1–10% of NSCLC, amplification in 5–22% | Older ages | Not clear | Smokers | Adenocarcinoma and SCC | Resistance to EGFR-TKIs. Response to MET inhibitors. |
HER2 | Mutations in exons 18–21, amplification | Mutations in 2–3% and amplifications in 2–5% of adenocarcinomas | Not clear | Mutations in females and amplifications in males | Mutations in never smokers and amplifications in ex-smokers | Adenocarcinoma Rare in SCC |
Resistance to EGFR-TKIs? Not clear |
NSCLC: non-small cell lung cancer; SCC: squamous cell carcinoma; TKIs: tyrosine kinase inhibitors; EML4: echinoderm microtubule-associated protein like 4.