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. 2019 Oct 30;10(12):2289–2299. doi: 10.1111/1759-7714.13226

Table 3.

Mutation analysis in adeno‐ versus squamous cell non‐small cell lung cancer

Adenocarcinomas (n = 59)
All Lepidic Acinar Papillary Solid
Mutation (n = 59) (n = 8) (n = 26) (n = 6) (n = 19)
AKT1 0 0 0 0 0
BRAF 1 (1.7%) 0 0 0 1 (5.3%)
EGFR 6 (10.2%) 2 (25%) 4 (15.4%) 0 0
ERBB2 0 0 0 0 0
IDH1 0 0 0 0 0
IDH2 1 (1.7%) 0 0 0 1 (5.3%)
JAK2 0 (0%) 0 0 0 0
KIT 2 (4.3%) 0 2 (7.7%) 0 0
KRAS 21 (35.6%) 4 (50%) 10 (38.5%) 1 (17%) 6 (31.6%)
PDGFRA 1 (1.7%) 0 0 0 1 (5.3%)
PIK3CA 0 0 0 0 0
TP53 42 (71.2%) 5 (62.5%) 19 (73.1%) 3 (50%) 15 (78.9%)
Mutation Squamous cell P‐value
carcinoma (n = 38) AC versus SCC
AKT1 1 (2.6%)
BRAF 0
EGFR 0 P = 0.042
ERBB2 0
IDH1 1 (2.6%)
IDH2 1 (2.6%)
JAK2 0
KIT 1 (2.6%)
KRAS 2 (5.3%) P = 0.001
PDGFRA 0
PIK3CA 4 (10.5%) P = 0.011
TP53 37 (97.4%) P = 0.001

AKT, protein kinase B; BRAF, v‐raf murine sarcoma viral oncogene homolog B; EGFR, epidermal growth factor receptor; IDH, isocitrate dehydrogenase; KIT, KIT proto‐oncogene receptor tyrosine kinase; KRAS, Kirsten rat sarcoma viral oncogene; PDGFRA, platelet‐derived growth factor receptor A; PIK3CA, gene encoding for the phosphatidylinositol 3‐kinase (PI3K) catalytic subunit; TP53: transformation‐related protein 53.