Table 4.
HNSCC gene mutations
| No | Nucleotide change | Amino acid Change | Primary tumor | Exon | Smoking (pack/year) | Age/Sex |
|---|---|---|---|---|---|---|
| 12 |
Substitution of G for C at nucleotide 35 |
G12A |
Oral Cavity (T3N0M0) |
KRAS Exon1 |
45 |
51/M |
| 21 |
Substitution of G for C at nucleotide 35 |
G12A |
Oropharyngeal (T2N0M0) |
KRAS Exon1 |
10 |
47 /M |
| 30 |
Substitution of G for C at nucleotide 35 |
G12A |
Oral Cavity (T3N1M0) |
KRAS Exon1 |
0 |
54/M |
| 10 |
Substitution of A for G at nucleotide 3140 |
H1047R |
Laryngeal (T3N0M0) |
PIK3CA Exon20 |
0 |
61/M |
| 51 |
Substitution of G for A at nucleotide 1633 |
E545K |
Oral Cavity (T1N1M0) |
PIK3CA Exon9 |
0 |
79/M |
| 53 | Substitution of G for A at nucleotide 1633 | E545K | Oral Cavity (T3N0M0) | PIK3CA Exon9 | 0 | 82/M |
We sequenced KRAS exon 1, BRAF exon 15 and PIK3CA exon 9 and exon 20 and identified mutations in six of the 115 patients (5.2%).