1Department of Pathology, Seoul National University Bundang Hospital, Seongnam, Korea
2Department of Pathology, Seoul National University College of Medicine, Seoul, Korea
3Department of Pathology, SMG-SNU Boramae Medical Center, Seoul, Korea
4Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
5Department of Pathology, Konkuk University School of Medicine, Seoul, Korea
6Department of Pathology, Inha University School of Medicine, Incheon, Korea
7Department of Pathology, Seegene Medical Foundation, Busan, Korea
8Department of Pathology, Kosin University Gospel Hospital, Kosin University College of Medicine, Busan, Korea
9Department of Pathology, Hallym University Dongtan Sacred Heart Hospital, Hwaseong, Korea
10Department of Pathology, Catholic University of Daegu School of Medicine, Daegu, Korea
11Department of Pathology, Yeungnam University College of Medicine, Daegu, Korea
12Department of Pathology, Seoul Red Cross Hospital, Seoul, Korea
13Department of Pathology, Inje University Sanggye Paik Hospital, Seoul, Korea
14Department of Pathology, Chung-Ang University College of Medicine, Seoul, Korea
15Department of Pathology, Wonju Severance Christian Hospital, Yonsei University Wonju College of Medicine, Wonju, Korea
© 2017 The Korean Society of Pathologists/The Korean Society for Cytopathology
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Conflicts of Interest
No potential conflict of interest relevant to this article was reported.
Gene | Classification | Core pathway | Process |
Mutational rate (%) |
Reference | ||
---|---|---|---|---|---|---|---|
Previous study | Hypermutated tumora | Nonhypermutated tumora | |||||
TP53 | TSG | Cell cycle/apoptosis, DNA damage control | Cell survival | 14–59 | 35 | 50 | 27,116–118,123–127 |
PIK3CAb | Oncogene | PI3K-AKT | Cell survival | 7–36 | 40 | 12 | 27,116–118,123–127 |
CDH1c | TSG | APC | Cell fate | 4–36 | - | 11 | 27,116–118,124–126 |
ARID1Ab | TSG | Chromatin modification | Cell fate | 8–27 | 44 | 14 | 27,116,118,123–126 |
PTEN | TSG | PI3K-AKT | Cell survival | 0–27 | 13 | - | 27,116,123,125,127 |
KRAS | Oncogene | RAS/RAF | Cell survival | 0–27 | 19 | 6 | 27,116,118,125,127 |
RHOAc | Oncogene | RHO/ROCK | Cell survival | 0–23 | - | 6 | 27,116,118 |
APC | TSG | APC | Cell fate | 3–14 | - | 7 | 27,116,118,123,124 |
ERBB3 | Oncogene | RTK | Cell survival | 0–10 | 25 | - | 27,116 |
ERBB2 | Oncogene | RTK | Cell survival | 2–9 | - | 3 | 27,116,118,126,127 |
CTNNB1 | Oncogene | APC | Cell fate | 2–9 | - | 4 | 27,116,118,124 |
MET | Oncogene | RTK | Cell survival | 0–9 | - | 116,127 | |
FBXW7 | TSG | NOTCH | Cell fate | 2–6 | 24 | - | 27,118,127 |
SMAD4 | TSG | TGF-β | Cell survival | 4–6 | - | 8 | 27,118 |
EGFR | Oncogene | RTK | Cell survival | 0–6 | - | - | 27,116,127 |
NRAS | Oncogene | RAS/RAF | Cell survival | 0–5 | - | - | 116,125,127 |
TSG, tumour suppressor gene; PI3K, phosphoinositide 3-kinase; RTK, receptor tyrosine kinase; TGF-β, transforming growth factor β.
a Data of mutation rates are from The Cancer Genome Atlas database; [25]
b More frequently mutated gene in gastric cancer with microsatellite instability–high frequency feature or Epstein-Barr virus positivity;
c More frequently mutated gene in gastric cancer with diffuse type of Lauren classification.
Gene | Classification | Core pathway | Process |
Mutational rate (%) |
Reference | ||
---|---|---|---|---|---|---|---|
Previous study | Hypermutated tumora | Nonhypermutated tumora | |||||
TP53b | TSG | Cell cycle/apoptosis, DNA damage control | Cell survival | 27–65 | 20 | 60 | 119–121,128,129 |
KRASb | Oncogene | RAS/RAF | Cell survival | 33–58 | 30 | 43 | 119–121,128–131 |
APCb,c | TSG | APC | Cell fate | 40–56 | 51 | 81 | 121,129 |
PIK3CAb | Oncogene | PI3K-AKT | Cell survival | 14–20 | - | 18 | 119,120,128,129,131 |
BRAFc | Oncogene | RAS/RAF | Cell survival | 5–14 | 46 | - | 119,120,128–131 |
PTEN | TSG | PI3K-AKT | Cell survival | 2–13 | - | - | 119,128,129 |
EGFR | Oncogene | RTK | Cell survival | 0–11 | - | - | 128,129,131 |
SMAD4b | TSG | TGF-β | Cell survival | 2–11 | - | 10 | 119,121,128,129 |
FBXW7b | TSG | NOTCH | Cell fate | 4–10 | - | 11 | 119,120,128,129 |
NRAS | Oncogene | RAS | Cell survival | 2–7 | - | 9 | 119,120,128–131 |
MET | Oncogene | RTK | Cell survival | 2–4 | - | - | 119,120 |
CTNNB1 | Oncogene | APC | Cell fate | 1–4 | - | 5 | 121,128,129 |
AKT1 | Oncogene | PI3K | Cell survival | 1–4 | - | - | 119,128,129 |
ERBB2 | Oncogene | RTK | Cell survival | 1–3 | - | - | 128,129 |
ALK | Oncogene | RTK | Cell survival | 1–2 | - | - | 120,128,129 |
MAP2K1 | Oncogene | RAS/RAF | Cell survival | 0–2 | - | - | 119–121,128 |
TSG, tumour suppressor gene; PI3K, phosphoinositide 3-kinase; RTK, receptor tyrosine kinase; TGF-β, transforming growth factor β.
a Data of mutation rates are from The Cancer Genome Atlas database; [26]
b More frequently mutated gene in nonhypermutated colorectal cancer;
c More frequently mutated gene in hypermutated colorectal cancer.