Table 4. Genetic and epigenetic alterations in circulating cell-free DNA pancreatic ductal adenocarcinoma and biliary tract cancer, 2013–2017.
| Author (year) | Target | PDAC
or BTC |
Cancer,
number |
Benign
lesions, number |
Healthy
volunteers, number |
Detected | Sensitivity | Specificity |
|---|---|---|---|---|---|---|---|---|
| Takai et al. (2016) 138 | K-ras | PDAC | 107 (non-
operable) |
- | - | 59% | - | - |
| Takai et al. (2015) 124 | cfDNA | PDAC | 48 | 29% | ||||
| Hadano et al. (2016) 139 | K-ras | PDAC | 105 | - | 20 | 31% | - | - |
| Zill et al. (2015) 140 | K-ras, TP53,
APC, FBXW7, SMAD4 |
PDAC | 26 | - | - | - | 92.3% | 100% |
| Earl et al. (2015) 135 | K-ras | PDAC | 31 | - | - | 26% | - | - |
| Kinusaga et al. (2015) 123 | G12V, G12D,
and G12R in codon 12 of K-ras gene |
PDAC | 141 | 20 | 20 | 62% | - | - |
| Sausen et al. (2015) 125 | cfDNA | PDAC | 77 | - | - | 43% | - | - |
| Wu et al. (2014) 128 | K-ras | PDAC | 24 | - | 25 | 72% | - | - |
BTC, biliary tract cancer; PDAC, pancreatic ductal adenocarcinoma.