Table 2.
Genetic alterations of type I and type II endometrial carcinomas, reported in percentages (references).
| Type I | Type II | |
|---|---|---|
| PTEN inactivation | Up to 83% [1, 4, 11, 12] | 11% [1, 2, 12] |
| PIK3CA mutation | 26–36% [7, 9] | 5% [7] |
| KRAS mutation | 10–30% [1, 2, 4, 7–12, 17] | 0–10% [2, 12] |
| β-catenin /CTNNB1 mutation | 14–44% [7, 8] | 0–5% [1, 7, 10, 11] |
| Microsatellite instability | 20–45% [1, 7–10] | 0–11% [8, 9] |
| p53 mutation | 10–20% [1, 4, 6, 7, 10, 11, 13, 17, 18] | 90% [1, 2, 4, 6, 7, 10–13, 17] |
| HER2/neu amplification | 10–30% [1, 4, 10, 17] | 18–80% [13] |
| p16 inactivation | 10% [1, 4, 7, 10, 11] | 40–45% [4, 7, 10] |
| E-cadherin loss | 10–20% [1, 4, 7, 10, 11] | 60–90% [4] |