Table 1.
Molecular characterization of endometrial cancers by histologic subtype
| Alteration | Endometrioid (%) | Non-endometrioid (%) |
| PTEN protein loss18,19 | 80 | 5 |
| PTEN mutation15–17,25 | 30–50 | 0–11 |
| PIK3CA mutation20,21,25 | 30–40 | 20 |
| PIK3R1 mutation157 | 43 | 12 |
| AKT mutation10,13,14 | 2–3 | 0 |
| KRAS mutation54–57 | 10–30 | 0–10 |
| IGFIR overexpression69,70 | 78 | Unknown |
| FGFR2 mutation11,87,88 | 12–16 | 1 |
| EGFR overexpression9,111 | 46 | 34 |
| EGFR mutation113,114 | Unknown | 0 |
| HER-2 overexpression9,111,124–126 | 3–10 | 32 |
| HER-2 amplification124,126 | 1 | 17 |
| β-catenin mutation133,134 | 15–50 | 0 |
| p53 mutation158 | 20 | 90 |
| E-cadherin loss129,130,133 | 5–50 | 60–90 |
| Microsatellite instability159,160 | 15–25 | 0–5 |
Abbreviations: PTEN, phosphatase and tensin homolog deleted on chromosome 10; PIK3CA, phosphatidylinositol 3 kinase, catalytic, α polypeptide; PIK3RI, phosphatidylinositol 3 kinase, regulatory polypeptide; AKT, v-akt murine thymoma viral oncogene homolog 1; KRAS, V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; IGFR1, insulin-like growth factor receptor 1; FGFR2, fibroblast growth factor receptor 2; EGFR, epidermal growth factor receptor; HER, human epidermal growth factor receptor