Table 2.
Types of endometrial cancer according to the Bokhman model and correlations with clinicopathological and molecular characteristics.
| Characteristics | Type I tumors | Type II tumors |
|---|---|---|
| Clinicopathological | ||
| Incidence | ~80% | ~20% |
| Age at initial diagnosis | Pre/peri-menopausal | Postmenopausal |
| Histology | Endometrioid | Non-endometrioid (predominantly serous and clear cell) |
| Grade | Usually low | Usually high |
| Premalignant phase | Atypical hyperplasia | Glandular dysplasia (for serous tumours) |
| Predisposing factors | Obesity, prolonged estrogen exposure | |
| ER, PgR | >90% | 0–31% |
| Molecular | ||
| HER-2/neu (overexpression) | 3% | 18% |
| EGFR expression | 46% | 34% |
| P53 mutations | 5–10% | 80–90% |
| Ploidy | 67% diploid | 45% diploid |
| PTEN (loss of function through deletion or mutation) | 50–80% | 10–11% |
| P16 inactivation | 10% | 40% |
| K-ras (mutational activation) | 13–26% | 0–10% |
| E-cadherin (reduced or non expression) | 10–20% | 62–87% |
| β-catenin CTNNB1 (gain of function mutation) | 25–38% | Rare |