Table 2.
Pathological, morphological, endocrine and common molecular genetic changes used to provide a dualistic clinical classification of endometrial cancers (Bokhman Classification).
| Factor | Type 1 EC | Type 2 EC | References |
|---|---|---|---|
| Frequency distribution | 80–90% | 10–20% | [71,74] |
| Prognosis | Favourable | Unfavourable | |
| Outcome (5-year survival) | 86% | 59% | |
| Onset of menopause | ≥50 years of age | ≤50 years of age | |
| Obesity, hyperlipidaemia and diabetes mellitus association | Yes | No | |
| Association with oestrogen stimulation | Yes | No | |
| Sensitivity to progestagens | High | Low | |
| Background endometrium histology | Hyperplasia | Atrophy | |
| Tumour grade | Low (grade 1–2) | High (grade 3) | |
| Myometrial invasion | Superficial | Deep | |
| Potential for metastatic spread through lymphatic system | Low | High | |
| Reproductive status | Decreased | No disturbance | |
| Clinicopathologic and molecular alterations | |||
| Prototypical histological type | Endometrioid | Non-endometrioid (serous, clear cell carcinoma) | [71,75,76,77,78] |
| Stage at diagnosis | Early (FIGO stage I–II) | Advanced (FIGO stage III–IV) | |
| ER and PR receptor expression | High | Low | |
| Common genetic alterations | |||
| Microsatellite instability * | 28–40% | 0–2% | [66,70,71,79,80,81,82,83] |
| PTEN mutation | 52–78% | 1–11% | |
| TP53 mutation | 9–12% | 60–91% | |
| POLE mutation | 11–20% | 0–7% | |
| KRAS mutation | 15–43% | 2–8% | |
| PIK3CA mutation | 36–52% | 24–42% | |
| PIK3R1 mutation | 21–43% | 0–12% | |
| ARID1A mutation | 25–48% | 6–11% | |
| CTNNB1 mutation | 23–24% | 0–3% | |
| PPP2R1A mutation | 5–7% | 15–43% | |
| ERRB2 mutation | 1–4% | 26–44% | |
| HER2 amplification | 0 | 27–44% | |
* Microsatellite instability is characterised by a deficiency in DNA repair mechanisms.