First principle: the unopposed‑estrogen axis (Concept 7 → oncology)
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Risk factors = more lifetime estrogen, less progesterone opposition: obesity (peripheral aromatisation), chronic anovulation/PCOS, nulliparity, early menarche/late menopause, unopposed estrogen therapy, tamoxifen, and Lynch syndrome.
The sign that makes this a curable cancer
Diagnosis (modern correction)
- Endometrial tissue sampling (office biopsy/hysteroscopy‑directed) is central; TVUS assesses endometrial thickness.
- "Fractional curettage = universal gold standard" is outdated — hysteroscopic assessment is preferred for focal lesions.
Premalignant terminology
Prefer hyperplasia without atypia vs atypical hyperplasia / EIN (the important premalignant category) over old simple/complex percentages.
Molecular class (the modern upgrade beyond Type I/II)
| Group | Prognosis |
|---|---|
| POLE‑mutated | favourable |
| MMR‑deficient (MMRd) | intermediate |
| NSMP (no specific molecular profile) | intermediate |
| p53‑abnormal | poor |
Management
Backbone = surgery (total hysterectomy + BSO ± sentinel nodes), with adjuvant radio/chemo/hormonal/immunotherapy by stage, histology and molecular risk.
Pitfalls
- Reassuring after a single episode of postmenopausal bleeding.
- Assuming all endometrial cancer is low‑grade/estrogen‑driven (serous/p53 types are aggressive).
Pearls
- 🎯 Unopposed estrogen → EIN → carcinoma; postmenopausal bleeding → biopsy. POLE good, p53 bad.
- 🩺 The PCOS–obesity–anovulation phenotype is a lifelong endometrial‑protection problem, not just a fertility one.
Next → A cancer with a known, preventable cause (Concept 38).