Epidemiology
Etiology
- Type I (Endometrioid Adenocarcinoma): Most common (~80%).
- Caused by unopposed estrogen leading to endometrial hyperplasia and malignant transformation.
- Occurs in perimenopausal or early postmenopausal women (ages 50-65).
- Perimenopause: Think anovulatory cycles. Estrogen is present, but progesterone is absent because there’s no ovulation/corpus luteum.
- Postmenopause: Think peripheral aromatization in adipose tissue. Adrenal androgens are converted to estrone, which is unopposed because the ovaries have failed and no longer produce progesterone. This is why obesity is the single most important risk factor.
- Associated with mutations like PTEN.
- Type II (e.g., Serous, Clear Cell): Less common, more aggressive.
- Estrogen-independent. Occurs via endometrial atrophy.
- Seen in older, postmenopausal women (>70).
- Associated with p53 mutations. Poorer prognosis.
Risk factors for estrogen-dependent tumors
- Nulliparity
- Early menarche and late menopause
- Polycystic ovary syndrome
- Metabolic syndrome (esp. obesity and diabetes mellitus type 2)
- Fat cells contain the enzyme aromatase and produce extra-ovarian estrogen, while anabolic insulin stimulates the production of extra-ovarian estrogen and also the proliferation of endometrial cells via IGF-1.
- Hypertension
- Unopposed estrogen replacement therapy (e.g., for menopausal symptoms)
- History of breast cancer and tamoxifen treatment
- Lynch syndrome (hereditary nonpolyposis colorectal cancer)
Pathophysiology
Clinical features
Diagnostics
Treatment
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