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).
- Decades of mitogenic stimulation without adequate progesterone counterbalance drive progressive glandular atypia: Normal → Endometrial Intraepithelial Neoplasia (EIN) → Adenocarcinoma (PTEN, PIK3CA, KRAS, ARID1A, MSI mutations).
- Postmenopausal Shift: Cessation of ovulatory cycles stops corpus luteum progesterone production; however, peripheral conversion of androstenedione to estrone via aromatase in adipose tissue continues indefinitely. This is why obesity is the single most important risk factor. c
- 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
Differential diagnostics
| Feature | Cervical Cancer | Endometrial Cancer |
|---|---|---|
| Main Etiology | High-risk HPV (types 16, 18). | Unopposed estrogen (Type I) / TP53 (Type II). |
| Key Risk Factors | • Smoking (SCC), HPV, HIV, multiple partners. • Lack of Pap screening. | • Obesity, Lynch syndrome, Tamoxifen. • Nulliparity, early menarche, late menopause, PCOS. |
| Protective Factors | HPV vaccine, barrier contraception. | COCs / Progestins, multiparity. |
| Typical Age | 35–55 yrs (bimodal; younger pts). | > 60 yrs (postmenopausal). |
| Histology | Squamous cell (SCC) (70–80%) > Adeno. | Endometrioid adeno (80%) > Serous/Clear cell. |
| Presentation | Postcoital bleeding, foul discharge. | Postmenopausal bleeding (PMB) / AUB. |
| Screening | Pap cytology ± HPV DNA (q3–5y, ages 21–65). | None (EMB screening only in Lynch syndrome). |
| Workup / Dx | • Visible mass: Direct punch biopsy. • Abnormal Pap: Colposcopy + biopsy. | • Endometrial biopsy (EMB) (gold standard). • TVUS: Stripe > 4 mm in PMB requires EMB. |
| Staging | Clinical / Radiologic (CT/MRI/PET). | Surgical (pathology post-TAH-BSO). |
| Early Tx | • Stage IA1: Conization or Simple Hysterectomy. • Stage IA2–IB2: Radical Hysterectomy + LND. | TAH-BSO + pelvic/para-aortic LND. |
| Advanced Tx | Stage IIB (parametrial spread): CCRT (Cisplatin + Radiation). No surgery. | Adjuvant Chemo + Radiation (Carbo/Paclitaxel ± EBRT/brachytherapy). |
| Key Pearl / COD | Hydronephrosis Uremia/AKI is leading COD (ureteral compression). | Any PMB = Cancer until proven otherwise (needs TVUS or EMB). |
Treatment
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