First principle: vague symptoms + early transcoelomic spread
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Many high‑grade serous carcinomas originate in the fimbrial fallopian tube — hence "ovarian/tubal/peritoneal" are grouped, and prevention removes tubes and ovaries. Symptoms are non‑specific → late presentation with peritoneal spread and ascites.
Genetic risk and risk reduction
- BRCA1/BRCA2, Lynch syndrome, family history, endometriosis (for clear‑cell/endometrioid) raise risk.
- 🚩 Correction: BRCA1 = chromosome 17; BRCA2 = chromosome 13 (older notes mis‑state BRCA1).
- Risk‑reducing bilateral salpingo‑oophorectomy after childbearing cuts ovarian/tubal cancer risk by >90% in BRCA carriers — timing individualised (variant, age‑specific risk, premature‑menopause consequences). It is risk‑reducing salpingo‑oophorectomy, not automatic hysterectomy.
Tumour markers — a one‑to‑one exam table
| Tumour | Marker / body |
|---|---|
| Epithelial | CA‑125 (monitoring, not screening) |
| Dysgerminoma | LDH (ovarian "seminoma," chemo/radiosensitive) |
| Yolk‑sac | AFP (Schiller–Duval bodies) |
| Granulosa‑cell | inhibin (Call–Exner bodies; estrogen → precocious puberty or PMB) |
| Choriocarcinoma/embryonal | β‑hCG |
| Fibroma | Meigs syndrome = fibroma + ascites + pleural effusion (benign!) |
Management
Epithelial: cytoreductive (debulking) surgery + platinum‑taxane chemotherapy, with PARP inhibitors/anti‑angiogenics as biomarker‑guided maintenance. Germ‑cell: often fertility‑sparing surgery + BEP with excellent outcomes.
Pitfalls
- Using CA‑125 to screen; mis‑stating BRCA1 chromosome; mistaking Meigs (benign) for advanced malignancy.
- Assuming a young woman's mass is epithelial — think germ‑cell.
Pearls
- 🎯 AFP = yolk‑sac; LDH = dysgerminoma; inhibin = granulosa. BRCA1 = chr17, BRCA2 = chr13. Meigs = fibroma + ascites + effusion.
- 🩺 Persistent bloating/early satiety in an older woman deserves a real work‑up — it is ovarian cancer's only early voice.