Ovarian cancer

Epidemiology


Etiology

The most likely pathogenesis of EOC is repeated injury and repair to the ovarian surface, which makes surface epithelial cells susceptible to malignant transformation (ie, acquiring oncogenic mutations).

Risk factors

Protective factors


Pathophysiology


Clinical features

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Tip

  • Surface epithelial-stroma: composed of cells that support the normal ovarian structure for ovulation (eg, serous, mucinous epithelial cells).
  • Germ cell: composed of cells that can develop into an embryo or placenta. These tumors are composed of varying amounts of germ layers (ie, endoderm, mesoderm, ectoderm), yolk sac, or placenta (eg, chorion). They often have associated hormonal activity (eg, increased hCG, alpha fetoprotein).
  • Sex cord-stroma: composed of cells that support and surround the oocyte. These cells secrete sex hormones including estrogen (granulosa cells) and testosterone (Sertoli-Leydig cells).

Histologic type Diagnosis Key features
Epithelial Serous cystadenocarcinoma Most common ovarian cancer
Often bilateral
Histology: psammoma bodies
Mucinous cystadenocarcinoma Pseudomyxoma peritonei
Mucin-producing epithelial cells
Germ cell Dysgerminoma Adolescents
β-hCG, ↑ LDH
Histology: "fried-egg" cells
Endodermal sinus (yolk sac) AFP
Aggressive
Schiller-Duval bodies resembling glomeruli
Stroma (sex cord) Granulosa cell tumor ↑ Estrogen (e.g., endometrial hyperplasia, postmenopausal bleeding)
↑ Inhibin
Histology: Call-Exner bodies, coffee-bean nuclei
Sertoli-Leydig cell tumor ↑ Androgens (e.g., hirsutism, clitoromegaly)

Ovarian germ cell tumors

Epithelial ovarian tumors

Cystadenoma

Ovarian germ cell tumors


Diagnostics

Tumor markers


Treatment