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| Endometrioid Carcinoma |
| Etiology • 10% of patients have evidence of ovarian or ovarian-breast cancer syndrome (see pathogenesis) • remainder sporadic • 15-30% associated with synchronous endometrial carcinoma • associated with endometriosis |
| Pathogenesis • mutations in BRCA1 in familial cases, |
| Epidemiology • peri- or post-menopausal women of low parity • gonadal dysgenesis • ovarian epithelial carcinoma = 6% of female cancer and 50% of female cancer deaths due to late detection and failure to determine high risk group • endometrioid = 20% of ovarian cancers; 40% bilateral |
| General Gross Description • smooth or irregular external surface • predominantly solid, although may be partially cystic • white, firm, focally necrotic and hemorrhagic on section |
| General Microscopic Description • indistinguishable from endometrial carcinoma • glands or glands mixed with solid areas • round to oval vesicular (clear) nuclei with • prominent nucleoli |
| Clinical Correlation • early symptoms vague, late abdominal distension with ascites and pain • rarely detected on routine examination • Stage I confined to ovary(ies), II confined to pelvis, III with extension to abdominal cavity, IV distant metasases • most women Stage III or IV at presentation • spread across serosal surfaces and to lymph nodes • removal of bulk of tumor and chemotherapy are major therapy |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1065-1068 |
| Endometrioid Carcinoma |
| Synopsis by: Melinda Sanders M.D. (T87000M83803)[42] |
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