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| Adenocarcinoma |
| Etiology •associated with unopposed estrogen use •may be exogenous (non-cycled estrogens) but generally •endogenous due to peripheral aromatization of adrenal androgens by adipose in obese women •also associated with granulosa cell tumors and other estrogen producing ovarian tumors as well as polycystic ovary syndrome •small group of women with high grade neoplasms lack evidence of hyperestrinism |
| Pathogenesis •estrogen drives continued proliferation with eventual acquisition of somatic mutations •in the absence of progesterone maturation of the endometrium and spiral arteries never occurs, nor does regular menses, |
| Epidemiology •obese post-menopausal women •may also have diabetes and hypertension (classic triad) •small group of women with high grade neoplasms lacks these correlates •increasing incidence with aging population •not reliably detected on pap smear |
| General Gross Description •fungating, friable, tan mass with irregular infiltration of underlying myometrium |
| General Microscopic Description •glands exhibit crowding so that they are "back-to-back" •stratified nuclei with mitotic activity •cells lose orientation to the lumen •nucleoli become prominent, nuclei are vesicular •lumenal necrosis •if >90% glandular grade 1, 10-90% glandular grade 2, <10% glandular grade 3 |
| Clinical Correlation •post-menopausal bleeding is usual symptom; other symptoms rare and indicative of advanced disease •most patients are Stage I (confined to endometrium) at diagnosis and respond completely to hysterectomy •neoplasm spreads to cervix, deep into myometrium, to ovary, regional lymph nodes and then to distant sites •when death occurs it is usually due to local disease in the pelvis |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1060-6 |
| Adenocarcinoma |
| Synopsis by: Melinda Sanders M.D. (T84000M81403)[20] |
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