Uterine body carcinoma. Etiology & pathogenesis. Precancer. Histological classification.
Endometrial carcinoma is the most frequent cancer of the female genital tract, commonly appearing ages 55-65. There are two types:
- Endometrioid
- Serous carcinoma
These are histologically and pathologically distinct. Endometrioid cancers arise in association with estrogen excess and endometrial hyperplasia in perimenopausal women, while serous carcinomas arise thanks to endometrial atrophy in
postmenopausal women. Endometrial hyperplasia can be simple without atypia, or complex hyperplasia.
Endometrioid cancer
- The majority of endometrial carcinomas - endometrial hyperplasia is an important precursor lesion
- Histologically similar to normal endometrial glands, risk factors are:
- Obesity
- Diabetes
- Hypertension
- Infertility
- Exposure to unopposed estrogen
- Breast carcinoma often occurs along with endometrioid carcinoma
- Mutation to PTEN gene common, along with PIK3CA mutation (TP53 less common)
- Histologically, closely resembles normal endometrium, may be infiltrative or exophytic, structure may be mucinous, tubal and/or squamous. Commonly metastasise to regional lymph nodes
H&E, endometrioid adenocarcinoma: crowded, back-to-back glands resembling endometrial glands with almost no stroma between them; pale pink nests are squamous differentiation.
Image: “Endometrioid endometrial adenocarcinoma intermed mag” by Nephron, CC BY-SA 3.0, via Wikimedia Commons.
Example: an obese, nulliparous 60-year-old woman with diabetes and hypertension presents with postmenopausal bleeding. Think of endometrioid carcinoma on a background of atypical hyperplasia: every postmenopausal bleed needs an endometrial biopsy.
Serous endometrial carcinoma
- Less common, 15%
- Nearly all have TP53 mutation whereas PTEN mutation is rare
- Forms small tufts and papillae rather than glands seen in endometrioid form
- Behave aggressively and are by definition high-grade