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uterine endometrioid carcinoma

Thursday 25 November 2010

type 1 endometrial carcinoma


Definition: Relatively indolent tumors that arise in background of endometrial hyperplasia.


- Back to back endometrial-type glands of varying differentiation/atypia with no intervening stroma
- May occasionally show a villoglandular pattern
- Stroma present is usually desmoplastic, may have foamy cells due to tumor necrosis (not specific for carcinoma, derived from stroma not histiocytes; fat positive, mucin negative)
- Adjacent endometrium often exhibits EIN or atypical hyperplasia
- Vascular invasion is associated with chronic inflammation around lymphatics
- May have trophoblastic differentiation with hCG+ cells
- Commonly has squamous metaplasia

FIGO grading

- Well differentiated (FIGO grade 1)

  • Extensive, complex epithelial growth pattern with little intervening stroma
  • Usually budding and branching of large glands causing papillary structures
  • May be villoglandular on low power
  • May have true papillae (DD: clear cell carcinoma, serous carcinoma), but without atypia
  • Mild to moderate atypia is allowed or only focal; if atypia is more severe, FIGO grade is increased to moderate (FIGO grade 2)
  • Some are myoinvasive
  • Often has benign squamous differentiation (adenoacanthoma), focal mucinous, secretory or ciliated features
  • Usually stage 1, with 95% relapse-free survival rate

- Moderately differentiated (FIGO grade 2)

  • 6%-50% of non-squamous tumor is composed of sheet-like tumor cells without glandular features
  • Tumor cells have moderate pleomorphism, prominent nucleoli

- Poorly differentiated (FIGO grade 3)

  • >50% of nonsquamous tumor is composed of sheet-like tumor cells without glandular features
  • Tumor cells have high grade features
  • Glands poorly formed when present
  • May contain malignant squamous cells
  • Angiolymphatic invasion common

Myometrial invasion

Myometrial invasion is an independent prognostic parameter of the endometrioid carcinomas which correlates with the risk of metastasis to pelvic and/or paraaortic lymph nodes.

Recognition of myometrial invasion is sometimes difficult. In fact, myoinvasion is overdiagnosed in routine practice in as many as 25% of the cases. Recently, it has been observed that tumor-associated macrophages stimulate angiogenesis and promote cancer dissemination.

There is a link between increased microvessel proliferation to stromal macrophage infiltrate and suggest that enhanced tumor angiogenesis, triggered by stromal macrophages, regulates the progression of endometrioid carcinomas.

The identical stroma microenvironment found in the primary and the corresponding metastatic tumor suggests that tumor stroma response is determined by the intrinsic biology of the tumor.

Differential diagnosis

- Ciliary metaplasia
- Papillary change
- Progesterone treatment related changes
- Shedding endometrium with papillary syncytial metaplasia
- Villoglandular endometrioid carcinoma
- Well differentiated tumors: atypical hyperplasia / EIN (Mod Pathol 2000;13:309)
- Poorly differentiated tumors: serous carcinoma


- Myometrial invasion and lymph node metastasis in endometrioid carcinomas: tumor-associated macrophages, microvessel density, and HIF1A have a crucial role. Espinosa I, José Carnicer M, Catasus L, Canet B, D’angelo E, Zannoni GF, Prat J. Am J Surg Pathol. 2010 Nov;34(11):1708-14. PMID: 20962622