[26] The mortality rate of uterine corpus cancer in the USA is high, being eighth among women’s cancers,[26] but in Japan it remains HSP targets low, ranking the 20th;[25] however, the mortality ratio is expected to increase.

Endometrioid adenocarcinoma is the most common epithelial malignancy of the endometrium, mimicking non-neoplastic endometrial glands. This tumor is usually graded by FIGO scale depending on the amount of solid components and cytological atypia. There is no substantial difference in the immunophenotype between differentiated endometrial carcinoma, namely, G1/2 EMA, and atypical endometrial hyperplasia. In general, EMA expresses common epithelial markers such as pancytokeratin, epithelial membrane antigen, epithelial antigen (BerEP4), B72.3 and carbohydrate antigen 125 (CA125). Carcinoembryonic antigen (CEA) expression is less striking compared to endocervical adenocarcinoma.

Squamous differentiation and morula formation with no or little proliferative activity, which are often observed in EMA, show CD10 (common buy BIBW2992 acute lymphoblastic leukemia antigen) expression as well as high molecule cytokeratin such as cytokeratin (CK) 34βE12. Vimentin is regarded as one of the markers available for distinguishing EMA from cervical adenocarcinoma. As its histogenesis-associated markers, estrogen receptor (ER), progesterone receptor (PgR), p53, β-catenin, p16, phosphatase and tensin (PTEN), and DNA mismatch repair proteins, Farnesyltransferase such as MutL protein homolog 1 (MLH1), MutS protein homolog (MSH)2, MSH6, and postmeiotic segregation increased 2 (PMS2) are listed. β-Catenin is involved in cell adhesion and is a component of the Wnt signal transduction pathway. Nuclear expression of β-catenin is observed in as many as 50% of EMA,[27-31] but is rarely observed in SEA.[27, 28] PTEN homolog deleted on chromosome 10 is a tumor suppressor

gene involved in the tumorigenesis of 40–75% of EMA.[28, 32-37] Mutation in PTEN occurs at a similar frequency in atypical endometrial hyperplasia and EMA,[38, 39] resulting in an immunohistochemical negative reaction. While PTEN is significant in the development of endometrial hyperplasia, PIK3CA mutations are considered to play a role in the transition of atypical endometrial hyperplasia to EMA.[38, 39] DNA mismatch repair proteins are found to be deficient in tumor cell nuclei in up to 33% of EMA, caused by MLH1 promoter hypermethylation in most cases or in mutation of MLH1, MSH2, MSH6 and PMS2 in the remaining cases.[40-43] The preponderance of G1/2 EMA shows clear expression of ER and PgR. But, according to upgrading from G1/2 to G3, these expressions decline considerably. Overexpression of p53 tends to be more evident in G3 EMA. Cervical muscular involvement of the endometrial carcinoma is defined as stage II, according to the FIGO 2008 scale.