To clarify the molecular mechanisms through which malignant changes are activated in endometrium, this study aims to examine the expression profiles of wild-type ER-alpha and their splice variants and to assess the number of coexisting mRNA isoforms of ER-alpha in normal endometrium as well as in endometrial hyperplasia and endometrial endometrioid adenocarcinoma.
Expression of cdc25B and phosphorylated ER-alpha was increased in endometrial hyperplasia and atypical hyperplasia compared with normal secretory endometrium.
In this study, we examined the alteration of the G2 pathway in endometrial hyperplasia (EH) and endometrioid-type endometrial cancer (EC), and analyzed the relationship between the G2 pathway status and the p53 pathway status.
A total of 56 frozen tissues, which included 14 normal endometria, 13 endometrial hyperplasias (10 without atypia and 3 with atypia), and 29 endometrial carcinomas, were examined for the expression of Bax, Bcl-2, and p53 using immunohistochemistry.
Whereas endometrioid carcinoma and endometrial hyperplasia are associated with microsatellite instability and ras and PTEN mutations, serous carcinoma and endometrial intraepithelial carcinoma are associated with p53 mutations and abnormal accumulation of p53 protein.
When 9%, 3.2 HNU (Human Neu Unit)/microgram protein, and 0.39 ng/mg protein were used as cut-off values for SPF. c-erbB-2, and p53 respectively, 13.9%, 20.2%, and 0% of endometrial hyperplasia and 50%, 56.3%, and 12.5% of endometrial carcinoma showed raised levels of the corresponding parameters.
The incidence of loss of expression of MSH2 and/or MLH1 protein in endometrial hyperplasia patients with personal (64%) or family (40%) histories was significantly higher than that in patients without such history (no personal: 21% and no family: 10%; P = 0.0035 and 0.0065).
Cyclical change of hMSH2 protein expression in normal endometrium during the menstrual cycle and its overexpression in endometrial hyperplasia and sporadic endometrial carcinoma.
Interestingly, an MSI-high phenotype was found in endometrial hyperplasias from MSH2 mutation carriers, in contrast to hyperplasias from MLH1 mutation carriers, which exhibited an MSI-stable phenotype.
We aimed to assess if immunohistochemical (IHC) expression of progesterone receptor isoforms, PR-A and PR-B, in endometrial glands and stroma in pre-treatment endometrial biopsies was related to relapse of EH.
This article reviews the role of KRAS in predicting transition from hyperplastic endometrium to early-stage well-differentiated EC, as well as further invasive proliferation of the tumour to advanced-stage disease.
The immunohistochemical staining of PR was nuclearly and cytoplasmatically positive in EH with/without atypia and cytoplasmatically negative in endometrioid carcinoma, and in ER, the immunohistochemical staining was cytoplasmatically negative in the forms of EH without atypia and positive in various stages of intensity in the rest of the cases.
The KRAS gene was most often mutated in carcinomas next to hyperplastic endometrium, whereas PIK3CA and CTNNB1 mutations were found in endometrioid carcinomas with adjacent atrophic endometrium.
Although a general increase in nuclear progesterone receptor (PR) expression occurred after E2 expression, a total loss in PR was noted in some endometrial glands as disease advanced to simple EH.
Down-regulated progesterone receptor A and B coinciding with successful treatment of endometrial hyperplasia by the levonorgestrel impregnated intrauterine system.