Electronic databases were searched from their inception to May 2018 for studies assessing immunohistochemical expression of PTEN in endometrial hyperplasia specimens.
The purpose of the current study was to characterize the role of PTEN in malignant transformation and to evaluate the significance of mutated PTEN exons as prognostic markers in the carcinogenesis of endometrial hyperplasia.
There was no higher frequency of PTEN mutations in endometrial hyperplasias with atypia (6 of 32; 19%) relative to those without atypia (4 of 19; 21%).
We aimed to determine the optimal immunohistochemical criteria to define PTEN loss in endometrial hyperplasia, through a systematic review and meta-analysis of diagnostic accuracy.
PTEN gene mutations were detected in 4 of 13 (30%) monoclonal endometrial hyperplasias with atypia and 2 of 17 (12%) monoclonal endometrial hyperplasias without atypia but were not detected in polyclonal endometrial hyperplasias, with or without atypia.
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.
The objective of this study was to evaluate the immunohistochemical expression of the estrogen receptor (ER) and progesterone receptor (PR), p14, p53, phosphatase and tensin homolog (PTEN), Ki67, in patients with endometrial hyperplasia (EH) with/without atypia versus endometrioid endometrial carcinoma type 1.
Our study evaluates an association between the morphological appearance of endometrial hyperplasia and endometrial carcinoma and the degree of PTEN alterations.
Furthermore, estrogen receptor (ER) expression in the nucleus of endometrial cells was reduced in disordered proliferation and increased when EH progressed to atypical EH and precancerous stages.
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.
Tissue microarrays of 368 endometrial carcinomas and large sections of 43 cases of endometrial hyperplasia were analysed for ESR1 gene amplification and ER protein expression by means of fluorescence in situ hybridization (FISH) and immunohistochemistry.
We used immunohistochemistry and quantitative real-time RT-PCR to examine the expression of WISP-1, the estrogen receptor (ER) and progesterone receptor (PR) in 86 cases of EEC, with 20 cases of endometrial hyperplasia, 20 of proliferative endometrium and 20 of secretory endometrium used as the control group.
Our findings suggest that decreased glycolysis and increased mitochondrial activity might contribute to the onset of ERα-dependent endometrial hyperplasia and that metformin might directly reverse impaired glycolysis and normalize mitochondrial function in PCOS patients with endometrial hyperplasia.
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.
A total of 22 patients with endometrial adenocarcinoma and 9 with endometrial hyperplasia (mean age, 56.0 +/- 15.3 y) underwent (18)F-FES PET for estrogen receptor imaging and (18)F-FDG PET.
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.
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.