scholarly journals Triple-high expression of phosphatase and tensin homolog (PTEN), estrogen receptor (ER) and progesterone receptor (PR) may predict favorable prognosis for patients with Type I endometrial carcinoma

2020 ◽  
Vol 11 (6) ◽  
pp. 1436-1445 ◽  
Author(s):  
Yanfang Liang ◽  
Bihua Lin ◽  
Ziyu Ye ◽  
Shasha Chen ◽  
Haibo Yu ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Progesterone Receptor ◽  
Endometrial Carcinoma ◽  
High Expression ◽  
Type I ◽  
Phosphatase And Tensin Homolog ◽  
Favorable Prognosis ◽  
Tensin Homolog

scholarly journals Insulin-Like Growth Factor Binding Protein 2 (IGFBP-2) Promotes Growth and Survival of Breast Epithelial Cells: Novel Regulation of the Estrogen Receptor

Endocrinology ◽  
2013 ◽  
Vol 154 (5) ◽  
pp. 1780-1793 ◽  
Author(s):  
Emily J. Foulstone ◽  
Li Zeng ◽  
Claire M. Perks ◽  
Jeff M. P. Holly
Keyword(s):  
Estrogen Receptor ◽  
Cancer Cells ◽  
Binding Protein ◽  
Chemotherapeutic Agents ◽  
Normal Breast ◽  
Proliferative Potential ◽  
Integrin Receptors ◽  
Phosphatase And Tensin Homolog ◽  
Growth And Survival ◽  
Tensin Homolog

Abstract In breast tumors IGF binding protein-2 (IGFBP-2) is elevated, and the presence of IGFBP-2 has been shown to correlate with malignancy. However, how IGFBP-2 contributes to the malignant state is still unclear. Silencing IGFBP-2 blocked cell proliferation and in MCF-7 cells increased cell death, indicating that IGFBP-2 was acting in both a mitogenic and a survival capacity. Exogenous IGFBP-2 acting via integrin receptors to reduce phosphatase and tensin homolog deleted from chromosome 10 (PTEN) levels protected these cells against death induced by various chemotherapeutic agents. This was dependent on a functional estrogen receptor (ER)-α because silencing ER-α blocked the ability of IGFBP-2 to confer cell survival. Loss of IGFBP-2 increased levels of PTEN and improved chemosensitivity of the cells, confirming its role as a survival factor. Silencing IGFBP-2 had no effect on the response to IGF-II, but responses to estrogen and tamoxifen were no longer observed due to loss of ER-α, which could be prevented by the inhibition of PTEN. Conversely, exogenous IGFBP-2 increased ER-α mRNA and protein in both normal and cancer cells via its interaction with integrin receptors. These actions of IGFBP-2 on ER-α involved the IGF-I receptor and activation of phosphatidylinositol 3-kinase in the cancer cells but were independent of this in normal breast cells. The production of IGFBP-2 by breast cancer cells enhances their proliferative potential, increases their survival, and protects them against chemotherapy-induced death. IGFBP-2 not only modulates IGFs and directly regulates PTEN but also has a role in maintaining ER-α expression.

scholarly journals Diagnostic utility of phosphatase and tensin homolog, β-catenin, and p53 for endometrial carcinoma by thin-layer endometrial preparations

Cancer ◽  
2008 ◽  
Vol 114 (3) ◽  
pp. 155-164 ◽  
Author(s):  
Yoshiaki Norimatsu ◽  
Motoyuki Miyamoto ◽  
Tadao K. Kobayashi ◽  
Takuya Moriya ◽  
Keiko Shimizu ◽  
...  
Keyword(s):  
Thin Layer ◽  
Endometrial Carcinoma ◽  
Diagnostic Utility ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog

scholarly journals PTENSequence Analysis in Endometrial Hyperplasia and Endometrial Carcinoma in Slovak Women

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
H. Gbelcová ◽  
P. Bakeš ◽  
P. Priščáková ◽  
V. Šišovský ◽  
I. Hojsíková ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Endometrial Carcinoma ◽  
Endometrial Hyperplasia ◽  
Female Genital Tract ◽  
Suppressor Gene ◽  
Serous Carcinoma ◽  
Tissue Samples ◽  
Phosphatase And Tensin Homolog ◽  
Coding Regions ◽  
Tensin Homolog

Phosphatase and tensin homolog (PTEN) is a protein that acts as a tumor suppressor by dephosphorylating the lipid second messenger phosphatidylinositol 3,4,5-trisphosphate. Loss of PTEN function has been implicated in the pathogenesis of a number of different tumors, particularly endometrial carcinoma (ECa). ECa is the most common neoplasia of the female genital tract. Our study evaluates an association between the morphological appearance of endometrial hyperplasia and endometrial carcinoma and the degree ofPTENalterations. A total of 45 endometrial biopsies from Slovak women were included in present study. Formalin-fixed and paraffin-embedded tissue samples with simple hyperplasia (3), complex hyperplasia (5), atypical complex hyperplasia (7), endometrioid carcinomas G1 (20) and G3 (5), and serous carcinoma (5) were evaluated for the presence of mutations in coding regions ofPTENgene, the most frequently mutated tumor suppressor gene in endometrial carcinoma. 75% of the detected mutations were clustered in exons 5 and 8. Out of the 39 mutations detected in 24 cases, 20 were frameshifts and 19 were nonsense, missense, or silent mutations. Some specimens harboured more than one mutation. The results of current study on Slovak women were compared to a previous study performed on Polish population. The two sets of results were similar.

scholarly journals IMMUNOHISTOCHEMICAL STUDY ON PTEN AND CYCLIN D1 IN NON-NEOPLASTIC AND NEOPLASTIC ENDOMETRIAL LESIONS

2021 ◽  
Vol 5 (7) ◽  
Author(s):  
Alpana Laisom ◽  
Gayatri Pukhrambam ◽  
Yumnam Shameen ◽  
Ningthibi Akoijam ◽  
Prasanta Sinam ◽  
...  
Keyword(s):  
Cyclin D1 ◽  
Endometrial Carcinoma ◽  
Endometrial Hyperplasia ◽  
Precancerous Lesions ◽  
Atypical Hyperplasia ◽  
Histopathological Diagnosis ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
Endometrial Carcinomas

Abstract Introduction: Endometrial carcinoma (EC) is the most common gynaecological malignancy in developed countries and has been classified into two groups, type 1 and type 2.  Type 1 or endometrioid endometrial carcinomas (EECA) accounts for 80% of EC and are thought to develop following a continuum of premalignant lesions ranging from endometrial hyperplasia without atypia (EH) and atypical hyperplasia (AH). PTEN (phosphatase and tensin homolog), a tumor suppressor gene is commonly inactivated in 83 % of endometrioid carcinoma and 55% of precancerous lesions. Cyclin D1, a cell cycle regulator is overexpressed in about 40% of endometrial carcinomas. Aim: To study the expression of PTEN (Phosphatase and tensin homolog) and Cyclin D1 in non-neoplastic and neoplastic endometrial lesions by immunohistochemistry (IHC). Methods: A 2 year cross-sectional study (September 2017 to August 2019) on 115 endometrial samples was done in the Department of Pathology, RIMS. Histomorphological features and IHC expression of PTEN and Cyclin D1 in the various endometrial lesions were studied and evaluated, data collected in IBM SPSS Statistics 21 was statistically analyzed using Chi - square  and Fisher’s Exact test. Results: Out of the 115 cases, 47(40.9%) were diagnosed as benign proliferative endometrium, 20(17.4%) benign secretory endometrium, 21(18.3%) hyperplasia without atypia, 15(13.0%)  atypical hyperplasia and 12(10.4%) endometrial carcinoma with an age group spanning from 26-68 years (mean age = 46.4).  Following IHC staining, 91.7%(11/12) and 83.3%(10/12) cases of EC and 80%(12/15) and 73.3%(11/15) cases of AH showed complete loss of PTEN expression and Cyclin D1 overexpression, respectively when compared to other benign lesions and was statistically significant  (p < .001). Conclusion: Loss of PTEN and Cyclin D1 overexpression was seen in a significant number of EECA and AH, suggesting both as an early event in endometrial carcinogenesis. Therefore, we propose the use of PTEN and Cyclin D1 immunostaining as an adjunct to histopathological diagnosis as it may be informative in the identification and further management of  premalignant endometrial  lesions that are likely to progress to carcinoma Keywords: PTEN, Cyclin D1, endometrial hyperplasia, endometrial carcinoma, endometrioid endometrial carcinomas.

scholarly journals Zebrafish pten Genes Play Relevant but Distinct Roles in Antiviral Immunity

Vaccines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 199 ◽  
Author(s):  
Patricia Pereiro ◽  
Antonio Figueras ◽  
Beatriz Novoa
Keyword(s):  
Nk Cell ◽  
Type I Interferon ◽  
Cytolytic Activity ◽  
Pten Gene ◽  
Type I ◽  
Replication Rate ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
In The Wild ◽  
Mutant Lines

The PTEN (phosphatase and TENsin homolog on chromosome 10) gene encodes a bifunctional phosphatase that acts as a tumor suppressor. However, PTEN has been implicated in different immune processes, including autophagy, inflammation, regulation of natural killer (NK) cell cytolytic activity and type I interferon responses. Unlike mammals, zebrafish possess two pten genes (ptena and ptenb). This study explores the involvement of both zebrafish pten genes in antiviral defense. Although ptena−/− and ptenb−/− larvae were more susceptible to Spring viremia of carp virus (SVCV), the viral replication rate was lower in the mutant larvae than in the wild-type larvae. We observed that both mutant lines showed alterations in the transcription of numerous genes, including those related to the type I interferon (IFN) system, cytolytic activity, autophagy and inflammation, and some of these genes were regulated in opposite ways depending on which pten gene was mutated. Even though the lower replication rate of SVCV could be associated with impaired autophagy in the mutant lines, the higher mortality observed in the ptena−/− and ptenb−/− larvae does not seem to be associated with an uncontrolled inflammatory response.

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