Expression of ER, PR and Her-2/neu in Endometrial Cancer: A Clinicopathological Study

Khunnarong, Jakkapan; Srijaipracharoen, Sunamchok; Tangjitgamol, Siriwan; Tanvanich, Sujitra; Manusirivithaya, S.

doi:10.4172/2155-9929.1000056

Cited by 2 publications

(2 citation statements)

References 37 publications

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“…Thus, type II is not completely estrogen-independent (5). Previous studies supported the role of ERα in the development of EC (4, 6). Additionally, G-protein-coupled receptor-30 (GPR30), which encodes a multi-pass membrane protein mediating the estrogen action of intracellular estrogen receptor (7, 8), has been suggested to be an indicator of EC progression (9).…”

Section: Introductionmentioning

confidence: 54%

“…In China, EC was diagnosed in 63,400 patients and accounted for more than 21,800 deaths in 2016 (3). EC has been proposed to be classified into two pathogenetic groups, of which type I mostly occurs in pre- and peri-menopausal women with a history of unopposed estrogen exposure (4). However, studies found no difference in the positivity of estrogen receptor (ER) or progesterone receptor (PR) as well as the level of sex hormones between these two types of EC.…”

Section: Introductionmentioning

confidence: 99%

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Chronic BDE-47 Exposure Aggravates Malignant Phenotypes and Chemoresistance by Activating ERK Through ERα and GPR30 in Endometrial Carcinoma

et al. 2019

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Environmental exposure to certain compounds contribute to cell plasticity, tumor progression and even chemoresistance. 2,2′,4,4′-tetrabromo diphenyl ether (BDE-47), one of the most frequently detected polybrominated diphenyl ethers (PBDEs) in environmental and biological samples, is a known estrogen disruptor closely associated with the development of hormone-dependent cancers. However, the effect of BDE-47 on endometrial carcinoma (EC), an estrogen-dependent cancer, remains to be elucidated. Mechanisms of estrogen receptor α (ERα) and G-protein-coupled receptor-30 (GPR30) involved in BDE-47 carcinogenesis are yet to be identified. This study aims to investigate the effect of BDE-47 on the invasive phenotype of estrogen-dependent EC cells. BDE-47-treated cells, such as Ishikawa-BDE-47 and HEC-1B-BDE-47 cells, exhibited increased cell viability and enhanced metastatic ability. In vivo studies showed larger tumor volumes and more metastasis in mice injected with Ishikawa-BDE-47 cells compared with parental Ishikawa cells. MTT assay showed that BDE-47 exposure could attenuate sensitivity of EC cells to cisplatin or paclitaxel treatment in vitro. Western blotting revealed overexpression of ERα, GPR30, pEGFR (phosphorylated epidermal growth factor receptor), and pERK (phosphorylated extracellular-regulated protein kinase) in Ishikawa-BDE-47 and HEC-1B-BDE-47 cells. Knockdown of ERα or GPR30 by small interfering RNA reversed the stimulating effect of BDE-47 on cell growth, migration and invasion of EC cells. Additionally, treatment with pEGFR or pERK inhibitor impaired cell viability, migration and invasion in Ishikawa-BDE-47 and HEC-1B-BDE-47 cells. Overall, our results indicate that chronic BDE-47 exposure triggers phenotypic plasticity, promotes progression and even chemoresistance in EC cells, at least in part, via ERα/GPR30 and EGFR/ERK signaling pathways.

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Section: Introductionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Chronic BDE-47 Exposure Aggravates Malignant Phenotypes and Chemoresistance by Activating ERK Through ERα and GPR30 in Endometrial Carcinoma

et al. 2019

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Immunohistochemical study of ER, PR, p53 and Ki67 expression in patients with endometrial adenocarcinoma and atypical endometrial hyperplasia

Swami¹,

Lakhe²,

Doshi³

et al. 2020

ACHR

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To study Immunohistochemistry pattern of ER, PR, p53 and Ki67 expression in patients with endometrial adenocarcinoma (EC) and endometrial hyperplasia. A retrospective study of 78 cases were studied for a period of 02 year from June 2018 to May 2020, where in the clinical data included age, presenting complaints, menopausal status, history of hormonal treatment, ultrasound examination.Histopathological parameters were analysed as per WHO 2014 classification of endometrial hyperplasia into typical and atypical endometrial hyperplasia / Endometrial Intraepithelial Neoplasia (EIN) and endometrial carcinoma. ER, PR, p53 and Ki 67 IHC markers were done on cases diagnosed as endometrial adenocarcinoma and endometrial hyperplasia. Among 78 cases, there were 20 cases of EC and 58 cases of endometrial hyperplasia. EC was most commonly seen in sixth to seventh decade and hyperplasia was seen in fourth to fifth decade .There were 11 surgical specimens and 09 biopsies of EC. Out of total 20 cases, there were 17 cases of endometrioid adenocarcinoma and 03 cases were of papillary serous adenocarcinoma.ER, PR expression was seen in 10 cases of grade 1 endometrial carcinomas and 5 cases of grade 2 EC. p53 expression was seen in 01 case of grade 1 EC and 03 cases grade 3 EC. ER, PR, p53 all were negative in one case. Ki67 was <10% in 11 cases, between 10-20% in 5 cases and >20% in 04 cases. We followed up 15 out of 20 cases, out of which only 01 patient died of disease who was grade 1 endometrial carcinoma. Rest 14 had progression free survival (PFS) till date.All 58 cases of endometrial hyperplasia were reclassified complex and simple hyperplasia to typical and atypical hyperplasia (as per WHO Classification 2014). Out of 58 cases, 56 cases were typical hyperplasia and 02 cases atypical hyperplasia. ER, PR expression was positive in all the cases of typical and atypical hyperplasia. p53 expression was absent in typical and atypical hyperplasia with low Ki 67 index (<10%). High ER, PR expression along with low p53 was seen in type 1 endometrial carcinomas compared to low or absent ER, PR along with strong p53 expression in papillary serous carcinoma (Type 2). The expression of ER, PR was high in typical hyperplasia as against high p53 expression observed in atypical hyperplasia.

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Expression of ER, PR and Her-2/neu in Endometrial Cancer: A Clinicopathological Study

Cited by 2 publications

References 37 publications

Chronic BDE-47 Exposure Aggravates Malignant Phenotypes and Chemoresistance by Activating ERK Through ERα and GPR30 in Endometrial Carcinoma

Chronic BDE-47 Exposure Aggravates Malignant Phenotypes and Chemoresistance by Activating ERK Through ERα and GPR30 in Endometrial Carcinoma

Immunohistochemical study of ER, PR, p53 and Ki67 expression in patients with endometrial adenocarcinoma and atypical endometrial hyperplasia

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