The Estrogen Receptor Joins Other Cancer Biomarkers as a Predictor of Outcome

Leslie, Kimberly K.; Thiel, Kristina W.; Pineda, Henry Reyes; Yang, Shujie; Zhang, Yuping; Carlson, Matthew J.; Kumar, Nirmala S.; Dai, Donghai

doi:10.1155/2013/479541

Cited by 16 publications

(16 citation statements)

References 44 publications

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“…Uterine proliferation seems to depend on ER mediated transcription, which may result from either the ligand ER-α activation (associated to estrogen stimulation) or a ligand-independent pathway [ 43 ]. Activation of the ER-α drives the transactivation of numerous growth factors, which in turn activate their cognate receptors, leading to multiple signalling cascades controlling cellular proliferation [ 44 ]. Estrogen receptor alpha may be induced in estrogen-driven tumours, and tumour growth is often limited by progesterone, once ER expression is down-regulated by activated PR [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

“…Activation of the ER-α drives the transactivation of numerous growth factors, which in turn activate their cognate receptors, leading to multiple signalling cascades controlling cellular proliferation [ 44 ]. Estrogen receptor alpha may be induced in estrogen-driven tumours, and tumour growth is often limited by progesterone, once ER expression is down-regulated by activated PR [ 44 ]. However, proliferation in a tumour may occur driven by the constitutive activation of a parallel growth factor pathway.…”

Section: Discussionmentioning

confidence: 99%

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An immunohistochemical study on the expression of sex steroid receptors, Ki-67 and cytokeratins 7 and 20 in feline endometrial adenocarcinomas

et al. 2015

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BackgroundEndometrial adenocarcinomas are a rare type of tumour in cats. Though different morphologies have been reported, the most frequent histological type of feline endometrial adenocarcinoma (FEA) is the papillary serous. Characterization of molecular markers expression in FEA may contribute to clarify the pathogenesis of these tumours and to assess the differences between normal endometrium and FEA regarding the expression pattern of several proteins. Therefore, this study aimed to evaluate the immunohistochemical profile of a wide panel of antibodies (specific for ER-α, PR, Ki-67, CK7 and CK20) in twenty-four cases of FEA. Comparisons were made between FEA and feline normal cyclic endometrium in follicular (n = 13) and luteal (n = 10) stages. Except for Ki-67, all other molecular markers were assessed independently for the intensity of immunolabeling and for the percentage of cells expressing the protein.ResultsThis study showed that in FEA a loss of expression occurs for ER-α (P ≤ 0.0001) and less markedly also for PR. The lost in sex steroid receptors concerns a decrease in both the proportion of labelled cells and the intensity of immunolabelling (P = 0.002 and P = 0.024, respectively). Proliferative activity, estimated via Ki-67 immunoreaction, significantly increased in FEA as compared to normal endometrium (P ≤ 0.0001). Feline endometrial adenocarcinomas maintained the CK7+/CK20+ status of normal endometrium. However, FEA showed decreased CK7 intensity of labelling compared to normal endometria (P ≤ 0.0001) and loss of CK20 expression, both in intensity (P ≤ 0.0001) and in percentage of positive cells (P = 0.01), compared to normal tissues.ConclusionsData gathered in this study suggest that proliferation in FEA accompanies ER-α down-regulation, possibly following activation of pathways mediated by local growth factors. Moreover, FEA retains combined expression of CK7 and CK20, as evidenced in normal endometrial epithelia, although a decrease in CK7 expression was observed.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

An immunohistochemical study on the expression of sex steroid receptors, Ki-67 and cytokeratins 7 and 20 in feline endometrial adenocarcinomas

et al. 2015

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“…Therefore, any shift to the endocrine balance in favor of high estrogen level will ultimately stimulate oncogenesis. Such overexposure to estrogen arises in the majority of type I tumors, which also becomes a high risk factor among women undergoing estrogen-only hormonal therapy, using tamoxifen as adjunct therapy for breast cancer, facing obesity as adipose tissue releases estrone, which is converted into estradiol in the uterus, or suffering from PCOS (polycystic ovary syndrome) [20,21].…”

Section: Introductionmentioning

confidence: 99%

Estrogen Receptor, Progesterone Receptor, and HER2 Receptor Markers in Endometrial Cancer

Wang¹,

Tran²,

Fu³

et al. 2020

J. Cancer

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Background: Endometrial cancer (EC) is a major gynecologic adenocarcinoma that arises from the endometrium. While the incidence of EC is on the rise worldwide, survivorship and clinical advancement have considerably lagged compared to other cancers. Given the sensitive nature of the endometrium and its high expression of hormone receptors, hormonal therapy has become a favorable alternative treatment compared to highly toxic chemotherapeutics and radiation therapy. Methods: Clinical samples from patients diagnosed with EC were obtained. ER and PR staining were performed according to the S-P kit, and HER2 staining was carried out according to the UltrasensitiveTM S-P immunohistochemistry kit protocol. Chi-square analysis was conducted using the SPSS. P-values of less than 0.05 were taken as an a priori value for statistical significance. Results: Immunohistochemical (IHC) analysis showed the overall positive expression rates of ER, PR, and HER2 to be 59.8%, 75.0%, and 71.1%, respectively. Significant co-expression was found among all three receptors, suggesting a cooperative, synergistic effect. More importantly, we found that ER expression was correlated with FIGO staging and cervical invasion, whereas PR expression was associated with histologic type. No clinicopathologic features were correlated with HER2 expression, but HER2 positivity was inversely associated with the degree of HER2 overexpression. Conclusions: These results suggest that EC is a heterogeneous disease that may not conform to traditional, prototypically defined subtypes. The status of ER, PR, and HER2 receptors may have the potential to serve as prognostic indicators for EC, but further analysis is needed to ascertain their prognostic significance.

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“…Patient characteristics such as body mass index and histopathologic features such as glandular cellularity have been correlated with response to progestin therapy [15, 17]. For endometrial cancer, expression of the hormone receptors estrogen receptor (ER) and progesterone receptor (PR) have been positively correlated with response [18–21]. However, identification of molecular biomarkers for progression from CAH to endometrial cancer has proven more challenging, with some studies providing conflicting results [15, 22].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of FOXO1 mRNA levels predicts treatment failure in patients with endometrial pathology conservatively managed with progestin-containing intrauterine devices

Pineda

Carlson

Devor

et al. 2016

Gynecologic Oncology

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Objective To examine hormone receptor expression levels and downstream gene activation in pre-treatment and post-treatment biopsies in a cohort of patients with endometrial pathology who were being conservatively managed with a progestin-containing intrauterine device (IUD). A molecular signature of treatment failure is proposed. Methods A retrospective analysis of pre- and post-treatment biopsy specimens from 10 women treated with progestin-containing IUD for complex atypical hyperplasia (CAH) or grade 1 endometrioid adenocarcinoma was performed. Expression of estrogen receptor (ER), progesterone receptor (PR) and PR target genes was examined by immunohistochemistry (IHC) and quantitative RT-PCR. Results The mean treatment duration was 14.3 months. Four CAH patients had stable disease or regressed after treatment, and four progressed to endometrioid adenocarcinoma. Both patients with an initial diagnosis of endometrioid adenocarcinoma regressed to CAH or no disease. In general, hormone receptor levels diminished post-treatment compared to pre-treatment biopsies; however, we noted unexpected higher expression of the B isoform of PR (PRB) as well as ER in those patients who progressed to frank cancer. There was a trend towards a non-nuclear cytoplasmic location of PRB in these patients. Importantly, the differentiating impact of PR signaling, as determined by the expression of the progestin-controlled tumor suppressor FOXO1, was lost in individuals who progressed on therapy. Conclusions FOXO1 mRNA levels may serve as a biomarker for response to therapy and an indicator of PR function in patients being conservatively managed with a progestin-containing IUD.

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The Estrogen Receptor Joins Other Cancer Biomarkers as a Predictor of Outcome

Cited by 16 publications

References 44 publications

An immunohistochemical study on the expression of sex steroid receptors, Ki-67 and cytokeratins 7 and 20 in feline endometrial adenocarcinomas

An immunohistochemical study on the expression of sex steroid receptors, Ki-67 and cytokeratins 7 and 20 in feline endometrial adenocarcinomas

Estrogen Receptor, Progesterone Receptor, and HER2 Receptor Markers in Endometrial Cancer

Downregulation of FOXO1 mRNA levels predicts treatment failure in patients with endometrial pathology conservatively managed with progestin-containing intrauterine devices

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