Journal articles: 'ER-positive'

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Susman, Ed. "ER-Positive Breast Cancer." Oncology Times 27, no. 4 (February 2005): 58. http://dx.doi.org/10.1097/01.cot.0000287844.29669.86.

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Solberg, Erik. "Idrettsutøvere er positive til screening." Tidsskrift for Den norske legeforening 131, no. 17 (2011): 1632. http://dx.doi.org/10.4045/tidsskr.11.0807.

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Mamounas, Terry. "Personalizing Treatment for Node-Positive, ER-Positive Breast Cancer." Oncology Times 39, no. 6 (March 2017): 36. http://dx.doi.org/10.1097/01.cot.0000515196.45322.1e.

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Deng, Hao, Li Yin, Xin-Tian Zhang, Li-Jiang Liu, Mo-Lin Wang, and Zhao-Yi Wang. "ER-α variant ER-α36 mediates antiestrogen resistance in ER-positive breast cancer stem/progenitor cells." Journal of Steroid Biochemistry and Molecular Biology 144 (October 2014): 417–26. http://dx.doi.org/10.1016/j.jsbmb.2014.08.017.

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Ruijtenbeek, R., A. Umar, L. van Houten, R. Hilhorst, J. A. Foekens, R. de Wijn, and J. W. Martens. "Differential protein kinase activity in ER-positive and ER-negative breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e22142-e22142. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22142.

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e22142 Background: Specific protein tyrosine kinases (PTKs) promote cancer progression and are potential drug targets. The presence of the estrogen receptor (ER) is an important criterion in deciding on treatment of patients with breast cancer. Since PTKs can affect the tumors' receptor function, we investigated in our first proof-of-principle study whether it is possible to discriminate ER-positive (ER+) from ER-negative (ER-) tumors based on PTK activity using microarrays containing many PTK peptide substrates. Methods: Cryosections of 12 ER+ and 12 ER- breast tumors were lysed in the presence of appropriate protease and phosphatase inhibitors. The protein kinase activity in the lysates was monitored in vitro using PamChip peptide microarrays, which comprise of 253 PTK peptide substrates derived from known human phosphorylation sites. Peptide phosphorylation through active kinases can be monitored in samples in real time, using a fluorescently labeled phospho-tyrosine specific antibody. Results: Phosphorylation activity profiles were determined in quadruplicate using multiple independent sample preparations. Using ANOVA analysis, out of 253 peptides, several peptides with a different phosphorylation signal in ER+ and ER- samples were found: 22 with p < 0.02 including VEGFR1, 2 and 3 and ADAM9. Multivariate unsupervised analysis using Principle Component Analysis showed a clustering of ER+ samples vs. ER- samples. Predictive analysis was performed using Partial-Least Squares Discriminant Analysis without explicit feature selection. The prediction error obtained from within experiment cross validation was typically in the range 10–20%. The error rate for between experiment prediction was 20%. An average predictive profile was constructed in which peptides with a relatively large weight were included, e.g. ADAM9 and BCAR1. Conclusions: Using PamChip peptide microarrays we have shown that differences in protein kinase activity exist between ER+ and ER- breast tumors. Our in vitro assay is a promising tool to investigate the interplay between kinase and nuclear receptor mediated signaling, with potential relevance to patient selection for targeted therapies. No significant financial relationships to disclose.

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Aasland, Aadne, Arne Backer Grønningsæter, and Peter Meylakhs. "Flere positive – men er alt negativt?" Nordisk Østforum 24, no. 04 (January 10, 2011): 375–95. http://dx.doi.org/10.18261/issn1891-1773-2010-04-03.

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Perron, Michelle. "Investigating Metformin for ER-Positive Breast Cancer." Oncology Times 42, no. 13 (July 5, 2020): 1,12–12. http://dx.doi.org/10.1097/01.cot.0000688420.18453.c6.

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Colleoni, M., and E. Montagna. "Neoadjuvant therapy for ER-positive breast cancers." Annals of Oncology 23 (September 2012): x243—x248. http://dx.doi.org/10.1093/annonc/mds305.

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Wang, Weiqi, Bing Xu, Zhaoxu Zhang, Kehua Fang, and Xiaotian Chang. "RCC2 Expression Stimulates ER-Positive Breast Tumorigenesis." Journal of Oncology 2020 (May 23, 2020): 1–13. http://dx.doi.org/10.1155/2020/5619462.

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Objective. Regulator of chromosome condensation 2 (RCC2) has been reported to be involved in the regulation of cell cleavage. This study investigated the effect of RCC2 expression on breast tumorigenesis. Methods. MCF-7 cells originating from estrogen receptor-positive (ER+) breast cancer were transfected with anti-RCC2 siRNA or RCC2-expressing plasmids. Cell proliferation, apoptosis, migration, and cytokine production in the transfected cells were examined using the CCK-8 assay, wound healing assay, and flow cytometry, respectively. PCR array was used to investigate the tumorigenic pathway of RCC2 in MCF-7 cells transfected with the anti-RCC2 siRNA. MCF-7 cells were also transfected with lentivirus-containing anti-RCC2 short hairpin RNA and were injected into BALB/c nude mice to generate tumor-bearing mice. Tumor growth in the mouse model was examined using magnetic resonance imaging by diffusion-weighted imaging analysis. Results. Western blotting and immunohistochemistry detected significantly increased expression of RCC2 in ER + breast tumor tissues compared with breast fibroadenoma samples. Inhibiting RCC2 expression decreased cell migration and stimulated apoptosis in MCF-7 cells, while overexpressing RCC2 stimulated cell migration and inhibited apoptosis. The inhibition of RCC2 expression significantly decreased breast tumor growth and IL-6 levels in the tumor-bearing mice. PCR array demonstrated that inhibiting RCC2 expression significantly decreased the expression of IGF1 and TWIST1, two well-known tumor-enhancing genes, in MCF-7 cells; conversely, overexpressing RCC2 increased the expression levels of these two genes in the transfected cells. This result was verified in the mouse model following inhibition of RCC2 expression in MCF-7 cells. Additionally, estradiol-17β suppressed MCF-7 cell apoptosis, stimulated cell proliferation and cell migration, and increased RCC2, IGF1, and TWIST1 expression. The siRNA-mediated inhibition of RCC2 expression alleviated the inhibitory effects of estrogen on apoptosis in MCF-7 cells, while overexpressing RCC2 enhanced the estrogen-driven inhibition of apoptosis. Modifying RCC2 expression had no impact on MCF-7 cell proliferation in the presence or absence of estradiol-17β. Conclusions. Our results suggest that estrogen-induced RCC2 expression prompts IGF1, TWIST1, and IL-6 expression, stimulates cell migration, and inhibits apoptosis to contribute to ER + breast tumorigenesis.

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McAndrew, Nicholas P., and Richard S. Finn. "Management of ER positive metastatic breast cancer." Seminars in Oncology 47, no. 5 (October 2020): 270–77. http://dx.doi.org/10.1053/j.seminoncol.2020.07.005.

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Asch-Kendrick, Rebecca J., Mark A. Samols, Mohammed T. Lilo, Andrea P. Subhawong, Rajni Sharma, Peter B. Illei, Pedram Argani, and Ashley Cimino-Mathews. "NKX3.1 is expressed in ER-positive and AR-positive primary breast carcinomas." Journal of Clinical Pathology 67, no. 9 (July 4, 2014): 768–71. http://dx.doi.org/10.1136/jclinpath-2014-202272.

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AimsNKX3.1 is an androgen-regulated tumour suppressor gene that is downregulated in prostate carcinoma. Immunohistochemistry for NKX3.1 is primarily specific for prostatic-derived tumours and tissue but is reported in a small number of breast carcinomas. NKX3.1 is also shown to inhibit estrogen receptor (ER) signalling in breast carcinoma models. Here, we investigate labelling of NKX3.1 in invasive ductal (IDC) and lobular (ILC) carcinomas of the breast with full characterisation of ER, progesterone receptor (PR), androgen receptor (AR) and Her2 status.MethodsTissue microarrays of 86 primary IDC and 37 ILC were labelled for NKX3.1. The IDC consisted of 20 luminal A, 7 luminal B, 14 Her2, and 45 triple negative carcinomas. The ILC consisted of 34 luminal A and 3 luminal B cases. NKX3.1 expression was scored as percentage nuclear labelling and labelling intensity.ResultsNuclear NKX3.1 labelling was seen in 2 IDC (2%) and 10 ILCs (27%). labelling intensity was weak in all cases (1–100% nuclear positivity). Positive NKX3.1 labelling was significantly associated with ILC (p<0.0001). NKX3.1 labelling was seen only in ER and AR-positive carcinomas, which showed a significant correlation (p=0.0003 and p=0.0079, respectively). Expression was not correlated with tumour stage, size, Her2 expression, presence of lymph node metastases or age.ConclusionsThis is the first study to evaluate NKX3.1 expression in breast carcinomas with known ER, PR, AR and Her2 status. Further studies are needed to evaluate what potential role NKX3.1 plays in ER and AR signalling and hormonal treatment response in breast carcinomas.

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Ju, Jie, Feng Du, Songlin Gao, Yiran Si, Nanlin Hu, Dongxu Liu, Xue Wang, et al. "The intra-tumor heterogeneity of ER and HER2 expression in patients with ER-positive and HER2-positive breast cancer." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e12550-e12550. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e12550.

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e12550 Background: ER- positive and HER2-positive (double-positive) breast cancers are known to display significant heterogeneity; however, traditional immunohistochemistry (IHC) only reflects inter-tumor heterogeneity. Studies are needed to demonstrate the intra-tumor heterogeneity of ER and HER2 expression and to further explore its impact. Methods: The retrospective study included three double-positive breast cancer cohorts. Data from a total of 141 patients from The Cancer Genome Atlas (TCGA) and 104 patients from the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) were used to investigate the molecular characteristics of double-positive breast cancers at the tissue level via somatic mutation and RNA-seq analyses, while 43 patients treated at our hospital were selected to analyze ER and HER2 expression and localization at a single-cell level using multiple IF. The rH/R was proposed to reflect ER and HER2 expression profiles based on multiple IF or RNA-seq results, as follows: rH/E = HER2+ cell percentage / (ER+ cell percentage + 1) or rH/E = ERBB2 expression quantity / (ESR1 expression quantity + 1). Results: In the first two cohorts, we found that the HER2-enriched subtype displayed unique molecular characteristics, including increased TP53, ERBB3, and PI3KCA mutation rates and the abnormal expression of important signaling pathways (e.g., G2/M cell cycle checkpoint and epithelial mesenchymal transition); The rH/E was a significant index for diagnosing HER2-enriched patients (area under the receiver operating characteristic curve [AUC] = 0.92 and 0.75, both P < 0.0001). In the third cohort, we found that 86 % of the patients contained all four tumor cell types (ER+HER2+, ER+HER2-, ER-HER2+, and ER-HER2- cells); The rH/E was an independent risk factor for recurrence (hazard ratio [HR] = 2.63, P = 0.02) and patients with a rH/E ≥ 1.5 had a significantly shorter 5-year disease-free survival (DFS = 67 % vs. 92 %, P = 0.046). Conclusions: The significant intra- and inter-tumor heterogeneity of double-positive breast cancers is closely related to the prognosis of patients, which is of great significance for precision treatment.

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Rangel, Nelson, Milena Rondon-Lagos, Laura Annaratone, Simona Osella-Abate, Jasna Metovic, Maria Piera Mano, Luca Bertero, Paola Cassoni, Anna Sapino, and Isabella Castellano. "The role of the AR/ER ratio in ER-positive breast cancer patients." Endocrine-Related Cancer 25, no. 3 (March 2018): 163–72. http://dx.doi.org/10.1530/erc-17-0417.

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The significance of androgen receptor (AR) in breast cancer (BC) management is not fully defined, and it is still ambiguous how the level of AR expression influences oestrogen receptor-positive (ER+) tumours. The aim of the present study was to analyse the prognostic impact of AR/ER ratio, evaluated by immunohistochemistry (IHC), correlating this value with clinical, pathological and molecular characteristics. We retrospectively selected a cohort of 402 ER+BC patients. On each tumour, IHC analyses for AR, ER, PgR, HER2 and Ki67 were performed and AR+ cases were used to calculate the AR/ER value. A cut-off of ≥2 was selected using receiver-operating characteristic (ROC) curve analyses. RNA from 19 cases with AR/ER≥2 was extracted and used for Prosigna-PAM50 assays. Tumours with AR/ER≥2 (6%) showed more frequent metastatic lymph nodes, larger size, higher histological grade and lower PgR levels than cases with AR/ER<2. Multivariate analysis confirmed that patients with AR/ER≥2 had worse disease-free interval (DFI) and disease-specific survival (DSS) (hazard ratios (HR) = 4.96 for DFI and HR = 8.69 for DSS, bothP ≤ 0.004). According to the Prosigna-PAM50 assay, 63% (12/19) of these cases resulted in intermediate or high risk of recurrence categories. Additionally, although all samples were positive for ER assessed by IHC, the molecular test assigned 47.4% (9/19) of BCs to intrinsic non-luminal subtypes. In conclusion, the AR/ER ratio ≥2 identifies a subgroup of patients with aggressive biological features and may represent an additional independent marker of worse BC prognosis. Moreover, the Prosigna-PAM50 results indicate that a significant number of cases with AR/ER≥2 could be non-luminal tumours.

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Chimge, Nyam-Osor, Sara Ahmed-Alnassar, and Baruch Frenkel. "Relationship between RUNX1 and AXIN1 in ER-negative versus ER-positive Breast Cancer." Cell Cycle 16, no. 4 (January 31, 2017): 312–18. http://dx.doi.org/10.1080/15384101.2016.1237325.

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Sun, M., M. Sun, J. Lyons-Weiler, A. E. Lokshin, F. Modugno, J. Marks, and W. L. Bigbee. "Serum proteomic profiling distinguishes estrogen receptor (ER) positive and ER negative breast cancers." Journal of Clinical Oncology 23, no. 16_suppl (June 2005): 578. http://dx.doi.org/10.1200/jco.2005.23.16_suppl.578.

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Wakako, Tajiri. "Abstract P4-05-11: The clinical importance of the new category, ER low-positive in the ER expression HER2 negative early breast cancer." Cancer Research 82, no. 4_Supplement (February 15, 2022): P4–05–11—P4–05–11. http://dx.doi.org/10.1158/1538-7445.sabcs21-p4-05-11.

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Abstract <Background>In the latest updated ASCO/CAP guideline, a new category, ER low-positive was introduced, which are determined by the 1% to10 % of positive staining of the tumor nuclei for ER. However clinical meaning of ER-low positive was unclear compared with ER- positive or ER-negative in HER2 negative breast cancer. <Purpose> In order to clarify the clinicopathological features of ER-low positive breast cancer, we compared the clinicopathological factors and prognosis among three groups, ER negative, ER-low positive, and ER-positive groups in the patients with HER2 negative breast cancer. <Patients and Method> A total of 1,882 patients with HER2 negative breast cancer who underwent surgery between 2001 and 2018 were included in this study. We divided them into three groups, ER negative (<1%), ER-low positive (1-10%), and ER positive (10%≦). The relationships between ER status and clinicopathological characteristics and prognosis were evaluated. <Result>According to ER status, 553(29.4%), 183(9.7%), 1146(60.9%) patients were divided into ER negative, low-positive and positive groups. Compared with ER-positive group, patients in the ER negative and low-positive groups were of higher age (p<.0001), and those tumors were significantly associated with the larger tumor size (p<.0001), higher histological grade (p<.0001) and more administration of adjuvant chemotherapy (p<0.0001). Most of the patients with ER low-positive and ER-positive tumors had received the adjuvant endocrine therapy. The prognosis of the patients with ER low-positive tumors were poorer than that of those with ER positive tumors in terms of relapse-free survival (RFS p<.0001), distant metastasis-free survival (DMFS p<.0001) and overall survival (OS p<.0001).In the node negative patients, the prognosis of the ER-negative and ER low-positive groups were equivalent, and poorer than that of the ER-positive group (RFS; p=0.0068, DMFS; p=0.0013, OS: p=0.0032). In addition, in pStage III patients, prognosis of the ER-negative and ER low-positive groups were also equivalent, and poorer than that of the ER-positive group (RFS; p=0.008, DMFS; p=0.0021, OS: p=0.0010). <Conclusion> This study showed that the prognosis of the patients with ER negative and ER low-positive were similar, and poorer than that of those with ER positive tumors. Therefore, the new category of ER-low positive is clinically especially important in order to determine the appropriate adjuvant therapy. Citation Format: Tajiri Wakako. The clinical importance of the new category, ER low-positive in the ER expression HER2 negative early breast cancer [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P4-05-11.

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Iwamoto, Takayuki, Daniel Booser, Vicente Valero, James L. Murray, Kimberly Koenig, Francisco J. Esteva, Naoto T. Ueno, et al. "Estrogen Receptor (ER) mRNA and ER-Related Gene Expression in Breast Cancers That Are 1% to 10% ER-Positive by Immunohistochemistry." Journal of Clinical Oncology 30, no. 7 (March 1, 2012): 729–34. http://dx.doi.org/10.1200/jco.2011.36.2574.

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Purpose We examined borderline estrogen receptor (ER) –positive cancers, defined as having 1% to 10% positivity by immunohistochemistry (IHC), to determine whether they show the same global gene-expression pattern and high ESR1 mRNA expression as ER-positive cancers or if they are more similar to ER-negative cancers. Patients and Methods ER status was determined by IHC in 465 primary breast cancers and with the Affymetrix U133A gene chip. We compared expressions of ESR1 mRNA and a 106 probe set ER-associated gene signature score between ER-negative (n = 183), 1% to 9% (n = 25), 10% (n = 6), and more than 10% (n = 251) ER-positive cancers. We also assessed the molecular class by using the PAM50 classifier and plotted survival by ER status. Results Among the 1% to 9%, 10%, and more than 10% ER IHC–positive patients, 24%, 67%, and 92% were also positive by ESR1 mRNA expression. The average ESR1 expression was significantly higher in the ≥ 10% ER-positive cohorts compared with the 1% to 9% or ER-negative cohort. The average ER gene signature scores were similar for the ER-negative and 1% to 9% IHC-positive patients and were significantly lower than in ≥ 10% ER-positive patients. Among the 1% to 9% ER-positive patients, 8% were luminal B and 48% were basal-like; among the 10% ER-positive patients, 50% were luminal. The overall survival rate of 1% to 9% ER-positive patients with cancer was between those of patients in the ≥ 10% ER-positive and ER-negative groups. Conclusion A minority of the 1% to 9% IHC ER–positive tumors show molecular features similar to those of ER-positive, potentially endocrine-sensitive tumors, whereas most show ER-negative, basal-like molecular characteristics. The safest clinical approach may be to use both adjuvant endocrine therapy and chemotherapy in this rare subset of patients.

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Kurbel, Sven. "Selective reduction of estrogen receptor (ER) positive breast cancer occurrence by estrogen receptor modulators supports etiological distinction between ER positive and ER negative breast cancers." Medical Hypotheses 64, no. 6 (January 2005): 1182–87. http://dx.doi.org/10.1016/j.mehy.2004.09.026.

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Qui, Wen-sheng, Lu Yue, Ai-ping Ding, Jian Sun, Yang Yao, Zan Shen, and Li-hong Fan. "Co-expression of ER-beta and HER2 associated with poorer prognosis in primary breast cancer." Clinical & Investigative Medicine 32, no. 3 (June 1, 2009): 250. http://dx.doi.org/10.25011/cim.v32i3.6114.

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Purpose: To assess the prognostic value of co-expression of estrogen receptor (ER)-beta and human epidermal growth factor receptor 2 (HER2) in primary breast cancer patients in China. Methods: Tumour specimens from 308 patients undergoing surgery for primary breast cancer were evaluated. Expression of ER-beta and HER-2 was investigated by the immunohistochemistry. Results: 123 patients (40%) were ER-beta positive and 58 (18.5 %) were HER2 positive. Among the 58 HER2 positive patients, 44 were ER-beta positive and 14 were ER-beta negative. ER-beta positive was associated with HER2 positive (75.9%, P=0.018) as well as ER-alpha positive (79.7%, P=0.023), poor cell differentiation (77.2% grade 2 or 3, P=0.010) and menopause age < 45 yr (55.3%, P=0.031). HER2 positive was associated with poor cell differentiation (93.1%, P=0.001), ?3cm tumour size (67.2%, P=0.011). Conclusion: Both ER-beta positive and HER2 positive status was associated with poorer overall survival (OS) by univariate analysis. In both HER2 positive and HER2 negative subgroups, ER-beta positive was associated with poorer distant disease free survival (DDFS) but not OS, which implied that ER-beta might relate to metastasis in breast cancer.

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Hutchinson, Samantha A., Priscilia Lianto, Hanne Roberg-Larsen, Sebastiano Battaglia, Thomas A. Hughes, and James L. Thorne. "ER-Negative Breast Cancer Is Highly Responsive to Cholesterol Metabolite Signalling." Nutrients 11, no. 11 (November 1, 2019): 2618. http://dx.doi.org/10.3390/nu11112618.

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Interventions that alter cholesterol have differential impacts on hormone receptor positive- and negative-breast cancer risk and prognosis. This implies differential regulation or response to cholesterol within different breast cancer subtypes. We evaluated differences in side-chain hydroxycholesterol and liver X nuclear receptor signalling between Oestrogen Receptor (ER)-positive and ER-negative breast cancers and cell lines. Cell line models of ER-positive and ER-negative disease were treated with Liver X Receptor (LXR) ligands and transcriptional activity assessed using luciferase reporters, qPCR and MTT. Publicly available datasets were mined to identify differences between ER-negative and ER-positive tumours and siRNA was used to suppress candidate regulators. Compared to ER-positive breast cancer, ER-negative breast cancer cells were highly responsive to LXR agonists. In primary disease and cell lines LXRA expression was strongly correlated with its target genes in ER-negative but not ER-positive disease. Expression of LXR’s corepressors (NCOR1, NCOR2 and LCOR) was significantly higher in ER-positive disease relative to ER-negative, and their knock-down equalized sensitivity to ligand between subtypes in reporter, gene expression and viability assays. Our data support further evaluation of dietary and pharmacological targeting of cholesterol metabolism as an adjunct to existing therapies for ER-negative and ER-positive breast cancer patients.

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Cuzick, Jack. "Predicting late recurrence in ER-positive breast cancer." Nature Reviews Clinical Oncology 16, no. 7 (May 15, 2019): 406–8. http://dx.doi.org/10.1038/s41571-019-0228-y.

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Chaudhry, Farrukh A., Leif Knutsen, and Rolf Kirschner. "Barneleger, gynekologer og fødselsleger er positive til gutteomskjæring." Tidsskrift for Den norske legeforening 133, no. 3 (2013): 264–65. http://dx.doi.org/10.4045/tidsskr.13.0046.

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Paik, Soonmyoung, Dan Paul Hartmann, Robert B. Dickson, and Marc E. Lippman. "Antiestrogen resistance in ER positive breast cancer cells." Breast Cancer Research and Treatment 31, no. 2-3 (1994): 301–7. http://dx.doi.org/10.1007/bf00666162.

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Sheffield, Brandon S., Zuzana Kos, Xiuqing Wang, Christine Chow, Sherman Lau, Robert Wolber, Cyril Blake Gilks, et al. "Molecular profiling of ER weakly-positive breast cancer." Journal of Clinical Oncology 33, no. 15_suppl (May 20, 2015): 525. http://dx.doi.org/10.1200/jco.2015.33.15_suppl.525.

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&NA;. "Endocrine therapy needed in younger, ER-positive women?" Inpharma Weekly &NA;, no. 1240 (June 2000): 15. http://dx.doi.org/10.2165/00128413-200012400-00036.

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Basappa, Basappa, Baburajeev Chumadathil Pookunoth, Mamatha Shinduvalli Kempasiddegowda, Rangappa Knchugarakoppal Subbegowda, Peter E. Lobie, and Vijay Pandey. "Novel Biphenyl Amines Inhibit Oestrogen Receptor (ER)-α in ER-Positive Mammary Carcinoma Cells." Molecules 26, no. 4 (February 3, 2021): 783. http://dx.doi.org/10.3390/molecules26040783.

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Herein, the activity of adamantanyl-tethered-biphenyl amines (ATBAs) as oestrogen receptor alpha (ERα) modulating ligands is reported. Using an ERα competitor assay it was demonstrated that ATBA compound 3-(adamantan-1-yl)-4-methoxy-N-(4-(trifluoromethyl) phenyl) aniline (AMTA) exhibited an inhibitory concentration 50% (IC50) value of 62.84 nM and demonstrated better binding affinity compared to tamoxifen (IC50 = 79.48 nM). Treatment of ERα positive (ER+) mammary carcinoma (MC) cells (Michigan Cancer Foundation-7 (MCF7)) with AMTA significantly decreased cell viability at an IC50 value of 6.4 μM. AMTA treatment of MC cell-generated three-dimensional (3D) spheroids resulted in significantly decreased cell viability. AMTA demonstrated a superior inhibitory effect compared to tamoxifen-treated MC cell spheroids. Subsequently, by use of an oestrogen response element (ERE) luciferase reporter construct, it was demonstrated that AMTA treatment significantly deceased ERE transcriptional activity in MC cells. Concordantly, AMTA treatment of MC cells also significantly decreased protein levels of oestrogen-regulated CCND1 in a dose-dependent manner. In silico molecular docking analysis suggested that AMTA compounds interact with the ligand-binding domain of ERα compared to the co-crystal ligand, 5-(4-hydroxyphenoxy)-6-(3-hydroxyphenyl)-7- methylnaphthalen-2-ol. Therefore, an analogue of AMTA may provide a structural basis to develop a newer class of ERα partial agonists.

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Shi, Liang, Tian-Song Xia, Xiao-Long Wei, Wenbin Zhou, Jinqiu Xue, Lin Cheng, Peipei Lou, et al. "Estrogen receptor (ER) was regulated by RNPC1 stabilizing mRNA in ER positive breast cancer." Oncotarget 6, no. 14 (March 26, 2015): 12264–78. http://dx.doi.org/10.18632/oncotarget.3654.

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Tao, J., M. Scaltriti, S. Marlow, M. Elkabets, N. Morse, D. Sgroi, and J. Baselga. "Antitumor Activity of Dual PI3K and ER Blockade in ER Positive Breast Cancer Models." Annals of Oncology 23 (September 2012): ix126. http://dx.doi.org/10.1016/s0923-7534(20)32912-4.

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Van Tine, Brian A., Robert J. Crowder, and Matthew J. Ellis. "ER and PI3K Independently Modulate Endocrine Resistance in ER-Positive Breast Cancer: Figure 1." Cancer Discovery 1, no. 4 (September 2011): 287–88. http://dx.doi.org/10.1158/2159-8290.cd-11-0192.

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Horiguchi, J. "Low ER level is one factor in the resistance of ER-positive and HER-2-positive tumors to hormone therapy." Journal of Clinical Oncology 22, no. 14_suppl (July 15, 2004): 809. http://dx.doi.org/10.1200/jco.2004.22.90140.809.

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Horiguchi, J. "Low ER level is one factor in the resistance of ER-positive and HER-2-positive tumors to hormone therapy." Journal of Clinical Oncology 22, no. 14_suppl (July 15, 2004): 809. http://dx.doi.org/10.1200/jco.2004.22.14_suppl.809.

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Sanford, Rachel Ann, Juhee Song, Angelica M. Gutierrez-Barrera, Jennifer Keating Litton, Isabelle Bedrosian, Constance T. Albarracin, Vicente Valero, and Banu Arun. "Incidence of germline BRCA mutation in patients with ER-low positive/PR negative/HER-2 neu negative tumors." Journal of Clinical Oncology 32, no. 26_suppl (September 10, 2014): 2. http://dx.doi.org/10.1200/jco.2014.32.26_suppl.2.

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2 Background: The 2011 ASCO/CAP guidelines recommend that breast cancers with estrogen receptor (ER) staining as low as 1% on immunohistochemistry be considered ER-positive. In practice, there remains significant variability in what clinicians consider ER-positive versus ER-negative. Current NCCN guidelines recommend that patients under age 60 with triple-negative breast cancer (TNBC) be referred for genetic counseling and consideration of germline BRCA mutation testing. With the 2011 ASCO/CAP guidelines, the definition of TNBC has changed to exclude patients with ER low-positive (1-9%) tumors; hence patients with ER-low positive tumors (formerly considered ER negative) may not be referred for genetic counseling and BRCA testing. This may lead to “undertesting” of appropriate patients. The incidence of BRCA germline mutations in patients with ER-low positive versus ER-negative (0%) tumors is unknown. We sought to identify whether the incidence of BRCA mutation differed between patients with ER-negative/PR-negative/HER-2 neu negative tumors and patients with ER-low positive/PR-negative/HER-2 neu negative tumors. Methods: We performed a review of a prospectively maintained research database of all patients with ER < 10%, PR 0% and HER-2 neu–negative breast cancers who were referred for genetic risk assessment and testing for BRCA mutation at UT MD Anderson Cancer Center. Results: Of 144 patients who underwent BRCA mutation testing, 22 (15%) had ER-low positive tumors while 122 (85%) had ER-negative tumors. Among patients with ER-low positive tumors, 7 of 22 (31.8%) were found to have a deleterious BRCA 1/2 mutation, while 33 of 122 (27%) with ER-negative tumors were found to have a deleterious BRCA 1/2 mutation. The incidence of deleterious BRCA 1/2 mutation in patients with ER-low positive tumors versus those with ER-negative tumors was not statistically significantly different (p = 0.6457). Conclusions: The rate of deleterious BRCA 1/2 germline mutations in ER-negative versus ER-low positive (1-9%) breast cancer is similar. Therefore, we strongly recommend that BRCA testing continue to be offered to women under age 60 with tumors that are ER-low positive/PR-negative/HER-2 neu negative.

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Maeda, Ichiro, Manabu Kubota, Jiro Ohta, Kimika Shinno, Shinya Tajima, Yasushi Ariizumi, Masatomo Doi, et al. "Effectiveness of computer-aided diagnosis (CADx) of breast pathology using immunohistochemistry results of core needle biopsy samples for synaptophysin, oestrogen receptor and CK14/p63 for classification of epithelial proliferative lesions of the breast." Journal of Clinical Pathology 70, no. 12 (June 19, 2017): 1057–62. http://dx.doi.org/10.1136/jclinpath-2017-204478.

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AimsThe aim of this study was to develop a computer-aided diagnosis (CADx) system for identifying breast pathology.MethodsTwo sets of 100 consecutive core needle biopsy (CNB) specimens were collected for test and validation studies. All 200 CNB specimens were stained with antibodies targeting oestrogen receptor (ER), synaptophysin and CK14/p63. All stained slides were scanned in a whole-slide imaging system and photographed. The photographs were analysed using software to identify the proportions of tumour cells that were positive and negative for each marker. In the test study, the cut-off values for synaptophysin (negative and positive) and CK14/p63 (negative and positive) were decided using receiver operating characteristic (ROC) analysis. For ER analysis, samples were divided into groups with <10% positive or >10% positive cells and decided using receiver operating characteristic (ROC) analysis. Finally, these two groups categorised as ER-low, ER-intermediate (non-low and non-high) and ER-high groups. In the validation study, the second set of immunohistochemical slides were analysed using these cut-off values.ResultsThe cut-off values for synaptophysin, <10% ER positive, >10% ER positive and CK14/p63 were 0.14%, 2.17%, 77.93% and 18.66%, respectively. The positive predictive value for malignancy (PPV) was 100% for synaptophysin-positive/ER-high/(CK14/p63)-any or synaptophysin-positive/ER-low/(CK14/p63)-any. The PPV was 25% for synaptophysin-positive/ER-intermediate/(CK14/p63)-positive. For synaptophysin-negative/(CK14/p63)-negative, the PPVs for ER-low, ER-intermediate and ER-high were 100%, 80.0% and 95.8%, respectively. The PPV was 4.5% for synaptophysin-negative/ER-intermediate/(CK14/p63)-positive.ConclusionThe CADx system was able to analyse sufficient data for all types of epithelial proliferative lesions of the breast including invasive breast cancer. This system may be useful for pathological diagnosis of breast CNB in routine investigations.

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Günther, Lukas, Peter Hufnagl, Klaus‐Jürgen Winzer, and Hans Guski. "Different Proliferation Patterns in Breast Cancer: AgNOR Measurements in ER-Negative and ER-Positive Tumor Cells." Analytical Cellular Pathology 20, no. 4 (2000): 155–62. http://dx.doi.org/10.1155/2000/914765.

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The relation between estrogen receptors (ER) and argyrophilic nucleolar organizer regions (AgNORs)in situwithin human breast cancer cells was analyzed. For AgNOR measurements in 49 invasive breast carcinomas, a new reproducible staining method for dual demonstration of ER and AgNORs was applied. Quantitative AgNOR variables were determined in ER‐positive and ER‐negative tumor cells by digital image analysis. The relationships between AgNOR parameters of ER‐positive and ER‐negative cells and other prognostic factors of breast cancer [Bloom–Richardson‐Grading and growth fraction (Ki‐67 index)] were investigated. A higher AgNOR content in ER‐negative cells and a special clustering phenomenon in ER‐positive tumor cells were found. Correlation with other criteria of malignant potential could be exclusively demonstrated for ER‐negative cells. ER‐negative cells of breast cancer can be characterized as the more malignant and possibly prognosis‐dictating cell fraction. Thus, ER‐negative cells probably contribute more to the progression of the tumor disease and furthermore to the prognosis than ER‐positive cells. We recommend measurement AgNORs exclusively in ER‐negative cells of breast cancer.

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Bartlett, John M. S., Ian O. Ellis, Mitch Dowsett, Elizabeth A. Mallon, David A. Cameron, Stephen Johnston, Emma Hall, et al. "Human Epidermal Growth Factor Receptor 2 Status Correlates With Lymph Node Involvement in Patients With Estrogen Receptor (ER) –Negative, but With Grade in Those With ER-Positive Early-Stage Breast Cancer Suitable for Cytotoxic Chemotherapy." Journal of Clinical Oncology 25, no. 28 (October 1, 2007): 4423–30. http://dx.doi.org/10.1200/jco.2007.11.0973.

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Purpose Human epidermal growth factor receptor 2 (HER-2) expression is associated with increased risk of high-grade disease, nodal metastasis, and absence of estrogen receptors (ERs) in early breast cancer. We tested interactions between ER and HER-2 to determine if they may modulate breast cancer nodal metastasis and proliferation. Patients and Methods Tumors from the Cancer Research UK Taxotere as Adjuvant Chemotherapy phase III trial were tested for HER-2 using current diagnostic procedures. ER status, progesterone status, clinicopathologic characteristics, and patient age were included in a logistic regression analysis to identify associations with HER-2 status (positive v negative). Results A total of 841 (23.6%) of 3,565 samples were HER-2 positive (3+ by immunohistochemistry or positive by fluorescent in situ hybridization). ER-negative tumors were more likely to be HER-2 positive than were ER-positive tumors (odds ratio [OR] = 1.87, ER negative v ER positive; P < .001). For ER-positive tumors, risk of HER-2 positivity increased by grade (OR = 7.6, grade 3 v grade 1; P < .001) but not nodal status (OR = 1.3, four or more positive nodes v node negative; P = .08). Conversely, ER negative node-positive tumors were markedly more frequently HER-2 positive than node-negative cases (OR = 3.05, four or more positive nodes v node negative; P < .001) but independent of grade (OR = 0.82, grade 3 v grade 1; P = .76). Conclusion In early breast cancer patients selected for cytotoxic chemotherapy, we identified significant interactions between HER-2 and ER expression that correlate with tumor pathology. In ER-positive breast cancers, HER-2 expression correlates with grade, not nodal metastasis. In ER-negative breast cancers, HER-2 expression correlates with increased nodal positivity, not grade. ER and HER-2 expression may modify tumor pathology via ER/HER-2–mediated cross talk.

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Long, Mengping, Chong You, Qianqian Song, Lina X. J. Hu, Zhaorong Guo, Qian Yao, Wei Hou, et al. "AR Expression Correlates with Distinctive Clinicopathological and Genomic Features in Breast Cancer Regardless of ESR1 Expression Status." International Journal of Molecular Sciences 23, no. 19 (September 29, 2022): 11468. http://dx.doi.org/10.3390/ijms231911468.

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Androgen receptor (AR) expression is frequently observed in breast cancer, but its association with estrogen receptor (ER) expression in breast cancer remains unclear. This study analyzed the clinicopathological and molecular features associated with AR negativity in both ER-positive and ER-negative breast cancer, trying to elucidate the molecular correlation between AR and ER. Our results showed that AR negativity was associated with different clinicopathological characteristics and molecular features in ER-positive and ER-negative breast cancer. Moreover, AR-positive breast cancer has better clinicopathological features than AR-negative breast cancer, especially in the ER-negative subtype. These results suggest that the role of AR in ER-negative breast cancer is distinctive from that in ER-positive breast cancer.

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Cui, Xiaojiang, Rachel Schiff, Grazia Arpino, C. Kent Osborne, and Adrian V. Lee. "Biology of Progesterone Receptor Loss in Breast Cancer and Its Implications for Endocrine Therapy." Journal of Clinical Oncology 23, no. 30 (October 20, 2005): 7721–35. http://dx.doi.org/10.1200/jco.2005.09.004.

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The response to endocrine therapy in breast cancer correlates with estrogen receptor (ER) and progesterone receptor (PR) status. ER-positive/PR-negative breast cancers respond less well to selective ER modulator (SERM) therapy than ER-positive/PR-positive tumors. The predictive value of PR has long been attributed to the dependence of PR expression on ER activity, with the absence of PR reflecting a nonfunctional ER and resistance to hormonal therapy. However, recent clinical and laboratory evidence suggests that ER-positive/PR-negative breast cancers may be specifically resistant to SERMs, whereas they may be less resistant to estrogen withdrawal therapy with aromatase inhibitors, which is a result inconsistent with the nonfunctional ER theory. Novel alternative molecular mechanisms potentially explaining SERM resistance in ER-positive/PR-negative tumors have been suggested by recent experimental indications that growth factors may downregulate PR levels. Thus, the absence of PR may not simply indicate a lack of ER activity, but rather may reflect hyperactive cross talk between ER and growth factor signaling pathways that downregulate PR even as they activate other ER functions. Therefore, ER-positive/PR-negative breast tumors might best be treated by completely blocking ER action via estrogen withdrawal with aromatase inhibitors, by targeted ER degradation, or by combined therapy targeting both ER and growth factor signaling pathways. In this review, we will discuss the biology and etiology of ER-positive/PR-negative breast cancer, highlighting recent data on molecular cross talk between ER and growth factor signaling pathways and demonstrating how PR might be a useful marker of these activities. Finally, we will consider the clinical implications of these observations.

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Kudo, A., H. Fukushima, H. Kawakami, M. Matsuda, T. Goya, and H. Hirano. "Use of serial semithin frozen sections to evaluate the co-localization of estrogen receptors and progesterone receptors in cells of breast cancer tissues." Journal of Histochemistry & Cytochemistry 44, no. 6 (June 1996): 615–20. http://dx.doi.org/10.1177/44.6.8666746.

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The extent of co-expression of estrogen receptors (ER) and progesterone receptors (PgR) in breast cancer cells was examined immunocytochemically. Eight surgical cases of infiltrating ductal carcinoma designated as ER-positive and PgR-positive (ER+/PgR+) by enzyme immunoassay (EIA) were used. They were fixed with 4% formaldehyde and cut into serial frozen semithin sections. Using sections stained with either anti-ER or anti-PgR antibody, we ascertained the co-localization of ER and PgR in a single cell and estimated the ratio of the number of cells co-expressing ER and PgR. Twenty-six to 95% of the cells were immunopositive for both ER and PgR, 2-25% of them, varying in cases, were positive for ER but not for PgR, and <3% of the cells were positive for PgR but not for ER. The remaining 5-60% cells were positive for neither ER nor PgR. A significant percentage of breast cancer cells in tissues designated as ER+/PgR+ by EIA showed the phenotype of ER-positive but PgR-negative. The co-expression ratio of ER and PgR in biochemically detected ER+/PgR+ breast cancer may reflect a particular clinical parameter, such as the heterogeneous responsiveness of ER+/PgR+ breast cancers to hormonal treatment. Immunostaining of serial semithin frozen sections for two or more different antigens is a useful method to assess the correlation of localization of antigens.

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Mehta, R. S., D. Jackson, T. Schubbert, and D. Hsiang. "HER2 FISH ratio cut-points and pathologic complete response (pCR), residual tumor (RT), HER2 status, and survival prediction in HER2-positive breast cancer (BC)." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e22033-e22033. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22033.

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e22033 Background: We demonstrated that pCR is correlated with increasing HER2-FISH ratio, while disease-free survival (DFS) with pCR and ER-positivity in HER2-positive breast cancer treated with trastuzumab (SABCS 2008). It is known that quantitative HER2-FISH ratio correlates with ER levels and HER2-positivity imparts a higher grade in ER-positive BC. Collectively, we hypothesized that combined ER (≥10) and a HER2 ratio cut-point may subdivide HER2-positive BC into pCR predictive subtypes.Methods: Of the 80 HER2-positive (IHC3+/FISH+) BC, quantitative HER2 FISH ratio (widely spread over 1–18.3) and ER correlation was noted (r=0.34, p=0.002). Moreover, HER2 ratio (>4) correlated with higher Ki-67 (r= 0.5, p=0.01) and grade (p trend=0.05) in ER-positive subtype, inferring a biologic cut-point. Results: Of patients with stage I-IV BC treated neoadjuvantly (92% trastuzumab-based), pCR was 0% (0/13) in ER-positive-low-HER2 compared to 77% (10/13, p=0.0001), 75% (24/32, p<0.0001) and 37.5% (3/8, p=0.043) in ER-positive-high-HER2, ER-negative-high-HER2 and ER-negative-low-HER2, respectively. DFS was 100, 90, 80% and 60% (logrank-trend p<0.05) in these 4 subtypes (excluding stage IV), respectively, at a median follow-up of 38 months (range 6–72). In ER-negative subtypes, DFS was 97% and 29% (logrank p=0.0001) in patients with or without pCR; of the six with RT, 0% DFS was noted in four with HER2-negative/HER2-reduced (HER2-R) RT, compared to 100% in the two with unchanged HER2 (p=<0.05, logrank test). In ER-positive subtypes, DFS is 95% overall, and 100% in patients with RT; 7 of 10 tested RT were HER2- R. Conclusions: pCR is crucial and high in ER-negative-high-HER2 and is crucial (but low) in ER-negative-low-HER2-positive BC for improved outcome. Improved DFS is associated with high pCR in ER-positive-high-HER2 BC, but is independent of the low pCR in ER-positive-low-HER2-subtype. Thus, combined HER2 and ER offer improved prediction. In hypothesis generating analysis, HER2-R may underlie relapse in ER-negative subtypes (HER2-basal-transitional-residual), while it may be beneficial in ER-positive subtypes (luminal-B- A-transitional) by reducing HER2-pathway mediated endocrine resistance. [Table: see text]

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Ignatiadis, Michail, Nikos Xenidis, Maria Perraki, Stella Apostolaki, Eleni Politaki, Maria Kafousi, Efstathios N. Stathopoulos, et al. "Different Prognostic Value of Cytokeratin-19 mRNA–Positive Circulating Tumor Cells According to Estrogen Receptor and HER2 Status in Early-Stage Breast Cancer." Journal of Clinical Oncology 25, no. 33 (November 20, 2007): 5194–202. http://dx.doi.org/10.1200/jco.2007.11.7762.

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Purpose To examine the prognostic value of cytokeratin-19 (CK-19) mRNA–positive circulating tumor cells (CTCs) in early-stage breast cancer patients focusing on clinically relevant subgroups based on estrogen receptor (ER) and HER2 expression. Patients and Methods CK-19 mRNA–positive CTCs were detected by real-time reverse transcriptase polymerase chain reaction in the blood of 444 consecutive, stage I-III, breast cancer patients before initiation of adjuvant chemotherapy. The association between detection of CK-19 mRNA–positive CTCs and clinical outcome was analyzed for patients with ER-positive, ER-negative, triple-negative, HER2-positive, and ER-positive/HER2-negative tumors. Results CK-19 mRNA–positive CTCs were detected in 181 (40.8%) of 444 patients; 109 (41.9%) of 260 patients with ER-positive tumors; 71 (40.6%) of 175 patients with ER-negative tumors; 27 (35%) of 77 patients with triple-negative tumors; 35 (39.8%) of 88 patients with HER2-positive tumors; and 82 (44.1%) of 186 patients with ER-positive/HER2-negative tumors. After a median follow-up of 53.5 months, patients with CK-19 mRNA–positive CTCs experienced reduced disease-free survival (DFS; P < .001) and overall survival (OS; P < .001); this was mainly observed in patients with ER-negative (P < .001 and P < .001, respectively) but not ER-positive tumors (P = .172 and P = .425, respectively) and in patients with triple-negative (P = .008 and P = .001, respectively) and HER2-positive (P = .023 and P = .040, respectively) but not ER-positive/HER2-negative tumors (P = .210 and P = .578, respectively). In multivariate analysis, the interaction between CK-19 mRNA–positive CTCs and ER status was the strongest independent prognostic factor for reduced DFS (hazard ratio [HR], 3.808; 95% CI, 2.415 to 6.003; P < .001) and OS (HR, 4.172; 95% CI, 2.477 to 9.161; P < .001). Conclusion Detection of CK-19 mRNA–positive CTCs before adjuvant chemotherapy predicts poor clinical outcome mainly in patients with ER-negative, triple-negative, and HER2-positive early-stage breast cancer.

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Ignatiadis, M., N. Xenidis, M. Perraki, S. Apostolaki, E. Politaki, M. Kafousi, E. Stathopoulos, C. Sotiriou, V. Georgoulias, and D. Mavroudis. "Different prognostic value of cytokeratin-19 mRNA-positive circulating tumor cells according to estrogen receptor status in early breast cancer." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 10500. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.10500.

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10500 Background: We have previously shown that the detection of cytokeratin-19 (CK-19) mRNA-positive circulating tumor cells (CTCs) predicts poor clinical outcome in node-negative breast cancer patients. Here, we examined the prognostic value of CK-19 mRNA-positive CTCs in early breast cancer patients focusing on clinically relevant subgroups based on estrogen receptor (ER) status. Methods: We analysed peripheral blood from 448 consecutive patients with stage I-III breast cancer after surgery and before the initiation of any adjuvant treatment for the presence of CK-19 mRNA-positive CTCs using a real-time RT-PCR assay. The effect of CK-19 mRNA-positive CTCs on clinical outcome of patients with ER-positive, ER-negative, and triple-negative (ER/PR/HER2-negative) tumors was investigated. Results: CK-19 mRNA-positive CTCs were detected in 181 (40.4%) of the 448 patients; 109 (41.5%) of 263 patients with ER-positive, 71 (40.6%) of 175 patients with ER-negative and 27 (35%) of 77 patients with triple-negative tumors. There was no significant difference in the proportion of patients with detectable CK-19 mRNA-positive CTCs in the ER-negative and ER-positive subgroups (p=0.856). After a median follow-up of 53 months, patients with CK-19 mRNA-positive CTCs experienced reduced disease-free survival (DFS) (p<0.0005) and overall survival (OS) (p<0.0005); this was mainly observed in patients with ER-negative (p<0.0005 and p<0.0005, respectively) and triple-negative (p=0.008 and p=0.001, respectively) but not with ER-positive (p=0.174 and p=0.364, respectively) tumors. In multivariate analyses, detection of CK-19 mRNA-positive CTCs was the strongest independent prognostic factor associated with reduced DFS and OS in the entire cohort (p<0.0005 and p=0.009, respectively), in ER-negative (p<0.0005 and p=0.003, respectively) and triple-negative (p=0.020 and p=0.022, respectively) but not in ER-positive tumors (p=0.350 and p=0.621, respectively). Conclusions: Detection of CK-19 mRNA-positive CTCs predicts poor clinical outcome at five years follow-up, only in patients with ER-negative and triple-negative, but not with ER-positive, early breast cancer. No significant financial relationships to disclose.

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Andreopoulou, E., C. Hatzis, D. Booser, V. Valero, M. J. Wallace, C. Sotiriou, G. Hortobagyi, L. Pusztai, and W. Symmans. "Correlations of estrogen receptor (ER) related genomic transcription and ER gene expression with increasing AJCC stage of ER-positive breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 1044. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.1044.

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1044 Background: Advanced stages of ER-positive breast cancer may have decreased tumor dependence on estrogen, possibly due to biological selection and/or progression. The sensitivity to endocrine therapy (SET) index measures transcriptional activity of the ER genomic pathway (165 ER-related genes). We investigated whether expression of genes for receptors ER (ESR1), progesterone receptor (PGR), or HER-2 (ERBB2), the SET index, or a housekeeper gene (GAPDH) vary by stage of ER-positive breast cancer. Methods: We evaluated gene expression profiles (Affymetrix U133 microarrays, Affymetrix, Santa Clara, CA) from 956 patients’ clinical samples of ER-positive breast cancer, including 290 new samples profiled at MDACC and 666 samples from published datasets. Microarray data were uniformly normalized, log-transformed, and expression levels for single genes and the SET index were compared to pathologic AJCC stage (315 patients were stage I, 362 stage IIA, 151 stage IIB, 29 stage III, 27 stage IV at initial presentation, and 72 stage IV previously treated and/or at relapse) using a median ordered regression analysis (p < 0.05 was significant). Results: SET index significantly decreased with advancing pathologic stage (p < 0.001), and PGR expression levels showed a similar, but lesser, effect (p = 0.014). However, expression levels of ESR1 and ERBB2 did not vary by stage. Overall, GAPDH gene expression increased with stage (p < 0.001), but that effect was only observed in stages III and IV. Expression of these genes was not significantly different between stage IV disease at initial presentation or at relapse. Conclusions: Expression levels of ESR1 and ERBB2 receptor genes did not vary, but ER-related genomic transcription (SET index and, to a lesser extent, PGR) declined significantly with increasing pathologic stage. This suggests that ER-positive breast cancer tends to have less transcriptional dependence on estrogen with increasing pathologic stage. The observed increase in expression of GAPDH in stages III and IV might reflect higher metabolic activity in advanced ER-positive breast cancer and deserves further study. [Table: see text]

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Guo, Peng, Xue-Yuan Dong, Ke-Wen Zhao, Xiaodong Sun, Qunna Li, and Jin-Tang Dong. "Estrogen-induced interaction between KLF5 and estrogen receptor (ER) suppresses the function of ER in ER-positive breast cancer cells." International Journal of Cancer 126, no. 1 (January 1, 2010): 81–89. http://dx.doi.org/10.1002/ijc.24696.

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Jatoi, Ismail, Bingshu E. Chen, William F. Anderson, and Philip S. Rosenberg. "Breast Cancer Mortality Trends in the United States According to Estrogen Receptor Status and Age at Diagnosis." Journal of Clinical Oncology 25, no. 13 (May 1, 2007): 1683–90. http://dx.doi.org/10.1200/jco.2006.09.2106.

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Purpose Since 1990, overall breast cancer mortality rates in the United States decreased 24%. This decline has been attributed to mammography screening and adjuvant systemic therapy. However, the efficacy of these modalities may depend on estrogen receptor (ER) expression and age. We therefore examined breast cancer mortality trends in the United States according to ER status and age. Methods Using the Surveillance, Epidemiology, and End Results (SEER) program (1990-2003), we calculated trends in incidence-based mortality (IBM), annual hazard rates for breast cancer deaths after diagnosis, and relative hazard rates for women with ER-positive and ER-negative tumors. Relative hazard rates were assessed with Cox proportional hazards models, adjusted for stage and grade, and stratified by age at diagnosis. Results During the study period, IBM and annual hazard rates for breast cancer deaths decreased among women with ER-positive and ER-negative tumors, although declines were greater for those with ER-positive tumors. Among women younger than 70 years, relative hazard rates declined 38% for those with ER-positive tumors versus 19% for those with ER-negative tumors. Among women 70 years or older, relative hazard rates declined 14% for those with ER-positive tumors versus no significant decline for those with ER-negative tumors. Conclusion In the United States, breast cancer mortality rates have declined among women with ER-positive and ER-negative tumors, with greater declines among younger women and those with ER-positive tumors. Although mortality in all groups remains unacceptably high, additional emphasis should be placed on improving outcomes of breast cancer patients older than 70 years and those of all ages with ER-negative tumors.

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LI, LONG, XIAOJUN LI, XIAOBING HAN, TING YANG, JING FU, YUNFENG ZHANG, and WENLI GOU. "An ovarian cancer model with positive ER: Reversion of ER antagonist resistance by Src blockade." Oncology Reports 32, no. 3 (June 23, 2014): 943–50. http://dx.doi.org/10.3892/or.2014.3284.

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Deng, Hao, Xin-Tian Zhang, Mo-Lin Wang, Hong-Yan Zheng, Li-Jiang Liu, and Zhao-Yi Wang. "ER-α36-Mediated Rapid Estrogen Signaling Positively Regulates ER-Positive Breast Cancer Stem/Progenitor Cells." PLoS ONE 9, no. 2 (February 18, 2014): e88034. http://dx.doi.org/10.1371/journal.pone.0088034.

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Koehler, M., T. L. VanArsdale, D. Shields, K. Arndt, J. Yuan, N. Lee, K. Eisele, J. Chionis, J. Cao, and C. L. Painter. "Mechanism of Action for Combined CDK4/6 and Er Inhibition in ER Positive Breast Cancer." Annals of Oncology 25 (May 2014): i21. http://dx.doi.org/10.1093/annonc/mdu069.2.

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Gökmen-Polar, Yesim, Rachel A. Toroni, Barbara A. Hocevar, Sunil Badve, Qianqian Zhao, Changyu Shen, Elizabeth Bruckheimer, Michael S. Kinch, and Kathy D. Miller. "Dual targeting of EphA2 and ER restores tamoxifen sensitivity in ER/EphA2-positive breast cancer." Breast Cancer Research and Treatment 127, no. 2 (July 3, 2010): 375–84. http://dx.doi.org/10.1007/s10549-010-1004-y.

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Vocka, Michal, Martina Zimovjanova, Zuzana Bielcikova, Petra Tesarova, Lubos Petruzelka, Martin Mateju, Ludmila Krizova, et al. "Estrogen Receptor Status Oppositely Modifies Breast Cancer Prognosis in BRCA1/BRCA2 Mutation Carriers Versus Non-Carriers." Cancers 11, no. 6 (May 28, 2019): 738. http://dx.doi.org/10.3390/cancers11060738.

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Breast cancer (BC) prognosis in BRCA1 and BRCA2 mutation carriers has been reported contradictorily, and the significance of variables influencing prognosis in sporadic BC is not established in BC patients with hereditary BRCA1/BRCA2 mutations. In this retrospective cohort study, we analyzed the effect of clinicopathological characteristics on BC prognosis (disease-free survival [DFS] and disease-specific survival [DSS]) in hereditary BRCA1/BRCA2 mutation carriers. We enrolled 234 BRCA1/BRCA2 mutation carriers and 899 non-carriers, of whom 191 carriers and 680 non-carriers, with complete data, were available for survival analyses. We found that patients with ER-positive tumors developed disease recurrence 2.3-times more likely when they carried a BRCA1/BRCA2 mutation (23/60; 38.3% ER-positive carriers vs. 74/445; 16.6% ER-positive non-carriers; p < 0.001). ER-positive mutation carriers also had a 3.4-times higher risk of death due to BC compared with ER-positive non-carriers (13/60; 21.7% vs. 28/445; 6.3%; p < 0.001). Moreover, prognosis in ER-negative BRCA1/BRCA2 mutation carriers was comparable with that in ER-positive non-carriers. Our study demonstrates that ER-positivity worsens BC prognosis in BRCA1/BRCA2 mutation carriers, while prognosis for carriers with ER-negative tumors (including early-onset) is significantly better and comparable with that in ER-positive, older BC non-carriers. These observations indicate that BRCA1/BRCA2 mutation carriers with ER-positive BC represent high-risk patients.

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Ningsi, Retno, Maha Elazezy, Luisa Stegat, Elena Laakmann, Sven Peine, Sabine Riethdorf, Volkmar Müller, Klaus Pantel, and Simon A. Joosse. "Detection and Characterization of Estrogen Receptor α Expression of Circulating Tumor Cells as a Prognostic Marker." Cancers 14, no. 11 (May 25, 2022): 2621. http://dx.doi.org/10.3390/cancers14112621.

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Abstract:

CTCs have increasingly been used as a liquid biopsy analyte to obtain real-time information on the tumor through minimally invasive blood analyses. CTCs allow for the identification of proteins relevant for targeted therapies. Here, we evaluated the expression of estrogen receptors (ER) in CTCs of patients with metastatic breast cancer. From sixty metastatic breast cancer patients who had ER-positive primary tumors (range of 1–70% immunostaining) at initial cancer diagnosis, 109 longitudinal blood samples were prospectively collected and analyzed using the CellSearch System in combination with the ERα monoclonal murine ER-119.3 antibody. Prolonged cell permeabilization was found to be required for proper staining of nuclear ER in vitro. Thirty-one cases were found to be CTC-positive; an increased number of CTCs during endocrine and chemotherapy was correlated with disease progression, whereas a decrease or stable amount of CTC number (<5) during treatment was correlated with a better clinical outcome. Survival analyses further indicate a positive association of CTC-status with progression-free survival (HR, 66.17; 95%CI, 3.66–195.96; p = 0.0045) and overall survival (HR, 6.21; 95%CI, 2.66–14.47; p < 0.0001). Only one-third of CTC-positive breast cancer patients, who were initially diagnosed with ER-positive primary tumors, harbored ER-positive CTCs at the time of metastasis, and even in those patients, both ER-positive and ER-negative CTCs were found. CTC-positivity was correlated with a shorter relapse-free survival. Remarkably, ER-negative CTCs were frequent despite initial ER-positive status of the primary tumor, suggesting a switch of ER phenotype or selection of minor ER-negative clones as a potential mechanism of escape from ER-targeting therapy.

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Journal articles on the topic 'ER-positive'

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