Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA381011 | ENA |
REPOSITORIES: ENA
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Project description:One of the greatest advances in therapy of estrogen receptor positive breast cancer has been the development of endocrine therapy. More than two thirds of primary breast tumors express estrogen receptor alpha (ERα) and their growth is mainly dependent on estrogen receptor activity. Several therapeutic approaches have thus been designed to inhibit ER activity in breast tissue. Tamoxifen, a selective ER modulator, is one of the main treatment options for premenopausal women with advanced ER positive breast cancer, and has also become well established as adjuvant therapy in the early breast cancer setting (Davies et al., 2011; Group, 1998; Jaiyesimi et al., 1995). In contrast to tamoxifen, which in other tissues such as bone and endometrium, can exert partial agonistic activity (Braithwaite et al., 2003; Fisher et al., 1994; Pietras, 2006), the selective ER downregulator, fulvestrant, is a potent ER antagonist. Binding of fulvestrant to ER inhibits receptor dimerization and nuclear uptake, prevents estrogen-response element binding and accelerates ER degradation (Dauvois et al., 1993; Dowsett et al., 2005; Fawell et al., 1990; Wakeling et al., 1991). Fulvestrant is approved for treatment of postmenopausal women with advanced breast cancer who have relapsed or progressed on first-line endocrine therapy (Howell et al., 2002; Osborne et al., 2002; Robertson et al., 2003). Estrogen deprivation by treatment with aromatase inhibitors (such as letrozole, anastrozole or exemestane) which block synthesis of estrogens is another effective therapy option in postmenopausal women (Bonneterre et al., 2000; Cuzick et al., 2010; Dowsett et al., 2010; Mouridsen et al., 2001; Nabholtz et al., 2000). The large majority of patients with ER+ breast cancer experience an initial response to endocrine therapy, however, in many of these patients, the disease subsequently progresses and eventually anti-estrogen therapy ceases to have effect. Biomarkers predicting response to estrogen deprivation and new alternative treatments targeting the pathways supporting estrogen independent growth are therefore urgently needed (Patani and Martin, 2014; Patani et al., 2013). In order to understand how tumors respond to withdrawal of their main growth signal, a comparison of molecular features of tumor before and during endocrine therapy is necessary, and the fate of individual cancer cell sub-clones should be monitored. Since studies of cellular dynamics are very difficult to perform with clinical material, we made use of a patient derived, estrogen dependent, orthotopically growing luminal-like primary breast cancer xenograft model (PDX) (Bergamaschi et al., 2009; Huuse et al., 2012). This PDX model is a representative model for luminal breast cancers as the molecular characteristics, cellular heterogeneity and estrogen dependency of the primary tumor are retained over many passages. Functionally different subpopulations of cancer cells were previously defined by expression of the markers CD24 and SSEA-4 in this model (Skrbo et al., 2014), and it is therefore a suitable model for comparison of cellular and molecular effects of estrogen deprivation and ER-signaling inhibition. In this study, a quantitative MS-based proteomic analysis using SILAC and a label-free approach were performed, aiming to map changes in protein expression induced by endocrine therapy. Inhibition of ER-signaling seemed to induce CD24 and SSEA-4 expression on residual tumor cells. Proteomic analysis revealed overexpression of enzymes involved in TCA cycle, oxidative phosphorylation and fatty acid beta-oxidation following endocrine treatment when compared to untreated tumors. These results indicated possible reprogramming of cell metabolism and utilization of aerobic respiration, i.e. oxidative phosphorylation, in response to endocrine therapy.
2022-02-28 | PXD002352 | Pride
Project description:Comparison between Estrogen receptor positive and Estrogen receptor negative breast cancer samples
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Project description:Integrative analysis of primary estrogen receptor-positive (ER+) breast cancer, triple-negative breast cancer (TNBC), and metaplastic breast cancer (MBC) tumors using Starfysh.
2024-02-10 | GSE218951 | GEO
Project description:Estrogen Receptor Positive Breast Cancer Aromatase Inhibitor Response Study
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Project description:Estrogen Receptor Positive Breast Cancer Aromatase Inhibitor Response Study
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Project description:In our previous analyses, we have identified that miR221&222 and miR206 are strongly up-regulated in Estrogen Receptor negative breast cancer cell lines and primary tumor. Moreover we have shown that miR221&222 and miR206 target the Estrogen Receptor. In order to identify the different function of miR221&222 and miR206 in breast cancer cells, an Estrogen Receptor positive breast cancer cells MCF7 was transfected with the different microRNAs and gene expression profile was carried out. We identified that miR221&222 up-modulation increase the tumorigenicity of breast cancer cells compared to miR206.
2009-12-11 | E-TABM-601 | biostudies-arrayexpress
Project description:Predicting prognosis using molecular profiling in estrogen receptor-positive breast cancer treated with tamoxifen
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Project description:Anacardic acid (AnAc) is a mixture of 6-alkylbenzoic acid congeners that are produced in a number of plants. Previously, we showed a specific congener AnAc 24:1n5 acts as a nuclear receptor alternate site modulator (NRAM) to inhibit breast cancer cells in an estrogen receptor (ER)-dependent manner by interfering with ER-DNA binding. AnAc 24:1n5 also inhibited the growth of a triple negative breast cancer (TNBC) cell line, through an undefined mechanism. Additional work from our labs indicated AnAc 24:1n5 inhibits prostaglandin synthase and that inhibition is more specific to COX-2. Reports from other investigators indicate AnAc has a number of interesting potential pharmacological targets. We previously used qRT-PCR to investigate expression changes in endogenous estrogen-regulated genes, i.e., TFF1, CCND1, and CTSD in breast cancer cell lines. However, since AnAc has the capacity of effect multiple molecular targets and since we detected an ER-independent inhibition of breast cancer cell proliferation, we suspect additional unknown molecular targets are affected in breast cancer cells. Identification of such targets using RNA-seq would be quite beneficial in targeting TNBC which primarily affects premenopausal women with a predominance in women of African and Latina ancestry. The goal of this portion of the project is to use next-generation RNA-SEQ to identify alterations in molecular target sequence levels in ER-positive and -negative breast cancer cell lines treated with AnAc.
2017-02-01 | GSE78011 | GEO
Project description:Comparison between Estrogen receptor positive and Estrogen receptor negative breast cancer samples Keywords: breast cancer type comparison
2008-09-17 | GSE10510 | GEO
Project description:RNA-seq was performed on breast cancer cell lines and primary tumors RNA-seq was performed on 28 breast cancer cell lines, 42 Triple Negative Breast Cancer (TNBC) primary tumors, and 42 Estrogen Receptor Positive (ER+) and HER2 Negative Breast Cancer primary tumors, 30 uninovlved breast tissue samples that were adjacent to ER+ primary tumors, 5 breast tissue samples from reduction mammoplasty procedures performed on patients with no known cancer, and 21 uninvolved breast tissue samples that were adjacent to TNBC primary tumors.
2014-06-11 | E-GEOD-58135 | biostudies-arrayexpress