Gene expression of primary breast cancers from patients before and after neo-adjuvant Tamoxifen treatment
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PROVIDER: PRJNA613650 | ENA |
REPOSITORIES: ENA
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Project description:Tumor gene expression data (microarray from FFPE) was obtained from breast cancer patients enrolled in a pre-operative window trial (ClinicalTrials.gov Identifier: NCT00738777). Patients received an oral loading dose of 40 mg of tamoxifen twice daily for the first seven days, followed by a daily dose of 20 mg until surgery. A core needle biopsy of the tumor was taken prior to treatment (n=62) and post-treatment tumor material (n=40) was obtained during surgery 20.7 (±9.6) days later. Paired material was available for 27/74 patients. Differential analysis comparing gene expression before and after Tamoxifen treatment implicated activation of the NFκB pathway and an enrichment of EMT/stemness features upon Tamoxifen treatment. In line with these findings, exposure of ER+ breast cancer cell lines to tamoxifen, in vitro and in vivo, gives rise to a tamoxifen-tolerant population with similar NFκB activity and EMT/stemness characteristics as described in the corresponding publication.
2020-04-06 | GSE147271 | GEO
Project description:Oesophageal adenocarcinoma exome sequence data from samples before and after neo-adjuvant chemotherapy
| PRJEB12657 | ENA
Project description:In the last decades platinum-based neo-adjuvant chemotherapy (NACT) has been recognized as a reliable therapeutic strategy in patients with un-resectable advanced epithelial ovarian cancer (EOC). However, the molecular changes induced by NACT at miRNA level, and their prognostic role has not been clarified until now. In order to uncover miRNAs that are altered in EOC tumor which received NACT, we performed whole-miRNA analysis on 82 FIGO Stage IIIC-IV high-grade serous (HGS) tumors, whose samples had been collected at complete primary debulking (PDS) and at interval-debulking surgery (IDS) after fter 4 courses of NACT.
2016-01-20 | E-MTAB-3696 | biostudies-arrayexpress
Project description:Purpose: Despite the benefits of estrogen receptor (ER)-targeted endocrine therapies in breast cancer, many tumors develop resistance. MicroRNAs (miRNAs) have been suggested as promising biomarkers and we here evaluated whether a miRNA profile could be identified, sub-grouping ER+ breast cancer patients treated with adjuvant Tamoxifen with regards to probability of recurrence. Experimental design: Global miRNA analysis was performed on 152 ER+ primary tumors from high-risk breast cancer patients with an initial discovery set of 52 patients, followed by 2 independent test sets (N=60 and N=40). All patients had received adjuvant Tamoxifen as mono-therapy (median clinical follow-up: 4.6 years) and half had developed distant recurrence (median time-to-recurrence: 3.5 years). MiRNA expression was examined by unsupervised hierarchical clustering and supervised analysis, including clinical parameters as co-variables.
2012-04-19 | GSE37405 | GEO
Project description:The beneficial effect of the selective estrogen receptor (ER) modulator tamoxifen in the treatment and prevention of breast cancer is assumed to be through its ability to antagonize the stimulatory actions of estrogen, although tamoxifen can also have some estrogen-like agonist effects. Here, we report that, in addition to these mixed agonist/antagonist actions, tamoxifen can also selectively regulate a unique set of >60 genes, which are minimally regulated by estradiol (E2) or raloxifene in ERalpha-positive MCF-7 human breast cancer cells. This gene regulation by tamoxifen is mediated by ERalpha and reversed by E2 or ICI 182,780. Introduction of ERbeta into MCF-7 cells reverses tamoxifen action on approximately 75% of these genes. To examine whether these genes might serve as markers of tamoxifen sensitivity and/or the development of resistance, their expression level was examined in breast cancers of women who had received adjuvant therapy with tamoxifen. High expression of two of the tamoxifen-stimulated genes, YWHAZ/14-3-3z and LOC441453, was found to correlate significantly with disease recurrence following tamoxifen treatment in women with ER-positive cancers and hence seem to be markers of a poor prognosis. Our data indicate a new dimension in tamoxifen action, involving gene expression regulation that is tamoxifen preferential, and identify genes that might serve as markers of tumor responsiveness or resistance to tamoxifen therapy. This may have a potential effect on the choice of tamoxifen versus aromatase inhibitors as adjuvant endocrine therapy.
2007-10-02 | E-GEOD-4025 | biostudies-arrayexpress
Project description:The primary objective is, first, the comparison of tamoxifen and anastrozole and, second, the comparison of zoledronate added to standard adjuvant therapy with controls according to disease-free survival (DFS) in premenopausal patients with non-metastatic breast cancer treated with tamoxifen or anastrozole. To assess whether zoledronate added to standard adjuvant therapy can decrease or even prevent bone loss in patients treated with hormonal blockade combined with an antiestrogen or aromatase inhibitor.
| 2026652 | ecrin-mdr-crc
Project description:Background: Estrogen receptor positive (ER+) breast cancers (BC) are heterogeneous with regard to their clinical behavior and response to therapies. The ER is currently the best predictor of response to the anti-estrogen agent tamoxifen, yet up to 30-40% of ER+BC will relapse despite tamoxifen treatment. New prognostic biomarkers and further biological understanding of tamoxifen resistance are required. We used gene expression profiling to develop an outcome-based predictor using a training set of 255 ER+ BC samples from women treated with adjuvant tamoxifen monotherapy. We used clusters of highly correlated genes to develop our predictor to facilitate both signature stability and biological interpretation. Independent validation was performed using 362 tamoxifen-treated ER+ BC samples obtained from multiple institutions and treated with tamoxifen only in the adjuvant and metastatic settings. Results: We developed a gene classifier consisting of 181 genes belonging to 13 biological clusters. In the independent set of adjuvantly-treated samples, it was able to define two distinct prognostic groups (HR 2.01 95%CI: 1.29-3.13; p=0.002). Six of the 13 gene clusters represented pathways involved in cell cycle and proliferation. In 112 metastatic breast cancer patients treated with tamoxifen, one of the classifier components suggesting a cellular inflammatory mechanism was significantly predictive of response. Conclusions: We have developed a gene classifier that can predict clinical outcome in tamoxifen-treated ER+ BC patients. Whilst our study emphasizes the important role of proliferation genes in prognosis, our approach proposes other genes and pathways that may elucidate further mechanisms that influence clinical outcome and prediction of response to tamoxifen. Experiment Overall Design: dataset of microarray experiments from primary breast tumors of patients treated by Tamoxifen in adjuvant setting. No replicate, no reference sample.
2008-06-20 | E-GEOD-9195 | biostudies-arrayexpress
Project description:Estrogen signaling pathway is critical for breast cancer development and has remained the major adjuvant therapeutic target for this disease. Tamoxifen has been used in clinic for many years to treat ER-positive breast cancer. However a great many (30%) suffer relapse due to drug resistance. In this study, the bromodomain inhibitor JQ1 was found to down-regulate ERalpha gene expression and have anti-tumor effect in cultured tamoxifen-resisant breast cancer cells. We used microarrays to detail the global programme of gene expression in tamoxifen-resistant MCF7 cells treated with the bromodomain inhibitor JQ1. Tamoxifen-resistant breast cancer MCF7 cells were treated with DMSO (vehicle) or JQ1 (0.2 uM) for 24 hours before total RNA was purified for microarray. Each sample was triplicated.
2014-03-01 | E-GEOD-49124 | biostudies-arrayexpress
Project description:Tamoxifen is the most widely administered adjuvant first-line hormone therapy for Estrogen receptor α (ERα) positive breast cancer patients. However, one from three patients will develop resistance, while the underlying molecular mechanisms are currently unclear. Recent studies reported that abnormal expression of miRNAs played a role in cancer progress. To study the potential function of miRNAs in tamoxifen resistance, Affymetrix GeneChip® miRNA 3.0 microarray was employed to identify differentially expressed miRNAs between tamoxifen sensitive MCF7 parent (MCF7-Pa) cells and induced resistant (MCF7-Re) cells.
2015-03-07 | GSE66607 | GEO
Project description:Gene expression profiling of 273 pre-treatment endoscopic FFPE oesophageal and oesophago-gastric junctional adenocarcinomas for validation of a DNA Damage Response Deficiency Assay. All patients were treated with neo-adjuvant chemotherapy followed by surgical resection and were collected at four UK centres in the Oesophageal Cancer Clinical and Molecular Stratification (OCCAMS) consortium between 2004 and 2013. Biopsies were reviewed for pathological subtype prior to marking for macrodissection and samples containing at least 50% adenocarcinoma tissue by area were taken forward. Total RNA was extracted using the RecoverallTM Total Nucleic Acid Isolation Kit for FFPE (Thermo Fisher Scientific, Waltham, MA) and amplified using the NuGen Ovation FFPE Amplification System v3 (NuGen San Carlos, CA). The amplified product was hybridized to the Almac Diagnostics Xcel™ array (Almac, Craigavon, United Kingdom), a cDNA microarray-based technology optimized for archival FFPE tissue, and analysed using the Affymetrix 7G scanner (Affymetrix, Santa Clara, CA)
2019-01-31 | E-MTAB-6969 | biostudies-arrayexpress