Analysis of early primary breast cancer to identify prognostic markers and associated pathways: mRNA and miRNA profiling
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE22220 | GEO | 2011/07/08
SECONDARY ACCESSION(S): PRJNA128775
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE22216: microRNA expression profiling of early primary breast cancer to identify prognostic markers and associated pathways GSE22219: Gene expression profiling of early primary breast cancer to identify prognostic markers and associated pathways Refer to individual Series. Supplementary file: Shows correspondence between mRNA and miRNA samples.
2011-07-08 | E-GEOD-22220 | biostudies-arrayexpress
Project description:Retrospective series of primary breast cancer patients who received surgery between 1989 and 1992. Patients received adjuvant chemotherapy and/or adjuvant hormone therapy, or no adjuvant treatment. Tamoxifen was used as endocrine therapy for 5 years in ER+ BC patients. Patients who were <50 years of age, with lymph node positive tumors, or ER– and/or >3 cm in diameter, received adjuvant cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) for six cycles, in a thrice weekly intravenous regimen. Patients >50 years of age with ER–, lymph node–positive tumors also received CMF. Retrospective clinical study to identify breast cancer prognostic markers and associated pathways. 216 early primary breast cancers were considered who had complete 10-years follow-up, clinical and demographics information. mRNA profiling data.
| S-ECPF-GEOD-22219 | biostudies-other
Project description:Retrospective series of primary breast cancer patients who received surgery between 1989 and 1992. Patients received adjuvant chemotherapy and/or adjuvant hormone therapy, or no adjuvant treatment. Tamoxifen was used as endocrine therapy for 5 years in ER+ BC patients. Patients who were <50 years of age, with lymph node positive tumors, or ER– and/or >3 cm in diameter, received adjuvant cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) for six cycles, in a thrice weekly intravenous regimen. Patients >50 years of age with ER–, lymph node–positive tumors also received CMF. Retrospective clinical study to identify breast cancer prognostic markers and associated pathways. 210 early primary breast cancers were considered who had complete 10-years follow-up, clinical and demographics information. miRNA profiling data.
| S-ECPF-GEOD-22216 | biostudies-other
Project description:Retrospective series of primary breast cancer patients who received surgery between 1989 and 1992. Patients received adjuvant chemotherapy and/or adjuvant hormone therapy, or no adjuvant treatment. Tamoxifen was used as endocrine therapy for 5 years in ER+ BC patients. Patients who were <50 years of age, with lymph node positive tumors, or ER– and/or >3 cm in diameter, received adjuvant cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) for six cycles, in a thrice weekly intravenous regimen. Patients >50 years of age with ER–, lymph node–positive tumors also received CMF.
2011-07-08 | GSE22216 | GEO
Project description:Retrospective series of primary breast cancer patients who received surgery between 1989 and 1992. Patients received adjuvant chemotherapy and/or adjuvant hormone therapy, or no adjuvant treatment. Tamoxifen was used as endocrine therapy for 5 years in ER+ BC patients. Patients who were <50 years of age, with lymph node positive tumors, or ER– and/or >3 cm in diameter, received adjuvant cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) for six cycles, in a thrice weekly intravenous regimen. Patients >50 years of age with ER–, lymph node–positive tumors also received CMF.
2011-07-08 | GSE22219 | GEO
Project description:Retrospective series of primary breast cancer patients who received surgery between 1989 and 1992. Patients received adjuvant chemotherapy and/or adjuvant hormone therapy, or no adjuvant treatment. Tamoxifen was used as endocrine therapy for 5 years in ER+ BC patients. Patients who were <50 years of age, with lymph node positive tumors, or ER– and/or >3 cm in diameter, received adjuvant cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) for six cycles, in a thrice weekly intravenous regimen. Patients >50 years of age with ER–, lymph node–positive tumors also received CMF. Retrospective clinical study to identify breast cancer prognostic markers and associated pathways. 210 early primary breast cancers were considered who had complete 10-years follow-up, clinical and demographics information. miRNA profiling data.
2011-07-08 | E-GEOD-22216 | biostudies-arrayexpress
Project description:Retrospective series of primary breast cancer patients who received surgery between 1989 and 1992. Patients received adjuvant chemotherapy and/or adjuvant hormone therapy, or no adjuvant treatment. Tamoxifen was used as endocrine therapy for 5 years in ER+ BC patients. Patients who were <50 years of age, with lymph node positive tumors, or ER– and/or >3 cm in diameter, received adjuvant cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) for six cycles, in a thrice weekly intravenous regimen. Patients >50 years of age with ER–, lymph node–positive tumors also received CMF. Retrospective clinical study to identify breast cancer prognostic markers and associated pathways. 216 early primary breast cancers were considered who had complete 10-years follow-up, clinical and demographics information. mRNA profiling data.
2011-07-08 | E-GEOD-22219 | biostudies-arrayexpress
Project description:BackgroundThyroid hormones (THs) inhibit hepatocellular carcinoma (HCC) through different mechanisms. However, whether microRNAs play a role in the antitumorigenic effect of THs remains unknown.MethodsBy next generation sequencing (NGS) we performed a comprehensive comparative miRNomic and transcriptomic analysis of rat hepatic preneoplastic lesions exposed or not to a short-term treatment with triiodothyronine (T3). The expression of the most deregulated miRs was also investigated in rat HCCs, and in human hepatoma cell lines, treated or not with T3.ResultsAmong miRs down-regulated in preneoplastic nodules following T3, co-expression networks revealed those targeting thyroid hormone receptor-β (Thrβ) and deiodinase1, and Oxidative Phosphorylation. On the other hand, miRs targeting members of the Nrf2 Oxidative Pathway, Glycolysis, Pentose Phosphate Pathway and Proline biosynthesis - all involved in the metabolic reprogramming displayed by preneoplastic lesions- were up-regulated. Notably, while the expression of most miRs deregulated in preneoplastic lesions was not altered in HCC or in hepatoma cells, miR-182, a miR known to target Dio1 and mitochondrial complexes, was down-deregulated by T3 treatment at all stages of hepatocarcinogenesis and in hepatocarcinoma cell lines. In support to the possible critical role of miR-182 in hepatocarcinogenesis, exogenous expression of this miR significantly impaired the inhibitory effect of T3 on the clonogenic growth capacity of human HCC cells.ConclusionsThis work identified several miRNAs, so far never associated to T3. In addition, the precise definition of the miRNA-mRNA networks elicited by T3 treatment gained in this study may provide a better understanding of the key regulatory events underlying the inhibitory effect of T3 on HCC development. In this context, T3-induced down-regulation of miR-182 appears as a promising tool.
| S-EPMC9530455 | biostudies-literature
Project description:INTRODUCTION:Few studies have performed expression profiling of both miRNA and mRNA from the same primary breast carcinomas. In this study we present and analyze data derived from expression profiling of 799 miRNAs in 101 primary human breast tumors, along with genome-wide mRNA profiles and extensive clinical information. METHODS:We investigate the relationship between these molecular components, in terms of their correlation with each other and with clinical characteristics. We use a systems biology approach to examine the correlative relationship between miRNA and mRNAs using statistical enrichment methods. RESULTS:We identify statistical significant differential expression of miRNAs between molecular intrinsic subtypes, and between samples with different levels of proliferation. Specifically, we point to miRNAs significantly associated with TP53 and ER status. We also show that several cellular processes, such as proliferation, cell adhesion and immune response, are strongly associated with certain miRNAs. We validate the role of miRNAs in regulating proliferation using high-throughput lysate-microarrays on cell lines and point to potential drivers of this process. CONCLUSION:This study provides a comprehensive dataset as well as methods and system-level results that jointly form a basis for further work on understanding the role of miRNA in primary breast cancer.
| S-EPMC3043070 | biostudies-literature
Project description:The aim of this study was to establish a novel competing endogenous RNA (ceRNA) network able to predict prognosis in patients with triple-negative breast cancer (TNBC). Differential gene expression analysis was performed using the GEO2R tool. Enrichr and STRING were used to conduct protein-protein interaction and pathway enrichment analyses, respectively. Upstream lncRNAs and miRNAs were identified using miRNet and mirTarBase, respectively. Prognostic values, expression, and correlational relationships of mRNAs, lncRNAs, and miRNAs were examined using GEPIA, starBase, and Kaplan-Meier plotter. It total, 860 upregulated and 622 downregulated differentially expressed mRNAs were identified in TNBC. Ten overexpressed and two underexpressed hub genes were screened. Next, 10 key miRNAs upstream of these key hub genes were predicted, of which six upregulated miRNAs were significantly associated with poor prognosis and four downregulated miRNAs were associated with good prognosis in TNBC. NEAT1 and MAL2 were selected as key lncRNAs. An mRNA-miRNA-lncRNA network in TNBC was constructed. Thus, we successfully established a novel mRNA-miRNA-lncRNA regulatory network, each component of which is prognostic for TNBC.
| S-EPMC7835059 | biostudies-literature