Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ena-DATASET-NCC-22-07-2016-00:14:52:391-1907 - samples

ABSTRACT: Corresponding data set is composed of whole exome sequencing of Korean ER positive breast cancer under 35. This set provides 100 alignment files from normal-tumor paired whole exome sequencing of 50 patients. This is a part of total project data set.

PROVIDER: EGAD00001002256 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

RNA sequencing of Korean ER positive breast cancer females aged under 35 years old - samples

Project description:Corresponding data set is composed of RNA sequencing of Korean ER positive breast cancer under 35 years old. This set provides 50 alignment files of 50 tumor samples. This is a part of total project data set.

| EGAD00001003243 | EGA

Expression data from breast cancer FNA biopsies from patients

Project description:We assess if distinct biological processes might be associated with chemotherapy sensitivity in the different clinical subsets of breast cancers. We performed gene set analysis (GSA) using functionally annotated gene sets corresponding to almost all known biological processes in ER-positive/HER2negative and ER-negative/HER2-negative breast cancer, respectively.

2010-12-31 | GSE22093 | GEO

Exome-seq of Glioblastoma Tumors and GBOs

Project description:Analysis of glioblastoma tissue and corresponding glioblastoma organoids by Exome sequencing.

2019-12-26 | GSE141944 | GEO

The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients

Project description:The goal of this study was to assess whether the presence of HLA-B*35 contributes to activation of ER stress/UPR and inflammation in lcSScPAH PBMC. HLA-B*35 is associated with increased risk of developing PAH in lcSSc patietns. Also we previously reported that HLA-B*35 induces ECs dysfunction via activation of ER stress/UPR and upregulation of the inflammatory response. Our study demonstrates that HLA-B*35 contributes to the dysregulated expression of selected ER stress, inflammation and proliferation related genes in lcSSc patient PBMCs, as well as healthy individuals, thus supporting a pathogenic role of HLA-B*35 as a risk factor for developing PAH in SSc patients.

2016-11-02 | GSE73355 | GEO

Expression data from breast cancer FNA biopsies from patients (US samples)

Project description:This is Phase II Trial of 4courses of 5-fluorouracil, doxorubicin and cyclophosphamide follwed by 4 additional courses of weekly docetaxel and capecitabine administered as Preoperative Therapy for Patients with Locally Advanced Breast Cancer, Stages II and III by US oncology (PROTOCOL 02-103) We performed gene set analysis (GSA) using functionally annotated gene sets corresponding to almost all known biological processes in ER-positive/HER2negative and ER-negative/HER2-negative breast cancer, respectively.

2011-02-07 | GSE23988 | GEO

Acquired FGFR and FGF alterations confer resistance to estrogen receptor (ER) targeted therapy in ER+ metastatic breast cancer

Project description:Beyond acquired mutations in the estrogen receptor (ER), mechanisms of resistance to ER-directed therapies in ER+ breast cancer have not been clearly defined. We conducted a genome-scale functional screen spanning 10,135 genes to investigate genes whose overexpression confer resistance to selective estrogen receptor degraders. Pathway analysis of candidate resistance genes demonstrated that the FGFR, ERBB, insulin receptor, and MAPK pathways represented key modalities of resistance. In parallel, we performed whole exome sequencing in paired pre-treatment and post-resistance biopsies from 60 patients with ER+ metastatic breast cancer who had developed resistance to ER-targeted therapy. The FGFR pathway was altered via FGFR1, FGFR2, or FGF3/FGF4 amplifications or FGFR2 mutations in 24 (40%) of the post-resistance biopsies. In 12 of the 24 post-resistance tumors exhibiting FGFR/FGF alterations, these alterations were not detected in the corresponding pre-treatment tumors, suggesting that they were acquired or enriched under the selective pressure of ER-directed therapy. In vitro experiments in ER+ breast cancer cells confirmed that FGFR/FGF alterations led to fulvestrant resistance as well as cross-resistance to the CDK4/6 inhibitor palbociclib, through activation of the MAPK pathway. The resistance phenotypes were reversed by FGFR inhibitors and, to a lesser extent, MEK inhibitors, suggesting potential treatment strategies.

2020-06-30 | GSE153509 | GEO

Gene profiling using archival formalin-fixed paraffin-embedded breast cancer specimens can generate informative microarray data: A comparison with matched fresh fine needle aspiration biopsy samples (FNA samples)

Project description:The Formalin-Fixed Paraffin-Embedded (FFPE) samples on selected breast cancer subtypes (ER+/Her2-, ER+/Her2+, ER-/Her2+, and ER-/Her2-) and their paired fresh fine needle aspirated biopsies (FNA) were investigated. The cases represented different subtypes of breast cancers based on their clinical receptors ER (E) and Her2 (H) status to demonstrate the ability of gene profiles to differentiate these tumors. Compared to FNA specimens, FFPE samples yielded relatively more degraded RNA, and 80% of the samples deemed suitable for cDNA-mediated annealing, selection, extension and ligation (DASL) assay. It is able to demonstrate that gene profiles from FFPE microarrays were reproducible and correlated well with the corresponding gene profiles from FNA microarrays. The gene profiles from both FNA and FFPE could differentiate the four breast cancer subtypes, and the expression levels of corresponding gene set were consistent with qRT-PCR and correlated to the clinical outcomes on published microarray data. It supports the use of FFPE specimens to develop a prognostic tool for breast cancers which can obviate the need for fresh specimens.

2011-06-22 | GSE23385 | GEO

2011-06-22 | GSE23384 | GEO