Genome-wide methylation analysis of human breast cancer subtype group (Luminal A, Luminal B, HER2+ and TNBC)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA480639 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7508950_1.fastq.gz | Fastqsanger.gz | |||
| SRR7508950_2.fastq.gz | Fastqsanger.gz | |||
| SRR7508960_1.fastq.gz | Fastqsanger.gz | |||
| SRR7508960_2.fastq.gz | Fastqsanger.gz | |||
| SRR7508951_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:To identify Differentially methylated regions (DMRs) in TNBCs, we performed methyl binding domain protein 2 enrichment of DNA followed by massively parallel sequencing (MBD-seq) using 10 breast tumors and 10 matched normal samples for each of the four subtypes (LumA, LumB, HER2, and TNBC), classified according to ER, PR, and HER2 expression. ~~. 468 genes were significantly hypomethylated and 353 genes were significantly hypermethylated in promoter and CDS regions in only TNBC.
2023-06-30 | GSE116877 | GEO
Project description:two luminal cell lines were added, MCF7 and BT-474 two TNBC cell line were added, MB231 and BT-549 microRNA expression profiles were conpared between the luminal group and the TNBC group
2014-10-03 | E-GEOD-62022 | biostudies-arrayexpress
Project description:Purpose In breast cancer, specific aberrant methylation patterns have been associated with different BC histologic and molecular subtypes and data suggest that DNA methylation profiles may play an important role in the development and progression of distinct breast subtypes. However, the epigenome of the newly defined luminal B and luminal B-HER2 positive breast cancers has not yet been characterized. Therefore the main goal of the current study is to deciphered the aberrant DNA methylation profiles associated with these breast cancer subtypes. Experimental Design 29 luminal subtype breast cancer samples along with 8 control tissue were epigenetically interrogated using the HumanMethylation27 DNA Analysis BeadChip. Results Luminal B-HER2 + subtype displays the most aggressive phenotype and shows the highest number of aberrantly methylated CpG markers. On the other hand, the luminal B subtype harbours an heterogeneous DNA methylation profile that seems to be half way between the luminal A and luminalB-HER2+ subtypes. Conclusions The heterogeneous epigenetic and genetic profile of the luminal B subtype, might indicate that a further stratification has to be done for this specific breast cancer subtype.
2016-12-18 | GSE73808 | GEO
Project description:We performed whole genome gene expression microarrays on short-term cultures of mammary tumors deriving from diagnostic Tru-cut procedures of patients to evaluate transcriptional response to the retinoid. Tissue slices were challenged with vehicle (DMSO) or ATRA 0.1µm for 48 hours. Included are 1 luminal (LumB, >70% ER+ cells), 1 Her2, and 2 triple negative (TN) primary tumors.
2016-10-01 | E-MTAB-4983 | biostudies-arrayexpress
Project description:two luminal cell lines were added, MCF7 and BT-474 two TNBC cell line were added, MB231 and BT-549
2014-10-03 | GSE62022 | GEO
Project description:Eribulin prolongs overall survival in patients with pre-treated advanced breast cancer. However, no biomarker exists to prospectively select patients who will benefit the most from this drug. SOLTI-1007-NeoEribulin is a phase II, open-label, two cohort, exploratory pharmacogenomic study in patients with clinical stage I-II HER2-negative breast cancer receiving neoadjuvant eribulin monotherapy treatment. Primary objective was to explore the association of baseline tumor gene expression with pathological complete response in the breast (pCRB) at surgery. Key secondary objectives were pCRB rates in all patients and according to HR status, gene expression changes during treatment and safety. 101 hormonal receptor-positive (HR+) and 73 triple negative breast cancer (TNBC) patients were recruited. The pCRB rates were 6.4% in all patients, 4.9% in HR+ disease and 8.2% in TNBC. The TNBC cohort was interrupted due to a progression disease rate of 30.1%. The pCRB rates differed according to intrinsic subtypes: 28.6% in HER2-E, 11.1% in Normal-like, 7.9% in Luminal B, 5.9% in Basal-like and 0% in Luminal A (HER2-E vs. others odds ratio=7.05, 95% CI 1.80-42.14; p-value = 0.032). Intrinsic subtype changes at surgery occurred in 33.3% of cases, mostly (49.0%) Luminal B converting to Luminal A or Basal-likes converting to Normal-like. Baseline tumor infiltrating lymphocytes (TILs) were significantly associated with pCR. Eribulin showed a good safety profile with a low response and pCRB rates. Patients with HER2-negative disease with a HER2-enriched profile may benefit the most from eribulin. In addition, significant biological activity of eribulin is observed in Luminal B and Basal-like subtypes.
2021-12-10 | GSE186102 | GEO
Project description:Recent meta-analyses suggest triple-negative breast cancer (TNBC) is a heterogenous disease. In this study we sought to define these TNBC subtypes and identify subtype-specific markers and targets. We identified and confirmed four distinct, stable TNBC subtypes: (1) Luminal-AR (LAR); 2) Mesenchymal (MES); 3) Basal-Like Immune-Suppressed (BLIS), and 4) Basal-Like Immune-Activated (BLIA). RNA profiling analysis was conducted on 198 TNBC tumors (ER-negativity defined as Allred Scale value â¤2) with >50% cellularity (discovery set: n=84; validation set: n=114)
2015-12-18 | E-GEOD-76124 | biostudies-arrayexpress
Project description:Breast cancer can classify molecular subtype, luminal A, B, and HER2-positive and triple-negative breast cancer. Especially TNBC, there is no therapeutic target compared to other molecular subtypes. To investigate dysregulated miRNAs in TNBC, we performed miRNA microarray using breast cancer tissue with matched normal tissue in each subtype.
2023-06-15 | GSE154255 | GEO
Project description:Breast cancer is a heterogeneous disease for which prognosis and treatment strategies are largely governed by the receptor status (estrogen, progesterone and Her2-neu) of the tumor cells. Gene expression profiling of whole breast tumors further stratifies breast cancer into several molecular subtypes which also co-segregate with the receptor status of the tumor cells. We postulated that cancer associated fibroblasts (CAFs) within the tumor stroma may exhibit subtype specific gene expression profiles and thus contribute to the biology of the disease in a subtype specific manner. Several studies have reported gene expression profile differences between CAFs and normal breast fibroblasts but in none of these studies were the results stratified based on tumor subtypes. To address whether gene expression in breast cancer associated fibroblasts varies between breast cancer subtypes, we compared the gene expression profiles of early passage primary CAFs isolated from twenty human breast cancer samples representing three main subtypes; seven ER+, seven triple negative (TNBC) and six Her2+. We observed significant expression differences between CAFs derived from Her2+ breast cancer and CAFs from TNBC and ER+ cancers, particularly in pathways associated with cytoskeleton and integrin signaling. In the case of Her2+ breast cancer, the signaling pathways found to be selectively up regulated in CAFs may contribute to the more invasive properties and unfavorable prognosis of Her2+ breast cancer. These data demonstrate that in addition to the distinct molecular profiles that characterize the neoplastic cells, CAF gene expression is also differentially regulated in distinct subtypes of breast cancer. We isolated CAFs from twenty primary breast cancer samples representing three main subtypes (ER+ (n=7), TNBC (n=7), Her2+ (n=6)) and performed gene expression profile analyses on RNA isolated from these early passage CAFs. Those samples were done in two batches with 4 samples repeated in both batches. One TNBC sample was found to be an outlier and not used in the analysis.
2013-12-20 | E-GEOD-37614 | biostudies-arrayexpress
Project description:Mechanisms driving tumor progression from less aggressive subtypes to more aggressive states represent key targets for breast cancer therapy. We identified a subset of Luminal A primary breast tumors to give rise to HER2-enriched (HER2E) subtype metastases, but remain clinically HER2 negative (cHER2-). By testing the unique genetic and transcriptomic features of these cases, we developed the hypothesis that fibroblast growth factor receptor 4 (FGFR4) drives this subtype switching. To evaluate this, we developed two FGFR4 genomic signatures using a PDX model treated with a FGFR4 inhibitor (BLU9931), which inhibited PDX growth in vivo. Examining patient outcomes in the METABRIC breast cancer cohort showed that the FGFR4-induced and FGFR4-repressed signatures each predicted overall survival (OS) (HR=6.30, P<0.0001; HR=0.33; P<0.0001, respectively). Multivariate analysis showed that the FGFR4-induced signature was also an independent prognostic factor beyond subtype and stage for OS (HR=2.34, P=0.014). Supervised analysis of 77 primary tumors with paired metastasis revealed that the FGFR4-induced signature was significantly higher in luminal/ER+ tumor metastases compared with their primaries. Finally, multivariate analysis demonstrated that the FGFR4-induced signature also predicted site-specific metastasis for lung, liver and brain, but not for bone or lymph nodes. These data identify a link between FGFR4-regulated genes and metastasis, suggesting a treatment options for FGFR4-positive patients, whose high expression is non-genetically determined.
2020-07-30 | GSE145326 | GEO