Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA275142 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The purpose of the present study was to investigate the association of glutathione S-transferase P1 (GSTP1) expression with resistance to neoadjuvant paclitaxel followed by 5-fluorouracil/epirubicin/cyclophosphamide (P-FEC) in human breast cancers. The relationship of GSTP1 expression and GSTP1 promoter hypermethylation with intrinsic subtypes was also investigated. In this study, primary breast cancer patients (n = 123, stage II-III) treated with neoadjuvant P-FEC were analyzed. Tumor samples were obtained by vacuum-assisted core biopsy before P-FEC. GSTP1 expression was determined using immunohistochemistry, GSTP1 promoter methylation index (MI) using bisulfite methylation assay and intrinsic subtypes using DNA microarray. The pathological complete response (pCR) rate was significantly higher in GSTP1-negative tumors (80.0%) than GSTP1-positive tumors (30.6%) (P = 0.009) among estrogen receptor (ER)-negative tumors but not among ER-positive tumors (P = 0.267). Multivariate analysis showed that GSTP1 was the only predictive factor for pCR (P = 0.013) among ER-negative tumors. Luminal A, luminal B and HER2-enriched tumors showed a significantly lower GSTP1 positivity than basal-like tumors (P = 0.002, P < 0.001 and P = 0.009, respectively), while luminal A, luminal B and HER2-enriched tumors showed a higher GSTP1 MI than basal-like tumors (P = 0.076, P < 0.001 and P < 0.001, respectively). In conclusion, these results suggest the possibility that GSTP1 expression can predict pathological response to P-FEC in ER-negative tumors but not in ER-positive tumors. Additionally, GSTP1 promoter hypermethylation might be implicated more importantly in the pathogenesis of luminal A, luminal B and HER2-enriched tumors than basal-like tumors. Fresh frozen tumor samples obtained by vacuum-assisted core biopsy from one hundred and fifteen patients were subjected to RNA extraction and hybridization on Affymetrix microarrays.
2012-03-20 | E-GEOD-32646 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of non-tumoral and infiltrating ductal breast cancer (tumoral) samples. The HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across approximately 450,000 CpG in non-tumoral and tumoral samples. Non-tumoral samples included six frozen non-neoplastic breast tissues from reduction mammoplasties and tumoral samples included eight frozen tumors from each BC subtype, i.e. luminal A (LA), luminal B (LB), luminal-HER2 (LH), HER2 (H) and triple-negative (TN) (Total: 40 tumors).
2020-02-17 | GSE141338 | GEO
Project description:The purpose of the present study was to investigate the association of glutathione S-transferase P1 (GSTP1) expression with resistance to neoadjuvant paclitaxel followed by 5-fluorouracil/epirubicin/cyclophosphamide (P-FEC) in human breast cancers. The relationship of GSTP1 expression and GSTP1 promoter hypermethylation with intrinsic subtypes was also investigated. In this study, primary breast cancer patients (n = 123, stage II-III) treated with neoadjuvant P-FEC were analyzed. Tumor samples were obtained by vacuum-assisted core biopsy before P-FEC. GSTP1 expression was determined using immunohistochemistry, GSTP1 promoter methylation index (MI) using bisulfite methylation assay and intrinsic subtypes using DNA microarray. The pathological complete response (pCR) rate was significantly higher in GSTP1-negative tumors (80.0%) than GSTP1-positive tumors (30.6%) (P = 0.009) among estrogen receptor (ER)-negative tumors but not among ER-positive tumors (P = 0.267). Multivariate analysis showed that GSTP1 was the only predictive factor for pCR (P = 0.013) among ER-negative tumors. Luminal A, luminal B and HER2-enriched tumors showed a significantly lower GSTP1 positivity than basal-like tumors (P = 0.002, P < 0.001 and P = 0.009, respectively), while luminal A, luminal B and HER2-enriched tumors showed a higher GSTP1 MI than basal-like tumors (P = 0.076, P < 0.001 and P < 0.001, respectively). In conclusion, these results suggest the possibility that GSTP1 expression can predict pathological response to P-FEC in ER-negative tumors but not in ER-positive tumors. Additionally, GSTP1 promoter hypermethylation might be implicated more importantly in the pathogenesis of luminal A, luminal B and HER2-enriched tumors than basal-like tumors.
2012-03-20 | GSE32646 | GEO
Project description:To investigate circadian clocks in human breast tumors, 43 pairs of human samples (tumor and matched normal breast tissues from the same patient) were collected to run bulk-RNAseq, including 29 pairs of Luminal A, 3 pairs of Luminal B, 2 pairs of HER2 and 9 pairs of Triple-negative breast cancer
2024-01-26 | GSE233242 | GEO
Project description:Triple-negative (TN) and Basal-like (BL) breast cancer definitions have been used interchangeably to identify breast cancers that lack expression of the hormonal receptors (HR) and overexpression and/or amplification of HER2. However, both classifications when compared to each other, show substantial discordance rates. Here, we molecularly characterize TN tumors, and Basal-like tumors, and compare and contrast the results in terms of common patterns and distinct patterns for each. In total, when testing 412 TN and 473 Basal-like tumors, 21.4% and 31.5% were identified as non-Basal-like and non-TN, respectively. TN tumors identified as Luminal or HER2-enriched showed undistinguishable overall gene expression profiles when compared versus Luminal or HER2-enriched tumors that were not TN. Similar findings were observed within Basal-like tumors regardless of the TN status. Interestingly, most TN tumors identified as HER2-enriched showed low HER2 expression and lack of HER2 amplification despite the similar overall gene expression profiles to HER2-E tumors that were not TN. Lastly, additional genomic classifications are examined within TN and Basal-like cancers, most of which are largely concordant with tumor intrinsic subtype. These results suggest that future clinical trials focused on TN disease should consider stratifying patients based on Basal-like versus non-Basal-like gene expression profiles as this appears to be the main biological difference seen within TN breast cancer patients. reference x sample
2014-07-29 | E-GEOD-41119 | biostudies-arrayexpress
Project description:Determination of recurrent chromosomal aberrations in Luninal A, Luminal B, HER2-positve, and triple negative breast cancers
2015-12-10 | GSE54140 | GEO
Project description:Kynureninase is a member of a large family of catalytically diverse but structurally homologous pyridoxal 5'-phosphate (PLP) dependent enzymes known as the aspartate aminotransferase superfamily or alpha-family. The Homo sapiens and other eukaryotic constitutive kynureninases preferentially catalyze the hydrolytic cleavage of 3-hydroxy-l-kynurenine to produce 3-hydroxyanthranilate and l-alanine, while l-kynurenine is the substrate of many prokaryotic inducible kynureninases. The human enzyme was cloned with an N-terminal hexahistidine tag, expressed, and purified from a bacterial expression system using Ni metal ion affinity chromatography. Kinetic characterization of the recombinant enzyme reveals classic Michaelis-Menten behavior, with a Km of 28.3 +/- 1.9 microM and a specific activity of 1.75 micromol min-1 mg-1 for 3-hydroxy-dl-kynurenine. Crystals of recombinant kynureninase that diffracted to 2.0 A were obtained, and the atomic structure of the PLP-bound holoenzyme was determined by molecular replacement using the Pseudomonas fluorescens kynureninase structure (PDB entry 1qz9) as the phasing model. A structural superposition with the P. fluorescens kynureninase revealed that these two structures resemble the "open" and "closed" conformations of aspartate aminotransferase. The comparison illustrates the dynamic nature of these proteins' small domains and reveals a role for Arg-434 similar to its role in other AAT alpha-family members. Docking of 3-hydroxy-l-kynurenine into the human kynureninase active site suggests that Asn-333 and His-102 are involved in substrate binding and molecular discrimination between inducible and constitutive kynureninase substrates.
| S-EPMC2531291 | biostudies-literature
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:We performed high throughput transcriptome of breast cancer and normal tissues, identifying lincRNA associated molecular subtype with powerful capacity to distinct breast cancer population and predict prognosis. We also identified subtype-specific lincRNAs that may be a useful complement to intrinsic molecular subtype classification when divergence emerges among pathologists.Paired-end transcriptome sequencing were carried out on a cohort of 33 breast tissues from 11 groups including five breast cancer subtypes including luminal A (LA), luminal B (HER2 negative)(LB, HER2-), luminal B (HER2 positive) (LB, HER2+), HER2 and tripple negative breast cancer (TNB), adjacent noncancerous breast tissue (ANT, three samples for each subtype) and the complete normal breast tissues (three samples)
2017-09-06 | GSE71651 | GEO
Project description:Microarrays have revolutionized breast cancer (BC) research by enabling studies of gene expression on a transcriptome-wide scale. Recently, RNA-Sequencing (RNA-Seq) has emerged as an alternative for precise readouts of the transcriptome. To date, no study has compared the ability of the two technologies to quantify clinically relevant individual genes and microarray-derived gene expression signatures (GES) in a set of BC samples encompassing the known molecular BC's subtypes. To accomplish this, the RNA from 57 BCs representing the four main molecular subtypes (triple negative, HER2 positive, luminal A, luminal B), was profiled with Affymetrix HG-U133 Plus 2.0 chips and sequenced using the Illumina HiSeq 2000 platform. The correlations of three clinically relevant BC genes, six molecular subtype classifiers, and a selection of 21 GES were evaluated. 58 tumors representing the different molecular subtypes [triple negative (ER-/PgR-/HER2-); HER2 positive (HER2+); luminal A (ER+/HER2-/histological grade 1), luminal B (ER+/HER2-/histological grade 3)] were obtained from patients recruited between 2007 and 2011 at the Institut Jules Bordet. RNA was profiled using the Affymetrix HG-U133 Plus 2.0 chips and sequenced on the Illumina platform, producing ~30 million 50 bp paired-end reads per sample. The reads alignment and expression quantification were performed using the Tophat/Cufflinks pipeline and the Ensembl genome version hg19. The Affymetrix microarray data were normalized using fRMA and probesets were selected based on the JetSet reannotation package. This submission represents the gene expression component of the study only.
2014-11-21 | E-GEOD-43358 | biostudies-arrayexpress