Bd852852-39c1-4bf0-954a-9d15b9ae5b53 - samples
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ABSTRACT:
PROVIDER: EGAD00001008106 | EGA |
REPOSITORIES: EGA
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Project description:Acute myeloid leukemia study. Supplementary Table 1: Clinical, morphological, cytogenetic and molecular genetic information on 116 AML patient samples. Supplementary Table 2: Summary of the distribution of clinical and molecular genetic characteristics within the AML sample set. Supplementary Table 3: Fluorescence ratios of the 6,283 well-measured and variably-expressed genes. Supplementary Table 4: Clinical and laboratory characteristics of normal karyotype predominant subtypes I and II. Supplementary Table 5: Supervised analysis of group-specific gene expression signatures. Supplementary Table 6: Gene-expression outcome class predictor. Supplementary Table 7: Multivariate proportional hazards analysis. Keywords: other
2004-04-15 | GSE425 | GEO
Project description:These is a collection of chromatin proteomics experiments that make up the 80 "in-house" biological conditions covered by ProteomeHD (see publication for more details). All experiments use SILAC, resulting in 80 SILAC ratios comparing the impact of various drugs (estradiol, TSA, hydroxytamoxifen, etc.), growth factors (TNFalpha) or other treatments (ionizing radiation) on chromatin composition. For a more detailed description see the Supplementary Table S2 of the publication, which can also be downloaded from here.
2019-11-11 | PXD008888 | Pride
Project description:Replication and expression of the mitochondrial genome depend on the sufficient supply ofnucleotide building blocks to mitochondria. Dysregulated nucleotide metabolism is detrimental tomitochondrial genomes and can destabilise mitochondrial DNA and trigger inflammation. Here, wereport that a mitochondrial nucleoside diphosphate kinase, NME6, supplies mitochondria withpyrimidine ribonucleotides to drive the transcription of mitochondrial genes. Perturbation of NME6leads to the depletion of mitochondrial transcripts, destabilisation of the electron transport chainand impaired oxidative phosphorylation. These deficiencies are rescued upon supplementation withpyrimidine ribonucleosides. Moreover, NME6 is required for the maintenance of mitochondrial DNAwhen the access to cytosolic pyrimidine deoxyribonucleotides is limited. Our results, therefore, shedlight on the importance of mitochondrial ribonucleotide salvage for the synthesis of RNA andmitochondrial gene expression.The repository contains two internal projects which are identified by the internal IDs: 0187 and 0196. The raw files are indicated by the internal ID, and each Supplementary Table contains a reference to the internal ID. The project with the ID 0187 contains whole cell (WC) and immunoprecipitation (IP) data. Please see the file: SampleNamesForProjects.xlsx for more details.
2023-05-04 | PXD038391 | Pride
Project description:Single-cell whole transcriptome and antibody expression for bone marrow samples from Cohorts A and B. CITEseq protocol was followed. 37 and 77 surface markers were measured in each cohort, respectively (see Supplementary Table 1). For details on cell sorting prior scRNAseq see the methods section of the manuscript.
| EGAD00001010187 | EGA
Project description:Because ST embryos may be at risk of procedure related chromosomal or sub-chromosomal abnormalities, we biopsied and examined expanded blastocysts derived from ST and control embryos. We examined copy number variations (CNVs) by SNP array to explore possible subchromosomal abnormalities (deletion or duplication) in selected ST ESCs. De novo CNVs were detected in both ST and intact controls but none carried clinical significance (Table S3 in the Supplementary Appendix).
2016-10-14 | GSE87897 | GEO
Project description:Intracranial aneurysm (IA) is a pathological dilation of the cerebral artery which has a potential to rupture leading to sub arachnoid haemorrhage (SAH). One third of the patients with aneurysmal SAH (aSAH) develop symptomatic narrowing of the blood vessels called cerebral vasospasm. The outcomes in the above clinical scenarios are variable and devastating. The study was designed to decipher the molecular mechanisms underlying the pathophysiology of intracranial aneurysm formation, its rupture and subsequent development of vasospasm at the proteomic level. The study was done in two phases – discovery phase and validation phase. We performed iTRAQ-based quantitative proteomic analysis of brain vessel tissue and serum samples in three subgroups of patients with IA and compared them with those of control group (subjects with no cerebrovascular disorder) during the discovery phase. In validation phase, dysregulated proteins of biological significance i.e. ORM1 as a biomarker for unruptured aneurysm and MMP9 as a biomarker for cerebral vasospasm were validated in larger cohort of patients.
2022-09-07 | PXD013442 | Pride
Project description:Description: These date form the basis for supplementary table 2 and supplementary figure 6 of the manuscript "Modelling glycan processing reveals Golgi-enzyme homeostasis upon trafficking defects and cellular differentiation" by P Fisher, H Spencer, J Thomas-Oates, AJ Wood, D Ungar in Cell Reports
2019-11-11 | PXD013211 | Pride
Project description:We used immunoprecipitation (IP) and mass spectrometry (MS) to identify proteins that interact with MFSD7C. Because an anti-MFSD7C monoclonal antibody is not available, we used MFSD7C tagged with both Myc and FLAG epitopes in a MFSD7C-expressing murine alveolar macrophage cell line MH-S (Supplementary Fig. 2a-c and see Methods for details). A total of 58 proteins were identified excluding MFSD7C and common contaminants of IP experiments such as keratin, actin, and ribosomal proteins (Table 1). Twenty-six of the 58 proteins are annotated as mitochondrial proteins and 4 (three Fc receptors and one integrin) are known to reside in the cytoplasmic membrane. The 58 proteins were classified into 10 different functional categories based on gene ontology.
2020-08-20 | PXD021016 | Pride
Project description:We have performed a comprehensive proteomic analysis of clinical patient samples of chronic lymphocytic leukemia (CLL) alongside genome-, transcriptome- and ex-vivo drug response profiling. Trisomy 12 and IGHV mutation status had the strongest impact on the proteome and transcriptome; and SF3B1 mutations preferentially affected the proteome. Unsupervised clustering of the proteome data partitioned CLL patients into six protein based subgroups (PG) with contrasting clinical behavior. PG1-4 could be explained by the impact of trisomy 12 and IGHV mutation status on protein abundances and another subgroup (PG6), was enriched for TP53 mutations. In addition we uncovered a new subgroup (PG5) only detectable from the proteome, characterized by low expression of central B-cell receptor proteins, altered splicing, metabolic reprogramming and increased sensitivity to proteasomal inhibition. We further validated the existence of this subgroup by conducting DIA based proteomics of an additional 167 patients. This entry contains the DIA-data for 167 patients used to validate the subgroups identified using HiRIEF-LC-MS/MS (see separate accession: PXD017453) as well as DIA data for 36 of the original discovery cohort. https://www.ebi.ac.uk/pride/archive/projects/PXD028936
2022-10-19 | PXD024544 | Pride
Project description:Purpose: The tet oncogene family member 2 (TET2) gene was recently identified mutated in myeloid disorders including acute myeloid leukemia (AML). To date, there is increasing evidence for a functional role of TET2 mutations (TET2mut) in AML. Thus, we explored frequency, gene expression pattern, and clinical impact of TET2mut in a large cohort of AML patients, in the context of other AML-associated aberrations. Patients and Methods: Samples from 783 younger adult AML patients were analyzed for the presence of TET2mut (coding exons 3-11), and results were correlated with data from molecular genetic analyses, gene expression profiling, and clinical outcome. Results: In total, 66 TET2mut were found in 60 (60/783; 7.6%) patients, including missense (n=37), frameshift (n=16), and nonsense (n=13) mutations, which with one exception were all heterozygous. TET2mut were not correlated with distinct clinical features or genetic alterations, except for isocitrate dehydrogenase mutations (IDHmut) that were almost mutually exclusive with TET2mut (p<0.001). TET2mut were characterized by only a weak gene expression pattern, which nevertheless reflected TET2mut-associated biology. TET2mut did not impact response to induction therapy and clinical outcome; combining patients exhibiting TET2mut and/or IDHmut revealed shorter overall survival (p=0.03), although this association was not independent from known risk factors. Conclusion: TET2mut were identified in 7.6% of younger adult AML patients and did not impact response to therapy and survival. Mutations were mutually exclusive with IDHmut, thereby supporting recent data on a common mechanism of action, which might obscure the impact of TET2mut if compared against all other AML cases. We performed a supervised class comparison analysis comparing 31 TET-mutated AML cases (TET2 mut) vs. 302 TET2-wildtype AML cases (TET wt) to see if a specific gene expression pattern associated with the presence of the identified TET2 mutations could be determined. No technical replicates were performed.
2011-12-31 | E-GEOD-32246 | biostudies-arrayexpress