Lymphocyte PanBody WGS H38
Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001003596 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:We study lymphocyte somatic evolution through the sequencing of normal healthy lymphocytes. We perform whole-genome sequencing of single-cell derived T and B cell colonies to identify somatic mutations, and perform targeted deep-sequencing of these mutations. The lineages of T and B cells, and the frequencies of these mutations reveals the neutral and non-neutral evolutionary processes underlying lymphocyte growth and function.
| EGAS00001003594 | EGA
Project description:We study lymphocyte somatic evolution through the sequencing of normal healthy lymphocytes. We perform whole-genome sequencing of single-cell derived T and B cell colonies to identify somatic mutations, and perform targeted deep-sequencing of these mutations. The lineages of T and B cells, and the frequencies of these mutations reveals the neutral and non-neutral evolutionary processes underlying lymphocyte growth and function.
| EGAS00001002948 | EGA
Project description:We study lymphocyte somatic evolution through the sequencing of normal healthy lymphocytes. We perform whole-genome sequencing of single-cell derived T and B cell colonies to identify somatic mutations, and perform targeted deep-sequencing of these mutations. The lineages of T and B cells, and the frequencies of these mutations reveals the neutral and non-neutral evolutionary processes underlying lymphocyte growth and function. .
This dataset contains all the data available for this study on 2021-02-02.
| EGAD00001006934 | EGA
Project description:We study lymphocyte somatic evolution through the sequencing of normal healthy lymphocytes. We perform whole-genome sequencing of single-cell derived T and B cell colonies to identify somatic mutations, and perform targeted deep-sequencing of these mutations. The lineages of T and B cells, and the frequencies of these mutations reveals the neutral and non-neutral evolutionary processes underlying lymphocyte growth and function. .
This dataset contains all the data available for this study on 2021-02-02.
| EGAD00001006935 | EGA
Project description:A variety of somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs), but the small number of CD34+ hematopoietic stem cells (HSCs) present in non-mobilized peripheral blood (PB) would be a convenient and desirable starting target. We report here a simple method for targeting derivation of iPSC from non-mobilized PB CD34+ HSCs using immunobead purification and 2-4 day culture to achieve enrichment of CD34+ HSCs to 80±9%, followed by reprogramming transduction with loxP-flanked polycistronic (Oct4, Klf4, Sox2, and c-Myc) STEMCCA-loxP lentivector at an MOI of 2. Our yield was 4.7±2.2 iPSC colonies (n=12) per 20 mL non-mobilized peripheral blood, where most colonies had single copy STEMCCA-loxP that was easily excised by transient transfection expression of Cre. Resultant iPSC clones expressed pluripotent cell markers, had genomic methylation pattern closely matching embryonic stem cells, and generated teratomas containing tissues of all three germ lineages in immunodeficient mice. Furthermore, we conclude that these iPSC are derived from the non-mobilized CD34+ HSCs enriched from PB rather than from any lymphocyte or monocyte contaminants because they lacked somatic rearrangements typical of T or B lymphocytes, and because we demonstrated that purified CD14+ monocytes do not yield iPSC colonies under these reprogramming conditions.
2013-04-26 | GSE40790 | GEO
Project description:In this study we will perform whole genome sequencing on in vitro colonies. Colonies of various sizes (100-300 cells) will be collected for somatic mutation analysis.
| EGAS00001003112 | EGA
Project description:Our results suggest that STAT3 can be activated independent of key oncogenic driver mutations in its SH2 domain in a subset of patients with large granular lymphocyte disorders. We examined the gene expression pattern in T-LGL leukemias compared to controls, and the impact of the presence of STAT3 mutations on the transcriptional regulation of a specific set of genes previously described.
2012-08-03 | GSE39838 | GEO
Project description:Prostate cancer-associated stroma (CAS) plays an active role in malignant transformation, tumor progression, and metastasis. Molecular analyses of CAS have demonstrated significant changes in gene expression; however, conflicting evidence exists on whether genomic alterations in benign cells comprising the tumor microenvironment (TME) underlie gene expression changes and oncogenic phenotypes. This study evaluates the nuclear and mitochondrial DNA integrity of prostate carcinoma cells, CAS, matched benign epithelium and benign epithelium-associated stroma by whole genome copy number analyses, targeted sequencing of TP53, and fluorescence in situ hybridization. Comparative genomic hybridization (aCGH) of CAS revealed a copy-neutral diploid genome with only rare and small somatic copy number aberrations (SCNAs). In contrast, several expected recurrent SCNAs were evident in the adjacent prostate carcinoma cells, including gains at 3q, 7p, and 8q, and losses at 8p and 10q. No somatic TP53 mutations were observed in CAS. Mitochondrial DNA (mtDNA) extracted from carcinoma cells and stroma identified 23 somatic mtDNA mutations in neoplastic epithelial cells but only one mutation in stroma. Finally, genomic analyses identified no SCNAs, no loss of heterozygosity (LOH) or copy-neutral LOH in cultured cancer-associated fibroblasts (CAFs), which are known to promote prostate cancer progression in vivo. Agilent whole human genome aCGH oligonucleotide microarrays were used to assess copy number aberrations in 79 specimens from 20 patients as well as two pairs of cancer-associated fibroblasts (CAF) and benign/normal associated fibroblasts (NAF). 3 CAF/NAF sample pairs were also assessed for DNA copy number aberrations and copy-neutral LOH using the Infinium HumanOmniExpressExome BeadChip Kit.
2016-02-12 | E-GEOD-76456 | biostudies-arrayexpress
Project description:This was a collaborative study to discover somatic mutations in 188 lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are likely to play a role in carcinogenesis. The observed mutational profiles correlate with clinical features, smoking status, and DNA repair defects. These results are complemented by data integration including SNP array data and gene expression array data (deposited here). Our findings shed further light on several key signaling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment. Experiment Overall Design: A subset of 75 RNAs from a corresponding set of 188 lung adenocarcinomas DNAs were resequenced across 623 genes.
2009-09-11 | E-GEOD-12667 | biostudies-arrayexpress
Project description:This goal of this study was to identify genes that are deregulated in the absence of EZH2 in early lymphocyte progenitors. Due to a requirement for EZH2 to repress Cdkn2a in early B and T cell development we generated Cdkn2a-/-Ezh2fl/fl Il7racre/+ mice. We examined gene expression by RNA-sequencing in sorted pro-B cells (B220+CD19+CD43+), DN3 cells (Lin- CD25+ CD117-), from Cdkn2a-/- Ezh2fl/fl Il7racre/+ and Cdkn2a-/- Il7racre/+ control mice. Reads were aligned to the mm10 reference genome by Tophat2.1.0. Reads were assigned to genes using the htseq-count tool from HTSeq v 0.6.1 and gene annotations from Ensembl release 78. Differential expression was calculated across 3 independent replicates by EdgeR. We found that pro-B and DN3 cells remain specified to their respective lineages despite loss of EZH2. In contrast, loss of EZH2 led to expression of alternate lineage determinants in pro-B but not DN3 cells indicating that EZH2 is required for lineage commitment in B, but not T lymphocyte progenitors.
2020-01-29 | GSE133993 | GEO