ET Exome
Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001000102 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Agilent whole exome hybridisation capture will be performed on genomic DNA derived from ~3 Splenic Marginal Zone Lymphoma with villous lymphocytes samples and matched normal DNA from the same patients. Samples will be multiplexed in one lane of Illumina HiSeq. Sequencing to a coverage of at least 30x will be performed and mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes.
| EGAS00001000139 | EGA
Project description:Agilent whole exome hybridisation capture will be performed on genomic DNA derived from FRCC patients. one lane of Illumina Hiseq sequencing will be performed on the resulting exome libraries and mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes.
| EGAS00001000176 | EGA
Project description:Agilent whole exome hybridisation capture will be performed on genomic DNA derived from 50 Polycythemia Vera Myeloproliferative Disease samples and matched normal DNA from the same patients. Three lanes of Illumina GA sequencing will be performed on the resulting 100 exome libraries and mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes.
| EGAS00001000028 | EGA
Project description:Agilent whole exome hybridisation capture will be performed on genomic DNA derived from 50 Primary Myelofibrosis Myeloproliferative Disease samples and matched normal DNA from the same patients. Three lanes of Illumina GA sequencing will be performed on the resulting 100 exome libraries and mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes.
| EGAS00001000175 | EGA
Project description:Agilent whole exome hybridisation capture will be performed on genomic DNA derived from 3 relatives from a family with multiple affected familial thrombocytosis (FT) patients. Germline DNA from 2-4 patients affected with FT will be used to prepare libraries and sequenced in one lane of HiSeq sequencing, mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes.
| EGAS00001000088 | EGA
Project description:Agilent whole exome hybridisation capture was performed on genomic DNA derived from Chondrosarcoma cancer and matched normal DNA from the same patients. Next Generation sequencing performed on the resulting exome libraries and mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes. Now we aim to re find and validate the findings of those exome libraries using bespoke pulldown methods and sequencing the products.
2016-05-17 | E-ERAD-37 | biostudies-arrayexpress
Project description:Agilent whole exome hybridisation capture will be performed on genomic DNA derived from 50 myeloproliferative disorder samples and matched normal DNA from the same patients. Three lanes of Illumina GA sequencing will be performed on the resulting 100 exome libraries and mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes. In addition, 500bp, NO_PCR total genomic libraries will be prepared from the same samples and five lanes of Illumina GA sequencing will be analysed to characterise genome wide, somatically acquired structural variation.
| EGAS00001000198 | EGA
Project description:Agilent whole exome hybridisation capture will be performed on genomic DNA derived from 50 myeloproliferative disorder samples and matched normal DNA from the same patients. Three lanes of Illumina GA sequencing will be performed on the resulting 100 exome libraries and mapped to build 37 of the human reference genome to facilitate the identification of novel cancer genes. In addition, 500bp, NO_PCR total genomic libraries will be prepared from the same samples and five lanes of Illumina GA sequencing will be analysed to characterise genome wide, somatically acquired structural variation.
| EGAS00001000199 | EGA
Project description:ChIP-seq experiments are standard experimental procedure for interrogating epigenetic states and protein-DNA interactions. Sequencing experiments are often designed according to the trade-off between the need to obtain maximum sequencing coverage limited funds. Multiplexing samples is a common approach to minimize cost and maximize information yield. We therefore performed an extensive ChiP-seq multiplexing study to gain a better understanding of the effect of multiplexing on the resulting peak detection and genomic annotation and to provide solid guidelines for multiplexing ChIP-seq studies. For a well characterized antibody, our results indicate that multiplexing to ~20M reads (roughly 8 samples per sequencing lane) is sufficient to capture most of the biological signal. Multiplexing samples in sequencing experiments is a common approach to maximize information yield while minimizing cost. In most cases the number of samples that are multiplexed is determined by financial consideration or experimental convenience with limited understanding on the effects on the experimental results. Here we set to examine the impact of multiplexing ChIP-seq experiments on the ability to identify a specific epigenetic modification. We performed an analysis of peak detection to determine the effects of multiplexing. These include false discovery rates, size, position and statistical significance of peak detection and changes in gene annotation. We found that, for histone marker H3K4me3, one can multiplex up to 8 samples (7 IP + 1 input) at ~21 million reads each and still detect over 90% of all peaks found when using a full lane for sample. Furthermore, there are no variations introduced by indexing or lane batch effects and importantly there is no significant reduction in the number of genes with neighboring H3K4me3 peaks. We conclude that, for a well characterized antibody and therefore, model IP condition, multiplexing 8 samples per lane is sufficient to capture most of the biological signal.
2015-06-01 | GSE64504 | GEO
Project description:To determine the genome-wide occupancy of the Plasmodium falciparum transcriptional regulator of invasion PfAP2-I (PfDd2_100013100/PF3D7_1007700), we used chromatin immunoprecipitation coupled with next-generation sequencing (ChIP-seq). Synchronized, schizont stage, 40 hours post-invasion, cultures of parasites expressing the AP2-I-GFP fusion protein were treated with formaldehyde to crosslink proteins to DNA and harvested. After shearing the DNA, the chromatin was incubated with anti-GFP antibody or IgG (as control) for immunoprecipitation. This material was used to generate Illumina sequencing libraries. The final libraries were multiplexed with fourteen barcoded samples per lane on an Illumina HiSeq 2500 system to generate 150 base pair single-end reads.
2017-06-01 | GSE80293 | GEO