DAC Accession Contact Person Email Access Information
EGAC00001000055 Frederic De gDAC-d@gene.com http://www.ebi.ac.uk/ega/dacs/EGAC00001000055

This DAC controls 24 datasets:

Dataset Accessionsort descending Technology Samples Description
EGAD00001000214 Illumina HiSeq 2000; 11 Whole genome sequencing of colon samples
EGAD00001000215 Illumina HiSeq 2000; 139 RNA sequencing of colon tumor/normal sample pairs
EGAD00001000216 Illumina HiSeq 2000; 144 Exome capture sequencing of colon tumor/normal pairs
EGAD00001000221 Illumina HiSeq 2000; 4 Whole genome sequencing of SCLC tumor/normal samples
EGAD00001000222 Illumina HiSeq 2000; 103 Exome capture sequencing of SCLC tumor/normal pairs and cell lines
EGAD00001000223 Illumina HiSeq 2000; 79 RNA sequencing of SCLC tumor/normal sample pairs and cell lines
EGAD00001000725 Illumina HiSeq 2000; 675 This dataset contains RNA sequencing data for 675 cancer cell lines. RNA libraries were made with the TruSeq RNA Sample Preparation kit (Illumina) according to the manufacturer protocol. The libraries were sequenced on an Illumnia HiSeq 2000
EGAD00001000815 Illumina HiSeq 2000; 102 Exome-seq, RNA-Seq, SNP array profiling of gastric tumor samples.
EGAD00001000817 Illumina HiSeq 2000; 34 Alternative splicing plays critical roles in differentiation, development, and cancer (Pettigrew et al., 2008; Chen and Manley, 2009). The recent identification of specific spliceosome inhibitors has generated interest in the therapeutic potential of targeting this cellular process (van Alphen et al., 2009). Using an integrated genomic approach, we have identified PRPF6, an RNA binding component of the pre-mRNA spliceosome, as an essential driver of oncogenesis in colon cancer. Importantly, PRPF6 is both amplified and overexpressed in colon cancer, and only colon cancer cells with high PRPF6 levels are sensitive to its loss. Our data clearly point to an important role for PRPF6 in colon cancer growth and suggest that a better understanding of its role in alternative splicing in colon cancer is warranted. To determine the specific alternative splice forms that PRPF6 regulates in colon cancer, we plan three experiments: 1. The first involves knocking down expression of PRPF6 in two different cancer cell lines with 3 different siRNAs, and then completing RNA-seq to determine the gene expression changes that occur relative to a non-targeting control siRNA. Because of the role for PRPF6 in pre-mRNA splicing, we especially want to quantify the changes in splice-specific forms of all genes genome-wide to identify genes whose splicing is altered upon PRPF6 knockdown. 2. The second involves immunoprecipitating PRPF6 from two different cancer cell lines and isolating any RNA that is bound to PRPF6, since PRPF6 is an RNA-binding protein. We then want to carry out RNA-seq to identify which RNA molecules co-immunoprecipitated with PRPF6. This will help us determine possible functions for PRPF6 in regulating colon cancer growth. 3. The third involves overexpressing PRPF6 in cell lines and then carrying out RNA-seq to identify any changes in splice-specific gene expression. This will allow us to determine whether increased PRPF6 expression is sufficient to drive alternative splicing changes.
EGAD00001000885 Illumina HiSeq 2000; 60 Exome read sequences for 30 tumor-normal pairs for the study "Diverse modes of genomic alterations in Hepatocellular Carcinoma".
EGAD00001000886 Illumina HiSeq 2000; 23 RNA-Sequencing data (raw read sequences) for 23 samples, from 12 patients, for the study "Diverse modes of genomic alterations in Hepatocellular Carcinoma"
EGAD00001001013 Illumina HiSeq 2000; 30 RNAseq and exome sequencing data of gastric cancer cell lines.
EGAD00001001034 24 Whole genome data (Complete genomics platform) for the study EGAS00001000824
EGAD00001001057 Illumina HiSeq 2000; 3 RNA-seq from normal human tissues (2 x 75 bp)
EGAD00001001104 Illumina MiSeq; 16 MMP-seq tumor samples, UDG treated (FASTQ)

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