DAC: WTSI CGP Data access committee

DAC Accession Contact Person Email Access Information
EGAC00001000000 Data Sharing datasharing@sanger.ac.uk http://www.ebi.ac.uk/ega/dacs/EGAC00001000000

This DAC controls 194 datasets:

Dataset Accessionsort ascending Technology Samples Description
EGAD00010000644 1022 Affymetrix SNP6.0 cancer cell line exome sequencing data
EGAD00010000488 Affymetrix_SNP6- 7 Chondroblastoma case sample genotype using Affymetrix SNP6.0
EGAD00010000452 Affymetrix_SNP6 36 Chondrosarcoma case sample genotype using Affymetrix SNP6.0
EGAD00010000395 Affymetrix_SNP6 19 Myeloma case sample genotype using Affymetrix SNP6.0
EGAD00001001898 HiSeq X Ten; 131 The study will investigate serial samples from the same patient taken at the time of MGUS or SMM diagnosis, and later at the time of evolution towards MM. Samples will be sequenced by whole genome along with a matched normal to obtain the highest possible amount of information toinvestigate genomic changes at disease evolution.
EGAD00001001890 HiSeq X Ten; 9 This study is to look at the effect of Myc and oxygen conditions on mutational signatures, to help establish causative roles for particular signatures.
EGAD00001001889 HiSeq X Ten; 9 ***THIS DATA CAN ONLY BE USED FOR NON-COMMERCIAL CANCER RESEARCH*** Sequencing of organoid cell lines derived from oesophageal tumour sections taken from patients diagnosed with primary oesophageal cancer who underwent tumour resection surgery.
EGAD00001001879 Illumina HiSeq 2000; 30 A pilot to establish the feasability of using a custom Agilent targeted pulldown of 110 genes implicated in colorectal tumourigensis to sequence for driver mutations in a set of 30 FFPE colorectal adenomas. If successful, we propose to sequence an additional 350 adenomas as part of a MRC research study in order to define the pattern of driver mutations across the spectrum of pathological subtypes including coventional adenomas, serrated adenomas and hyperplastic polyps
EGAD00001001873 Illumina HiSeq 2000; 215 AML emerges as a consequence of accumulating independent genetic aberrations that direct regulation and/or dysfunction of genes resulting in aberrant activation of signalling pathways, resistance to apoptosis and uncontrolled proliferation. Given the significant heterogeneity of AML genomes, AML patients demonstrate a highly variable response rate and poor median survival in response to current chemotherapy regimens. For the past 4 years we have conducted gene expression profiling on purified bone marrow populations equating to normal haematopoietic stem and progenitor cells from healthy subjects and patients with de novo AML in order to identify AML signatures of aberrantly expressed genes in cancer versus normal. We are now applying a series of bioinformatic methodologies combined with clinical and conventional diagnostic data to establish novel genomics strategies for improved prognostication of AML. Additionally, we use our AML signatures to unravel oncogenic signalling pathway activities in AML patients and test inhibitory drugs for these pathways inn preclinical therapeutic programmes. We consider that superimposing GEP and clinical data for our AML patient cohort with additional data on their mutational status will significantly improve the prognostic power of the study as well as unravel yet unknown mutations associated with aberrant signalling activities of oncogenic pathways.
EGAD00001001872 Illumina HiSeq 2000; 333 Targeted exome sequencing of patient derived xenografts from primary colorectal tumours and liver metastases.
EGAD00001001855 HiSeq X Ten; 15 This study is interested in lineage tracing of the adrenal gland. It will aid our understanding of phylogenetic relationships and contrasting mutational signatures between multiple functional and non-functional adrenal tumours and geographically sampled adrenal tissue.
EGAD00001001846 HiSeq X Ten; 4 2 BRAFV600E cell lines that have been made resistance to 1. the BRAF inhibitor PLX4720 and 2. the combination therapy of dabrafenib and trametinib seem to have a internal duplication in the kinase domain. We would like to know if this is caused by a translocation.
EGAD00001001845 Illumina HiSeq 2000; 16 Leeds Melanoma Cohort
EGAD00001001659 HiSeq X Ten; 12 Genome-wide analysis of mutations induced by ionizing radiation in human cells in different conditions.
EGAD00001001629 HiSeq X Ten; 20 Whole-genome somatic rearrangement and point mutation analysis in cell lines with induced telomere fusions.

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