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• Genomic_profiling_of_B_other_Adult_ALL_RNA

  Adult ALL is an aggressive leukaemia, affecting adults of all ages. It is associated with a rapid onset and poor outcomes. Our understanding of adult ALL genome has been limited to molecular markers first described in paediatric ALL and validated in adult ALL and to date there have been no studies investigating the genomics of Adult ALL. We will perform whole genome sequencing on at least 100 Adult ALL cases. Priority will be given on ALL cases without a known primary lesion by cytogenetic analysis which are categorised as “B-other”. We will also sequence representative cases of each known subtype. This will deliver a comprehensive annotation of the genomic landscape of Adult ALL to include acquired somatic mutations (substitutions, indels, structural variants/fusion genes) and copy number profiles. The focus on B-other Adult ALL is likely to result in new and previously undescribed genomic lesions.

  Study EGAS00001003428

• Wistar PDX Development and Trial Center

  Overall the outcomes of patients with metastatic melanoma have improved dramatically over the last decade due to an improved understanding of the molecular drivers of this disease. In particular, multiple targeted therapy regimens have been approved for patients with a BRAFV600E/K mutation, which are present in ~50% of cutaneous melanomas. These treatments achieve clinical responses in ~80% of patients with a BRAFV600E/K mutation, thus providing proof-of-concept of the therapeutic potential for personalized therapeutic strategies. However, most of the patients will progress within 2 years of starting those therapies. Further, currently there are no targeted therapies that have been shown to be effective in patients with a wild-type BRAF. Thus, there are unmet clinical needs to develop treatments that prevent or overcome resistance to existing therapies for patients with a BRAFV600E/K mutation, and that are effective in patients without a BRAF mutation. In order to facilitate the development of new therapeutic strategies, over the last 5 years we have led a major effort to develop a broad collection of PDX models to reflect the clinical, histological, and genetic heterogeneity of this disease. Our collection of PDX models represents one of the largest collections for any human malignancy, and our initial testing demonstrates that the collection accurately recapitulates the oncogenic drivers and molecular heterogeneity that is observed in patients. This collection also includes a subset of PDX established from patients with acquired resistance to targeted therapies that have been maintained on those agents in vivo to sustain their resistant phenotype. Together these efforts have generated a robust resource to develop, refine, and prioritize new personalized combinatorial therapies for patients. Thus, we propose to establish a multi-disciplinary and multi-institutional PDTC Program focused on the use and continued expansion of our robust melanoma PDX collection to identify new therapeutic approaches that fill important clinical gaps in this disease.

  Study phs002432

• ZFHX4 is necessary for dopaminergic neuron differentiation and controls cell cycle by regulating LIN28A

  ZFHX4 as a transcription factor specifically induced during the in vitro differentiation of iPSC-derived mDANs. Depletion of ZFHX4 during neuronal differentiation led to a significant reduction in the number of mDANs while its overexpression did not lead to any changes in mDAN count. Identification of ZFHX4 target genes using CUT&Tag profiling and RNA-seq upon ZFHX4 knock-down (KD) revealed its involvement in cell cycle regulation during mDAN differentiation

  Dataset EGAD50000001605

• Non-invasive prenatal diagnosis by genome-wide haplotyping of cell-free plasma DNA

  This dataset contains a total of 10 families and 51 samples presented in 'Non-invasive prenatal diagnosis by genome-wide haplotyping of cell-free plasma DNA' study, in which 9 of them are cfDNA samples and the rest of samples are gDNA samples. All the samples are targeted sequencing data with a custom 45Mb capture library . Raw pair-end fastq files for each sample is available.

  Dataset EGAD00001004989

• BAM files from capture-based targeted sequencing of 12 agressive B-cell lymphoma tumour samples (IG-MCL-panel)

  This dataset contains BAM files from capture-based targeted sequencing of 12 agressive B-cell lymphoma tumour samples for cases 1 to 6 and 8 to 13. The sequencing panel used is a MCL-oriented panel containing 159 genes.

  Dataset EGAD50000000801

• Single cell TotalSeqC protein data of 20 PMBC pools of HCC patients

  Single cell TotalSeqC protein data serial peripheral blood mononuclear cell (PBMC) samples taken from advanced HCC patients. TotalSeqC is available for 41 out of 72 PBMC samples included in the study, and were combined into 20 pools.

  Dataset EGAD00001011346

• Autosomal Recessive CD55 Deficiency is Associated with Protein Losing Enteropathy, Thrombosis, and Complement Dysregulation

  We describe 11 patients from 8 families with homozygous LOF mutations in the complement regulatory protein CD55. Loss of CD55 is associated with increased complement activation, severe protein losing enteropathy accompanying a primary intestinal lymphangiectasia, and deep vein thrombotic events. We have named this disease CHAPLE after the principle components of the disease.

  Study phs001376

• CALGB 80303:Genome-Wide Association Study of Advanced Pancreatic Cancer Patients - A Randomized Phase III trial of Gemcitabine Plus Bevacizumab versus Gemcitabine Plus Placebo in Patients with Advanced Pancreatic Cancer

  CALGB 80303 was a randomized, phase III study in advanced pancreatic cancer patients treated with Gemcitabine plus either Bevacizumab or placebo. No difference in overall survival (OS) was observed between the two arms. We prospectively collected germline DNA and conducted a genome-wide association study (GWAS).

  Study phs000250

• Single Cell DNA amplicon sequencing of 12 B-ALL patients (at diagnosis and during treatment)

  This dataset contains single cell DNA amplicon sequencing of 12 B-ALL patients. For all patients a diagnosis sample was processed, while 4 patients were also followed up during treatment, summing up to a total of 23 samples. Mutations were called in the predefined set of amplicons.

  Dataset EGAD00001006955

• Dataset for LCPlus_WES

  WES/WGS sequencing data of 86 chromothriptic tumor and control runs, which were uploaded to umbrella studies. The sequencing was always paired

  Dataset EGAD00001009273