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• Circulating tumor cell copy-number heterogeneity in ALK-rearranged non-small-cell lung cancer resistant to ALK inhibitors

  Gatekeeper mutations are identified in only 50% of the cases at resistance to Anaplastic Lymphoma Kinase (ALK)-tyrosine kinase inhibitors (TKIs). Circulating tumor cells (CTCs) are relevant tools to identify additional resistance mechanisms and can be sequenced at the single-cell level. Here, we provide in-depth investigation of copy number alteration (CNA) heterogeneity in phenotypically characterized CTCs at resistance to ALK-TKIs in ALK-positive non-small cell lung cancer.

  Study EGAS00001005301

• MSI_Cancer_Models___RNAseq

  The study will use RNAseq to aid in define determinants of WRN dependency in MSI Cell lines.

  Study EGAS00001004180

• WTCCC case-control study for Multiple Sclerosis - Combined controls

  WTCCC genome-wide accosication study for Multiple Sclerosis (MS) - Combined controls

  Study EGAS00000000023

• Container Study for ICGC Malignant Lymphoma Master Study (MMML)

  Master Container Study for Malignant Lymphoma data (ICGC - Germany)

  Study EGAS00001001600

• Exome sequencing for LySeqST

  Exome sequencing of 120 lymphoma samples and 13 normal samples for LySeqST: A targeted sequencing assay for robust genomic classification of diffuse large B-cell lymphoma.

  Dataset EGAD50000002289

• Summary statistics from genome-wide association study in glioma of 12,488 cases and 18,169 controls.

  Genome-wide association studies (GWAS) have transformed our understanding of glioma susceptibility, but individual studies have had limited power to identify risk loci. We performed a meta-analysis of existing GWAS and two new GWAS, which totaled 12,488 cases and 18,169 controls. We identified five new loci for glioblastoma (GBM) at 1p31.3 (rs12752552; P = 2.04 × 10-9, odds ratio (OR) = 1.22), 11q14.1 (rs11233250; P = 9.95 × 10-10, OR = 1.24), 16p13.3 (rs2562152; P = 1.93 × 10-8, OR = 1.21), 16q12.1 (rs10852606; P = 1.29 × 10-11, OR = 1.18) and 22q13.1 (rs2235573; P = 1.76 × 10-10, OR = 1.15), as well as eight loci for non-GBM tumors at 1q32.1 (rs4252707; P = 3.34 × 10-9, OR = 1.19), 1q44 (rs12076373; P = 2.63 × 10-10, OR = 1.23), 2q33.3 (rs7572263; P = 2.18 × 10-10, OR = 1.20), 3p14.1 (rs11706832; P = 7.66 × 10-9, OR = 1.15), 10q24.33 (rs11598018; P = 3.39 × 10-8, OR = 1.14), 11q21 (rs7107785; P = 3.87 × 10-10, OR = 1.16), 14q12 (rs10131032; P = 5.07 × 10-11, OR = 1.33) and 16p13.3 (rs3751667; P = 2.61 × 10-9, OR = 1.18). These data substantiate that genetic susceptibility to GBM and non-GBM tumors are highly distinct, which likely reflects different etiology.

  Study EGAS00001003372

• Hi-C Profiling of Solid Tumor Samples

  Structural variants, such as translocations, inversions, duplications, and deletions, have long been recognized as mutations that can contribute to the initiation and progression of cancer. This can occur through a variety of mechanisms, including changes in gene dosage and the generation of fusion genes. In recent years, it is becoming increasingly clear that these events also can alter how genomes are organized in 3D space in the nucleus and contribute to changes in enhancer-promoter regulation. However, it remains poorly understand how often 3D genome structural changes occur in cancers, what genes are affected by these events, and in which tumor types. This study is part of ongoing work to better characterize 3D genome structural changes across a variety of tumor types to better understand where and when 3D genome structure changes as the result of structural variation in cancer genomes and to characterize the genes and tumor types affected.

  Study phs003227

• TCR Repertoire Sequencing to Evaluate the Diversity of Follicular Helper T Cells in HIV Infected Lymph Nodes

  The TCR repertoire of CD4+ T cells in human lymph nodes is a case-based analysis of the TCR repertoire of CD4+ T cells in human lymph nodes. The study aims to determine how HIV infection alters the repertoire complexity of follicular helper T cells (TFH) in relationship to other T cell subsets in the lymphoid compartment. This study performs TCR repertoire sequencing using Molecular Identifier Clustering-based Immune Repertoire Sequencing (MIDCIRS). We found TFH cells become clonally expanded and convergently selected in LNs from patients with chronic HIV infection.

  Study phs001548

• Circulating RNAs in Acute Heart Failure (CRUCIAL)

  The purpose of this American Heart Association-funded and NIH-funded study is to examine circulating RNAs in the acute congestive heart failure (CHF) setting, and how they change with decongestive therapy, and their function in vitro and in vivo. The investigators are testing the hypothesis that ex-RNA levels change significantly during decongestion therapy and can be used as a marker of those individuals who respond to CHF therapy (in terms of cardiac structure or outcome). Additionally, the translational research design allows the investigators to assay the effects of these RNAs on tissue phenotypes in vitro.

  Study phs003403

• Integrated Transcriptomic and Regulatory RNA Profiling Reflects Complex Pathophysiology and Uncovers a Conserved Gene Signature in End Stage Heart Failure RNA-Seq data

  Heart failure (HF) is a complex syndrome. Despite availability of multiple treatment options, the mortality remains high and the quality of life poor. Better understanding of the underlying pathophysiological processes can lead to development of novel therapies. Multiple comparative transcriptomics studies, which revealed gene level changes in the key pathophysiological pathways in failing hearts, point towards heterogeneity from interplay of disease stage, etiologies and ethnicity. Transcriptomic characterization of HF in patients from different ethnicities can potentially help in understanding the heterogeneity imparted by various factors and the core elements in heart failure.

  Study EGAS50000000810