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• Accelerating Medicines Partnership-Systemic Lupus Erythematosus (AMP-RA/SLE)

  This project is analyzing tissue and blood samples from people with rheumatoid arthritis (RA) and lupus to pinpoint genes, proteins, chemical pathways, and networks involved at a single cell level. This type of modular, molecular analysis will allow comparisons across the diseases and will provide insights into key aspects of the disease process. The project will identify differences between those RA patients who respond to therapies and those who do not, as well as provide a better systems level understanding of disease mechanisms in both RA and lupus. This knowledge is essential for the development of targeted therapies and for the application of existing and future therapies to appropriate patient populations. Additional datasets can be accessed through ImmPort (http://www.immport.org/immport-open/public/home/studySearch), accession: SDY997

  Study phs001459

• Genomic sequencing of Pediatric Rhabdomyosarcoma

  Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma of childhood accounting for approximately 350 newly diagnosed cases yearly in the United States. With the development of multimodal chemotherapy regimens, relapse-free survival rates have improved to 70-80% in patients with localized disease albeit with significant toxicity. Unfortunately, despite aggressive treatment, patients with metastatic or recurrent disease continue to suffer from high mortality. Further characterization of the genetic events underlying this tumor type is critical for the development of more effective diagnostic, prognostic and therapeutic strategies. In a collaborative effort between the National Cancer Institute, the Children's Oncology Group, and the Broad Institute, we use a combination of whole-genome and whole-exome sequencing to characterize the landscape of somatic alterations in 147 tumor/normal pairs.

  Study phs000720

• Accelerating Medicines Partnership-Rheumatoid Arthritis (AMP-RA/SLE)

  This project is analyzing tissue and blood samples from people with RA and lupus to pinpoint genes, proteins, chemical pathways, and networks involved at a single cell level. This type of modular, molecular analysis will allow comparisons across the diseases and will provide insights into key aspects of the disease process. The project will identify differences between those RA patients who respond to therapies and those who do not, as well as provide a better systems level understanding of disease mechanisms in both RA and lupus. This knowledge is essential for the development of targeted therapies and for the application of existing and future therapies to appropriate patient populations. Additional datasets can be accessed through ImmPort (http://www.immport.org/immport-open/public/home/studySearch), accession: SDY998, SDY999.

  Study phs001457

• Adeno-associated virus in the liver: natural history and consequences in tumor development

  Adeno-associated virus (AAV) is a defective mono-stranded DNA virus, endemic in human population (40-80%). AAV infection has long been considered as non-pathogenic1, however few years ago we reported for the first time recurrent clonal AAV2 insertion in the pathogenesis of human hepatocellular carcinoma (HCC) developed on normal liver. These clonal viral insertions target cancer driver genes, including CCNA2, CCNE1, TERT, TNFSF10 and MLL4, leading to their overexpression. The viral inserted sequences involved in almost all the cases the 3’ inverse tandem repeat (ITR) of AAV2, which is important for virus integration in host DNA and exhibits a promoter/enhancer activity. Here, we used RNA sequencing (RNA-seq) to investigate their functional impact on the tissue, such as fusion transcript generation events.

  Study EGAS00001003310

• Small_molecule_inhibitors_in_melanoma___Kenski___Kong___WES

  Small-molecule inhibitors targeting the most commonly activated pathway in melanoma, MAPK pathway (either alone or in combination) are already given to melanoma patients for few years, and initially reduce tumour burden dramatically, eventually melanomas become resistant and tumours progress while on treatment. Resistance to this treatment occurs by acquisition of additional mutations or other alterations that affect the mitogen-activated protein kinase (MAPK) pathway by either direct or indirect signalling. Many resistance mechanisms somehow lead to reactivation of extracellular signal-regulated kinase (ERK), thereby restoring signalling of the oncogenic BRAF/MEK/ERK pathway. In addition, PI3K pathway activation contributes to resistance to BRAF inhibition. Less frequent but equally important to the phenomenon of targeted drug resistance is the observation that B15–20% of BRAF mutant melanoma patients fail to respond to BRAF inhibition already early on treatment, owing to intrinsic resistance. These patients have little therapeutic options, unless immunotherapy can be given. To better understand the resistance mechanisms in MAPK inhibitor-treated melanoma patients and melanoma biology, our lab generated a big panel of MAPK inhibitor resistant melanoma cell lines by continuous drug exposure. The understanding of the genetic landscape and gene expression as well as cross resistance to other treatment regimens, and other aspects of melanoma biology such as phenotype switch, will allow us to better exploit new therapeutic strategies for melanoma patients.

  Study EGAS00001002863

• Genome wide variation in the Angolan Namib desert reveals unique Pre-Bantu ancestry

  The populations of the Angolan Namib Desert have been largely neglected in previous surveys of the genomic landscape of southern Africa. Although at present, the Namib is culturally dominated by Southwest Bantu-speaking cattle-herders, the region exhibits an extraordinary ethnographic diversity which includes an array of semi-nomadic peoples whose subsistence strategies fall outside the traditional division between foraging and food production and can thus be referred to as “peripatetic”. Among these small-scale populations are the last speakers of the Kwadi branch of the Khoe-Kwadi language family associated with the introduction of pastoralism into southern Africa (Kwepe), as well as a range of groups whose origins remain enigmatic (Kwisi, Twa and Tjimba). Using genome-wide data from 208 individuals belonging to nine ethnically diverse groups from the Angolan Namib and adjacent areas (Kwepe, Kwisi, Twa, Tjimba, !Xun, Kuvale, Himba, Nyaneka, Ovimbundu) in combination with published data from other regions of Africa, we reconstruct in detail the histories of contact emerging from pre-historic migrations to southern Africa and show that peripatetic groups from southwestern Angola stand out for exhibiting elevated levels of an unique, regionally-specific and highly divergent Pre-Bantu ancestry. These findings highlight the importance of the Namib for understanding the deep genetic structure of Africa.

  Study EGAS00001007011

• RNA-seq dataset of patient and healthy donors

  RNA-seq dataset on a patient (P) presenting with defects of immunity and three healthy donors (C1, C5, C6). This dataset contains raw and processed files from RNA-seq transcriptome analysis performed according to the Smart-seq2. There are 24 single-read (50 bp) fastq files, 6 per patient/donor consisting of 2 cell types and 3 replicates per cell type. There is one count matrix file generated using featureCounts against Ensembl v98 gene models.

  Dataset EGAD00001008371

• NHLBI TOPMed: Study of Asthma Phenotypes and Pharmacogenomic Interactions by Race-Ethnicity (SAPPHIRE)

  Started in 2007, the Study of Asthma Phenotypes and Pharmacogenomic Interactions by Race-ethnicity (SAPPHIRE) is one of the largest asthma cohort studies in the United States. Its overarching goal is to elucidate the genetic underpinnings of asthma and asthma medication treatment response. The cohort was recruited from a large health care system serving southeast Michigan and the Detroit metropolitan area, and the participants broadly represent the demographic and socioeconomic diversity of the region. Control participants (i.e., patients without a diagnosis with asthma) were recruited from the same health system and geographic region. By virtue of their health system enrollment, both asthma case and control patients have longitudinal clinical information which was routinely collected as part of their care. Both case and control patients underwent at detailed evaluation at the time of enrollment which included lung function testing and bronchodilator response. The SAPPHIRE cohort is a member of the Asthma Translational Genomics Collaborative (ATGC). The latter was selected for whole genome sequencing in Phase 3 of the National Heart Lung and Blood Institute's TOPMed Program. The SAPPHIRE sample selected for sequencing includes African American and/or Latino individuals with and without asthma.

  Study phs001467

• A small cell lung cancer genome reports complex tobacco exposure signatures

  Cancer is driven by mutation. Worldwide, tobacco smoking is the major lifestyle exposure that causes cancer, exerting carcinogenicity through 60 chemicals that bind and mutate DNA. Using massively parallel sequencing technology, we sequenced a small cell lung cancer cell line, NCI-H209, to explore the mutational burden associated with tobacco smoking. 22,910 somatic substitutions were identified, including 132 in coding exons. Multiple mutation signatures testify to the cocktail of carcinogens in tobacco smoke and their proclivities for particular bases and surrounding sequence context. Effects of transcription-coupled repair and a second, more general expression-linked repair pathway were evident. We identified a tandem duplication that duplicates exons 3-8 of CHD7 in-frame, and another two lines carrying PVT1-CHD7 fusion genes, suggesting that CHD7 may be recurrently rearranged in this disease. These findings illustrate the potential for next-generation sequencing to provide unprecedented insights into mutational processes, cellular repair pathways and gene networks associated with cancer.

  Study EGAS00000000051

• Single cell epigenomic study of H3-K27M mutant diffuse midline glioma across age and location

  Histone 3 lysine27-to-methionine (H3-K27M) mutations most frequently occur in childhood diffuse midline gliomas (DMGs) of the pons, but are also increasingly recognized in adult DMGs. Their potential heterogeneity at different ages and midline locations are vastly understudied. Here, through dissecting the single-cell epigenomic architectures of a comprehensive cohort of patient H3-K27M DMGs, we delineate how age and anatomical location shape glioma cell-intrinsic and -extrinsic features in light of the shared driver mutation. We analyzed the open chromatin profiles of 8 tumors utilizing the single-cell/nucleus assay for transposase-accessible chromatin using sequencing (snATAC-seq)

  Study EGAS00001007035