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• Pathogenesis and Immunity in Endemic Burkitt Lymphoma

  This genomic landscape of Burkitt lymphoma represents a multimodal sequencing of tumors and control tissues and individuals to better understand the etiology, and molecular pathogenesis of Burkitt lymphoma including the roles of the associated Plasmodium falciparum malaria and EBV infections. Comprehensive sequencing set includes genomic, transcriptomic, and epigenomic datasets in concert with variable clinical phenotypes and outcome information such as anatomical presentation site, in-hospital survival rates, and EBV genome type. This deposit includes additional small RNA-seq data from endemic BL (eBL) tumors and RNA-sequencing data from sorted NK cell subsets from the peripheral blood of eBL patients. The additional small RNA-seq data are from tumor specimens from 17 eBL cases, of the previously deposited polyA RNA-seq data from 28 eBL cases (phs1282.V1). The additional RNAseq data from Fluorescence-activated cell sorting (FACS) of NK cell subsets, isolated from the peripheral blood of 7 eBL cases. The additional RNAseq data are from eBL tumor samples of 5 eBL cases, BL cell lines established from these tumor samples and also NSG mouse tumors created by implanting the established BL cell lines into NSG mice. The dataset also includes RNAseq data of the NSG mouse tumors after treatment with Rituximab (RIT) and Phosphate buffered saline (PBS). The fifth batch of data includes mRNA-seq from different passages of a single eBL cell line that have variable EBV phenotypes (low passage with lytic EBV and high passage with latent EBV). This batch also includes lytic and latent lymphoblastoid cell line (LCL) clones from a single blood donor generated through infection with the strain of EBV isolated from the aforementioned eBL cell line. For initial transcriptome analysis see: Kaymaz et al. "Comprehensive Transcriptome and Mutational Profiling of Endemic Burkitt Lymphoma Reveals EBV Type-specific Difference." Molecular Cancer Research, 2017, PMID: 28465297. For initial microRNA analysis see: Oduor et al. "Human and Epstein-Barr Virus miRNA Profiling as Predictive Biomarkers for Endemic Burkitt Lymphoma." Frontiers in Microbiology 8, 2017, PMID: 28400759. For initial NK subsets RNA expression analysis see: Forconi et al. "A new hope for CD56negCD16pos NK cells as unconventional cytotoxic mediators: an adaptation to chronic diseases." Frontiers in Cellular and Infection Microbiology, 2020, PMID: 32373555.For initial eBL cell line and mouse avatar RNA expression analysis see: Saikumar et al. "Endemic Burkitt lymphoma avatar mouse models for exploring inter-patient tumor variation and testing targeted therapies." Life Science Alliance, 2023, PMID: 36878637. For general overview of cohort study see: Buckle et al. "Factors influencing survival among Kenyan children diagnosed with endemic Burkitt lymphoma between 2003 and 2011: A historical cohort study." Int J Cancer. 15:1231, 2016, PMID: 27136063.

  Study phs001282

• Androgen deprivation therapy promotes an inflammatory and obesity-like microenvironment in periprostatic fat

  Prostate cancer is a leading cause of cancer-related death and morbidity worldwide. Androgen deprivation therapy (ADT) is the cornerstone of management for advanced disease. The use of androgen deprivation therapies is associated with multiple side effects, including metabolic syndrome and truncal obesity. At the same time, obesity has been associated with both prostate cancer development and disease progression, linked to its effects on chronic inflammation at a tissue level. The connection between androgen deprivation therapy, obesity, inflammation, and prostate cancer progression is well-established in clinical settings; however, an understanding of the changes in adipose tissue at the molecular level induced by castrating therapies is missing. Here we investigated the transcriptional changes in periprostatic fat tissue induced by profound androgen deprivation therapy in a group of patients with high-risk tumours compared to a matching untreated cohort. We find that androgen deprivation therapy is associated with a pro-inflammatory and obesity-like adipose tissue microenvironment. This study suggests that the beneficial effect of androgen deprivation therapy may be partially counteracted by metabolic and inflammatory side effects in the adipose tissue surrounding the prostate.

  Study EGAS00001003286

• Vanderbilt Genome-Electronic Records (VGER) Project: QRS Duration

  An important potential enabling resource for Personalized Medicine is the combination of a DNA repository with Electronic Medical Record (EMR) systems sufficiently robust to provide excellence in clinical care and to serve as resources for analysis of disease susceptibility and therapeutic outcomes across patient populations. The Vanderbilt EMR is a state of the art clinical and research tool (that includes >1.7 million records), and is associated with a DNA repository which has been in development for over 3 years; these are the key components of VGER, the Vanderbilt Genome-Electronic Records project, a part of NHGRI's eMERGE network. The VGER model acquires DNA from discarded blood samples collected from routine patient care, and can link these to de-identified data extracted and readily updated from the EMR. The phenotype we analyze here is the QRS duration on the electrocardiogram, since slow conduction (indicated by longer QRS duration) is a marker of arrhythmia susceptibility.

  Study phs000188

• Whole-Genome Sequencing of a Healthy Aging Cohort.

  Studies of long-lived individuals have revealed few genetic mechanisms for protection against age-associated disease. Therefore, we pursued genome sequencing of a related phenotype-healthy aging-to understand the genetics of disease-free aging without medical intervention. In contrast with studies of exceptional longevity, usually focused on centenarians, healthy aging is not associated with known longevity variants, but is associated with reduced genetic susceptibility to Alzheimer and coronary artery disease. Additionally, healthy aging is not associated with a decreased rate of rare pathogenic variants, potentially indicating the presence of disease-resistance factors. In keeping with this possibility, we identify suggestive common and rare variant genetic associations implying that protection against cognitive decline is a genetic component of healthy aging. These findings, based on a relatively small cohort, require independent replication. Overall, our results suggest healthy aging is an overlapping but distinct phenotype from exceptional longevity that may be enriched with disease-protective genetic factors.

  Study EGAS00001002306

• Combined clinical and gene expression score identifies high-risk individuals among follicular lymphoma patients on immunotherapy

  Follicular lymphoma (FL) is usually an indolent malignant B-cell lymphoma, but at least 30% of the patients experience transformation to Diffuse Large B-cell Lymphoma (DLBCL) with inferior survival. Early identification of patients with poor prognosis is essential for tailoring treatment. Here, we describe a network-based integrative analysis of 168 FL-biopsies from 127 patients with long clinical follow-up and transformation status. A distinct shift in expression towards a DLBCL expression phenotype is observed in BTK associated genes in cases with transformation. This shift is present years prior to transformation. An integrated score combining the BTK score and a clinical index is proposed, termed the BTK-FLIPI score. It identifies patients (16%) with very poor prognosis, with median time to progression 21.7 months (95% CI: 14.3-42.6) versus 70.9 months (95% CI: 41.5-95.0) for the remainder. The results suggest BTK as a potential target for treatment of high-risk FL-patients.

  Study EGAS00001002566

• Genomic analysis of a hypermutated gliosarcoma

  Gliosarcoma is a variant of glioblastoma with equally poor prognosis and characterized by mixed glial and mesenchymal pathology. Metastasis is not uncommon but involvement of the spinal cord is rare, and comprehensive genetic characterization of spinal gliosarcoma is lacking. We describe a patient initially diagnosed with a low-grade brain glioma via biopsy, followed by adjuvant radiation and temozolomide treatment. Nearly two years after diagnosis, she developed neurological deficits from an intradural, extramedullary tumor anterior to the spinal cord at T4, which was resected and diagnosed as gliosarcoma. Whole-exome sequencing (WES) of this tumor revealed a hypermutated phenotype, characterized by somatic mutations in key DNA mismatch repair (MMR) pathway genes, an abundance of C>T transitions within the identified somatic SNVs, and microsatellite stability, together consistent with temozolomide-mediated hypermutagenesis. This is the first report of a hypermutator phenotype in gliosarcoma, which may represent a novel genomic mechanism of progression from lower-grade glioma.

  Study EGAS00001004864

• The Proteogenomic Subtypes of Acute Myeloid Leukemia

  Acute myeloid leukemia (AML) is an aggressive blood cancer with poor prognosis. We report a comprehensive proteogenomic analysis of bone-marrow biopsies from 252 uniformly treated AML patients to elucidate the molecular pathophysiology of AML in order to inform future diagnostic and therapeutic approaches. In addition to in-depth quantitative proteomics, our analysis includes cytogenetic profiling and DNA/RNA sequencing. We identify five proteomic AML subtypes, each reflecting specific biological features spanning genomic boundaries. Two of these proteomic subtypes correlate with patient outcome, but none are exclusively associated with specific genomic aberrations. Remarkably, one subtype (Mito-AML), which is only captured in the proteome, is characterized by high expression of mitochondrial proteins and confers poor outcome, with reduced remission rate and shorter overall survival upon treatment with intensive induction chemotherapy. Functional analyses reveal that Mito-AML is metabolically wired towards stronger complex I dependent respiration and is more responsive to treatment with the BCL2 inhibitor venetoclax.

  Study EGAS00001005950

• RB1 Loss Triggers Dependence on ESRRG in Retinoblastoma

  Retinoblastoma (Rb) is a deadly childhood eye cancer that is classically initiated by inactivation of the RB1 tumor suppressor. Clinical management continues to rely on nonspecific chemotherapeutic agents that are associated with treatment resistance and toxicity. Here, we analyzed whole exomes from primary Rb tumors to identify novel Rb dependencies. Several recurrent genomic aberrations implicate estrogen-related receptor gamma (ESRRG) in Rb pathogenesis. ESRRG is an essential mediator of hypoxic adaptation and cell survival in retinoblastoma, representing a promising new therapeutic target.

  Study phs002859

• Longitudinal Assessment of Methylmercury and Gut Microbes During Pregnancy

  Methylmercury is a potent neurotoxin, and the fetal period is the most vulnerable exposure period. There is significant variability in methylmercury metabolism, which has been attributed to differences in the structure and function of the gut microbiome. Our main objective was to better understand the interplay between gut microorganisms and methylmercury metabolism during pregnancy. To address this aim, associations were investigated between maternal biomarkers (blood, hair, stool) for prenatal methylmercury exposure and maternal gut microbiota during early and late gestation.

  Study phs001768

• Epigenetic memory of SARS-CoV-2 mRNA vaccination in monocyte-derived macrophages

  Immune memory is key to effective antimicrobial responses, but the impact of mRNA vaccines on this process is not fully understood. Our research shows that SARS-CoV-2 mRNA vaccines alter the epigenetic profile of human macrophages, specifically enhancing histone acetylation, which is linked to immune training. Significant epigenetic changes, along with increased cytokine release, require two vaccine doses. However, these effects diminish over time but can be restored with a booster dose six months later, maintaining a strong pro-inflammatory response.

  Study EGAS50000000341