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• A study of the molecular pathogenesis of Splenic Marginal Zone and Diffuse Large B-Cell Lymphoma

  We will perform exome sequencing on selected cases of splenic marginal zone lymphoma (SMZL) and diffuse large B-cell lymphoma (DLBCL) in order to characterise their genetic makeup and identify biomarkers for prognosis and prediction of treatment response.

  Dataset EGAD00001000410

• Best Endovascular vs. Best Surgical Therapy in Patients With Critical Limb Ischemia (BEST CLI-BioLINCC)

  Data Access NOTE Please refer to the “Authorized Access” section below for information about how access to the data from this accession differs from many other dbGaP accessions. Objectives To compare the effectiveness of surgical treatment to the effectiveness of endovascular treatment in adults with chronic limb-threatening ischemia who are eligible for both treatment options. Background Peripheral artery disease (PAD) affects more than 200 million people worldwide. A portion of those individuals develop chronic limb-threatening ischemia (CLTI). CLTI is associated with severe health outcomes. CLTI is defined by ischemic foot pain at rest, ischemic ulcerations, or gangrene. Treatment for CLTI includes revascularization to improve limb perfusion and limit the risk of amputation. However, the choice of surgery or endovascular therapy for revascularization varies greatly. The extent to which this variability affects clinical outcomes in patients with CLTI is unknown. The BEST-CLI trial was initiated to determine whether endovascular revascularization was superior to surgical revascularization in patients with CLTI. Participants A total of 1434 participants with a single segment of great saphenous vein comprised cohort 1. Of these, 718 participants were randomly assigned to the surgical treatment group and 716 participants were randomly assigned to the endovascular therapy group. A total of 396 participants needing an alternative conduit comprised cohort 2. Of these, 197 participants were randomly assigned to the surgical treatment group and 199 participants were randomly assigned to the endovascular therapy group. Design BEST-CLI was an international, randomized, open-label trial. Participants were assigned to one of two cohorts based on the availability of a single segment of great saphenous vein. Participants in both cohorts were randomly assigned to either surgery or endovascular therapy. Follow-up was performed at 30 days after the procedure, 3 months, 6 months, and every 6 months thereafter up to 84 months after randomization. Telephone visits in lieu of clinic visits were planned at 30 months and every 12 months thereafter and at the end of the trial. Participants were followed for major adverse cardiovascular events (myocardial infarction, stroke, or death from any cause), quality of life, level of pain, and performance on the six-minute walk test. The primary outcome was a composite of major adverse limb events or death from any cause. A major adverse limb event was defined as above ankle amputation of the index limb or a major index-limb reintervention (new bypass, interposition graft revision, thrombectomy, or thrombolysis). Conclusions Among patients with CLTI who had an adequate great saphenous vein for surgical revascularization (cohort 1), the incidence of a major adverse limb event or death was significantly lower in the surgical group than in the endovascular group. Among the patients who lacked an adequate saphenous vein conduit (cohort 2), the outcomes in the two groups were similar. Farber A, Menard MT, Conte MS, et al. Surgery or Endovascular Therapy for Chronic Limb-Threatening Ischemia. N Engl J Med. 2022;387(25):2305-2316. PMID 36342173

  Study phs003844

• Human Lung Tissue eQTL Study

  Genetic risks underlying respiratory diseases (e.g. COPD and asthma) are carefully studied by large genome-wide association studies (GWAS), where many loci were identified. In the post-GWAS era, the main challenge is to find the causal genes and pathways in GWAS-nominated chromosomal regions and to characterize etiology mechanism. The Lung eQTL Consortium is an international effort to systematically capture the genetic architecture of gene expression regulation in human lung. By studying lung specimens from 1,103 individuals of mostly European ancestry, we report a large number of genetic variants affecting gene expression in the lung, or lung expression quantitative trait loci (eQTL). These lung eQTLs will serve as an important resource to aid in the understanding of the molecular underpinnings of lung biology and its disruption in disease.

  Study phs001745

• Multimodal Mapping of the Immune Landscape in Human Pancreatic Cancer

  Pancreatic ductal adenocarcinoma (PDA) is characterized by an immune-suppressive tumor microenvironment that has rendered it largely refractory to immunotherapy. We used single-cell RNA sequencing on patient tumors and matched blood, and we uncovered a previously unappreciated, complex environment of immune-suppressive cellular interactions. These experiments reveal immune checkpoint expression heterogeneity on individual patient T cells, with corresponding ligands on neoplastic and myeloid cells. TIGIT was upregulated on tumor infiltrating CD8+ T cells and was the only checkpoint receptor consistently expressed by exhausted CD8+ T cells. Clinical annotation of the samples revealed that the exhausted signature is most prominent in patients with advanced stages of disease. Our findings suggest individualized combination therapy, involving anti-TIGIT therapies, may be necessary to extend the benefits of immunotherapy to pancreatic cancer patients.

  Study phs002071

• International Genetics of Parkinson Disease Progression (IGPP) Consortium: EPIPARK and HBS2 Cohorts

  EPIPARK and HBS2 cohorts were analyzed as part of the International Genetics of Parkinson Disease Progression (IGPP) Consortium. EPIPARK is a population-based cohort to study non-motor symptoms in parkinsonism in the city of Lübeck, Germany led by Drs. Meike Kasten and Christine Klein. HBS2 is a recently enrolled subset of participants in the Harvard Biomarkers Study led by Dr. Clemens Scherzer (www.bwhparkinsoncenter.org/biobank) of 89 participants with a diagnosis of Parkinson Disease (PD). Genotyping with Illumina Infinium Multi-Ethnic Genotyping Arrays (MEGA chip) was performed by Dr. Scherzer, Harvard Medical School and Brigham and Women’s Hospital. 179 participants with a diagnosis of PD from EPIPARK and 89 participants with a diagnosis of PD from HBS2 met Q/C criteria were analyzed.

  Study phs002328

• National Sleep Research Resource (NSRR): Hispanic Community Health Study/Study of Latinos

  The Hispanic Community Health Study / Study of Latinos (HCHS/SOL) is a multi-center epidemiologic study in Hispanic/Latino populations to determine the role of acculturation in the prevalence and development of disease, and to identify risk factors playing a protective or harmful role in Hispanics/Latinos. The study is sponsored by the National Heart, Lung, and Blood Institute (NHLBI) and six other institutes, centers, and offices of the National Institutes of Health (NIH) contributed to the first phase of the project. Raw polysomnography data are available from the HCHS/SOL Baseline visit and raw actigraphy data are available from the Sueño Ancillary visit. Primary HCHS/SOL data can be requested through dbGaP phs000810 Hispanic Community Health Study /Study of Latinos (HCHS/SOL).

  Study phs003543

• Single cell multi-omics analysis of chromothriptic medulloblastoma highlights genomic and transcriptomic consequences of genome instability

  Chromothripsis is a form of genome instability, whereby a presumably single catastrophic event generates extensive genomic rearrangements of one or few chromosome(s). However, little is known about the heterogeneity of chromothripsis across different clones from the same tumor, as well as changes in response to treatment. We analyzed single-cell genomic and transcriptomic alterations linked with chromothripsis in human p53-deficient medulloblastoma (n=7). We reconstructed the order of somatic events, identified early alterations likely linked to chromothripsis and depicted the contribution of chromothripsis to malignancy. We characterized subclonal variation of chromothripsis and its effects on double-minute chromosomes, cancer drivers and putatively druggable targets. Furthermore, we highlighted the causative role and the fitness consequences of specific rearrangements in neural progenitors.

  Study EGAS00001005410

• Single cell transcriptomics of human adrenal gland reveal chromosomal alterations in adrenocortical cells

  Adrenocortical cells get replenished throughout our lifetime and as such they are a cellular population of high interest in relation to adrenocortical tumours. Single cell transcriptomics of human adrenal gland were performed to identify rare subpopulations of cells, dynamics of cellular turnover and clone expansions in the adrenal cortex. The adrenal gland of this particular individual is characterized by the presence of mutant clone charecterized by aneuploidy in chromosomes 8, 9, 13 and 22, occupying the zona glomerulosa and zona fasciculata. Differential expression analysis of the mutant cells revealed upregulation of MC2R (adrenocorticotropic hormone receptor), CYP21A2, HSD3B2 genes (enzymes involved in cortisol production). Overall, this donor sample is an example of clonal tissue expansions carrying chromosomal rearrangements that likely impact organ morphology and function but are seemingly benign.

  Study EGAS00001007488

• Persistent Mutation Burden Drives Sustained Anti-Tumor Immune Responses

  Tumor mutation burden is an imperfect proxy of tumor foreignness and has therefore failed to consistently demonstrate clinical utility in predicting responses in the context of immunotherapy. We evaluated mutations in regions of the genome that are unlikely to undergo loss and discovered that clonal mutations in single-copy regions and those present in multiple copies per cell constitute a persistent tumor mutation burden (pTMB) that is linked with therapeutic response to immune checkpoint blockade. Persistent mutations were retained in the context of tumor evolution under selective pressure of immunotherapy and tumors with a high pTMB content were characterized by a more inflamed tumor microenvironment. pTMB imposes an evolutionary bottleneck that cancer cells cannot overcome and may thus drive sustained immunologic tumor control in the context of immunotherapy.

  Study EGAS00001006660

• Maintenance of Brain Tumor Profile on Organotypic Brain Slice Culture (OBSC)

  We used uncultured tumor resection tissue from an NF2 mutation-driven grade II meningioma (MG-II) to investigate whether tumors engrafted onto organotypic brain slice cultures (OBSCs) maintained the genetic profile of the parent tumor. We prepared three groups of samples for whole exome sequencing (WES) from the same pool of dissociated MG-II tissue. Group HT is the original uncultured human tumor tissue (n = 3). Group CL is the parent tumor tissue expanded in standard in vitro cell culture until the minimum number of cells required for WES had grown. Because of initial cell loss and subsequent clonal expansion, this required six passages over the span of approximately one month (n = 3). Group BSHT is the uncultured tumor resection tissue engrafted onto OBSCs and subsequently dissected from the OBSCs at the conclusion of our standardized assay length (4 days; n = 4). WES analysis showed that tumor tissue engrafted onto OBSCs maintained a significant genetic resemblance to the parent tumor, while tumor tissue expanded in vitro displayed a distinctly different profile. Furthermore, the mutational profiles of all four BSHT biological replicates were markedly similar, indicating that each OBSC-engrafted tumor indeed contained a representative sample of the original patient tumor. A closer look at the hallmark NF2 mutations existing within all samples revealed that while all samples from the original tumor (HT1-3) and the OBSC-engrafted tumor (BSHT1-4) maintain the frame shift deletion at V24, this mutation was lost in all samples expanded in vitro (CL1-3) and replaced by mutations in other areas. Together, this data suggests that the rapid assay design and tumor-accommodating niche of our OBSC platform enables effective maintenance of the original patient tumor profile. The BBsplit algorithm from the BBtools suite was run on all samples to eliminate rat DNA contamination in the BSHT samples as well as to account for any biases that may result as a part of that process. Only the reads that were binned to the human reference were used for subsequent analysis. Reads were then mapped to the GRCh38 version of the human genome with BWA v0.7.17 and realigned together with ABRA2 v.23. Quality control was implemented using the GATK/Picard v4.1.7.0 toolkit. Somatic variants were called for each sample using the MuTect2 algorithm v4.1.7.0. Variants were merged into a single cohort variant call file and then converted to MAF via vcf2maf v1.6.21 tool. Variants were annotated using VEP v87. To identify mutations with potentially high biological impact, multiple filtering steps were applied to somatic mutation calling. First, we selected only the somatic variants that passed all filters from the MuTect2 FilterMutectCalls algorithm and second, only high/moderate impact (change coding) variants as defined by the VEP annotation were further analyzed. Over 1900 single nucleotide variants (SNVs) were detected across all samples. Figures that summarized the results were generated using maftools.

  Study phs003268