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• ICGC PCAWG Dataset: OV-AU_PCAWG_RNA-Seq_TopHat2

  ICGC PCAWG Dataset for RNA-Seq BAM aligned using TopHat2. Project: OV-AU.

  Dataset EGAD00001003416

• ICGC PCAWG Dataset: LIRI-JP_PCAWG_RNA-Seq_TopHat2

  ICGC PCAWG Dataset for RNA-Seq BAM aligned using TopHat2. Project: LIRI-JP.

  Dataset EGAD00001003546

• Genomic Landscape of Chordoid Glioma

  This data set consist genomic information of 10 Chordoid Glioma samples: - Exome sequencing: 10 tumors and matched normal DNA for four of them (BAM files) - RNAseq : 10 tumors (fastq files) - CNV array: 9 tumors (IDAT files)

  Dataset EGAD00001004112

• SNV vcf files for CPCG Subclonal Heterogeneity in multiple and single regions

  SNV calls generated using the MuTect-TITAN-PhyloWGS from the CPC-GENE Subclonal Heterogeneity study using single and multiple regions

  Dataset EGAD00001004433

• ICGC PCAWG Dataset: LAML-KR_PCAWG_WGS_BWA

  ICGC PCAWG Dataset for WGS BAM aligned using BWA MEM. Project: LAML-KR.

  Dataset EGAD00001002119

• ICGC PCAWG Dataset: BTCA-SG_PCAWG_WGS_BWA

  ICGC PCAWG Dataset for WGS BAM aligned using BWA MEM. Project: BTCA-SG.

  Dataset EGAD00001002121

• ICGC PCAWG Dataset: BRCA-UK_PCAWG_WGS_BWA

  ICGC PCAWG Dataset for WGS BAM aligned using BWA MEM. Project: BRCA-UK.

  Dataset EGAD00001002122

• ICGC PCAWG Dataset: PAEN-IT_PCAWG_WGS_BWA

  ICGC PCAWG Dataset for WGS BAM aligned using BWA MEM. Project: PAEN-IT.

  Dataset EGAD00001002153

• Exploration of neuroblastoma xenograft models for tumor extracellular RNA profiling in murine blood plasma

  Total RNA sequencing (SMARTer Stranded Total RNA-Seq Kit v2) data of extracellular RNA (exRNA) from liquid biopsies of neuroblastoma xenograft models.

  Dataset EGAD00001010905

• Bulk RNA from sorted CD8+ T cells after 48h co-culture with human Mito-DsRed MSCs.

  For human samples, total cellular RNA was isolated from post-sorted Mito+ and Mito CD8+ cells using the RNeasy Mini Kit (Qiagen). Stranded RNA libraries were created using SMARTSeq Stranded.

  Dataset EGAD00001011082

• ICGC PCAWG Dataset: CMDI-UK_PCAWG_WGS_BWA

  ICGC PCAWG Dataset for WGS BAM aligned using BWA MEM. Project: CMDI-UK.

  Dataset EGAD00001002664

• BLUEPRINT DNA methylation profiles of human hematopoietic progenitors

  DNA methylation was analyzed for stem/progenitor cell types and terminally differentiated cell types of the human blood lineage (HSC, MPP, CMP, MEP, GMP, CLP, MLP0, MLP1, MLP2, MLP3, MK, CD4+ Tcell, CD8+ Tcell, Bcell, NK, Neut, Mono).

  Dataset EGAD00001002732

• Benchmarking CRISPR Whole-genome Drop-out Screen - B&S (2019-08-07)

  This study is a benchmarking exercise to explore potential source of variation between different CRISPR drop out libraries. . This dataset contains all the data available for this study on 2019-08-07.

  Dataset EGAD00001005233

• SF11979 snATAC seq IDHR132H Wildtype GBM Female

  SF11979 snATAC, IDHR132H WT GBM Female, 76 Single Nuclei ATAC seq data from high grade human glioma samples. NovaSeq6000 was used for ATAC seq. The files uploaded are bam files created with grch38 reference.

  Dataset EGAD00001005418

• Multi-region sequencing of a RET fusion positive cancer patient

  Deep WGS sequencing (160x) of 2 different sites of disease of a patient with a RET fusion positive cancer. Amplicon sequencing of 19 other sites of the same patients for the RET fusion.

  Dataset EGAD00001005776

• Dataset for RNA and Exome sequencing of Glioblastoma samples

  This dataset contains RNA Seq, 10x scRNA Seq and Exome sequencing of glioblastoma samples. Sequencing was performed on a Illumina NovaSeq 6000 and Illumina HiSeq 4000. The sequencing was always paired.

  Dataset EGAD00001012235

• HV31 - PacBio long-read circular consensus (CCS) senquencing

  PacBio long-read circular consensus (CCS) sequencing data for individual HV31 generated on PacBio Sequel II instrument, using size-selected (10-15 kb) DNA from CD14+ monocytes, to a sequencing depth of ~12×. Sequencing was performed at the Wellcome Sanger Institute.

  Dataset EGAD00001006979

• Exome sequencing data for 40 cases of alopecia areata and vitiligo

  Sequencing of independent unrelated cases of alopecia areata (total/ universal) and vitiligo (>10%, affected family member). DNA obtained from blood

  Study EGAS00001003831

• The Melbourne Urological Research Alliance (MURAL) Collection of Patient-Derived Models of Prostate Cancer

  1. Low-Dose Carboplatin Modifies the Tumor Microenvironment to Augment CAR T Cell Efficacy in Human Prostate Cancer Models.Single-cell RNA sequencing (scRNA-seq) was performed to analyze the transcriptional modifications in the tumor microenvironment of prostate cancer patient-derived xenografts (PDX). The analyzed PDX tumor was PDX-287R from the MURAL collection of PDXs (PMID: 34413304). Mice harboring PDX tumors were treated with the carboplatin chemotherapy, and tumors were harvested 3 weeks later. RNA sequencing (RNA-Seq) was used to define immune and non-immune cell populations and anti-tumor innate immune signaling within the tumor microenvironment.To investigate the response of tumor cells to carboplatin treatment in more detail, RNA-Seq was performed on FACs-isolated tumor cells from PDX-287R at one week post-treatment. Gene set enrichment analysis showed an enrichment for apoptotic pathways, with significantly increased expression of the pro-apoptotic genes FAS, BAX, BBC3, IFI6, and JUN. Previously, carboplatin has been shown to activate the cGAS/STING pathway, and here we also found an increase in STING signaling, with an enrichment for the cytosolic DNA sensing pathway and increased expression of STING1, STAT1 and STAT2. There was also a significant increase in the expression of genes involved in T cell chemotaxis, including CXCL10, CXCL11, and CCL20. Collectively, carboplatin-induced cell death in tumor cells likely initiated a pro-inflammatory phenotype in prostate cancer PDXs.2. Co-Targeting BET, CREBBP, and EP300 Inhibits Neuroendocrine Signaling in Androgen Receptor-Null Prostate Cancer.The landscape of castration-resistant prostate cancer (CRPC) is characterized by a multitude of phenotypes, among which neuroendocrine disease holds a prominent position, each displaying unique responses to therapeutic interventions. The efficacy of inhibitors targeting BET and CREBBP/EP300 in prostate cancer treatment is widely acknowledged, primarily due to their ability to attenuate androgen receptor (AR) signaling. However, the effectiveness of these inhibitors in prostate cancers devoid of AR remains uncertain.This investigation sought to elucidate the role of BRD4, CREBBP, and EP300, which are co-expressed in both AR-positive and AR-null prostate cancer. Our study revealed that a compound targeting all three proteins, NEO2734, exhibited efficacy in suppressing the growth of organoids from both AR-positive and AR-null tumors, as evidenced by alterations in viability, size, and cellular composition. Furthermore, NEO2734 treatment consistently led to transcriptional downregulation of cell cycle pathways across various models. In the context of neuroendocrine prostate cancer (NEPC), NEO2734 demonstrated notable efficacy. Treatment with NEO2734 resulted in decreased expression of ASCL1 and other neuroendocrine markers (including SYP) , accompanied by a reduction in tumor growth in vivo. These findings collectively underscore the potential of epigenome-targeted inhibitors in impeding the growth of neuroendocrine prostate cancer, by disrupting lineage regulators in a phenotype-dependent manner. Consistent with the NEPC organoids and explants, NKX3-1 was upregulated in NEO2734-treated PDXs.In this study, we examined the impact of NEO2734 treatment on 6 organoids (treated for 24 hrs), 3 explants treated with JQ1 (for 48 hrs) and 2 PDXs (at two time points) using bulk RNA sequencing (RNA-Seq). These results are available through this dbGaP submission. The implications of these results warrant further exploration and development of compounds possessing similar activities for clinical applications. The ability of NEO2734 to mitigate the growth of both AR-positive and AR-null prostate cancer underscores its potential as a versatile therapeutic agent. Moreover, its efficacy in targeting neuroendocrine phenotypes offers promising avenues for addressing a subtype of CRPC that poses significant clinical challenges. In conclusion, this study sheds light on the intricate interplay between epigenetic regulators and prostate cancer phenotypes. The observed effects of NEO2734 on growth inhibition and phenotype-specific disruption highlight the importance of continued research into compounds with similar epigenome-targeting mechanisms for advancing precision medicine approaches in the treatment of prostate cancer.3. Defining Focal Neuroendocrine Differentiation as a Transcriptionally Distinct Form of Prostate Cancer Pathology Characterized by the Expression of Androgen ReceptorsThe study aimed to understand the transcriptional differences among different neuroendocrine pathologies of prostate cancer. The study hypothesized that the diverse neuroendocrine pathology observed in prostate might be attributable to differences in transcriptional level that remain hidden in bulk RNA-Seq data. To investigate, we employed scRNA-seq to generate gene expression profiles of 18,632 individual tumor cells from 9 PDX models representing five distinct neuroendocrine pathologies of prostate cancer. Our analysis identified 3-8 transcriptionally distinct sub-populations per PDX. The expression of key oncogenic signaling pathways and master regulator activity varied across in neuroendocrine pathologies, with each type of pathology displaying a unique set of transcriptional sub-populations. We discovered that, like the amphicrine pathology, focal neuroendocrine differentiation (focal NED) cells maintain androgen receptor (AR) signaling. However, the expression profiles of focal NED cells differed from the other pathologies, indicating it should be considered as a distinct type of neuroendocrine pathology in prostate cancer. Analysis of copy number alterations suggested little clonal divergence between focal NED cells and neighboring adenocarcinoma cells, emphasizing the transcriptional distinctiveness of focal NED.Overall, the findings suggest potential differences in treatment approaches for tumors from prostate cancer patients showing neuroendocrine pathology, especially focal NED.4. Reprogramming of Androgen Receptor Activity in Castration-Resistant Prostate Cancer is Shaped by Truncated Variants.Under the influence of treatments that target the androgen receptor (AR) axis, prostate cancer cells undergo various changes to the AR gene. This includes the production of truncated AR variants that lack the ligand binding domain and are constitutively active. However, the exact role of these truncated variants in shaping the AR signaling axis and their importance in therapy resistance is not yet fully understood. By examining the AR cistrome in a group of patient-derived prostate cancer models with different mechanisms of castration resistance, we observed diverse changes in AR activity in metastatic prostate cancer, including castration-resistant models. Specifically, we identified a unique subset of tumors characterized by the expression of ARv567es, a variant resulting from structural rearrangements of the AR gene. Tumors positive for ARv567es showed a distinct AR binding profile and epigenome compared to those without ARv567es, which was linked to an altered transcriptional profile. The presence of ARv567es is associated with poor responses to treatments, such as castration and bipolar androgen therapy (BAT), regardless of the presence of full-length AR. This involves disruption of the autoregulatory loop that controls AR gene transcription and reduced transcriptional responses to treatment. Overall, this study demonstrates that ARv567es can lead to transcriptional reprogramming in advanced prostate cancer and drive therapy resistance. 5. The MURAL Collection of Prostate Cancer Patient-Derived Xenografts Enables Discovery Through Preclinical Models of Uro-Oncology.We created a comprehensive PDX resource for prostate cancer to facilitate the rapid and systematic evaluation of new therapies. This collection includes 59 tumors from 30 patients, gathered between 2012 and 2020, aligning with the availability of abiraterone and enzalutamide in the clinic. The PDXs cover the clinical, pathological, and genomic spectrum of prostate cancer, ranging from treatment-naïve primary tumors to castration-resistant metastases. We characterized heterogeneity in adenocarcinoma and neuroendocrine phenotypes using bulk and single-cell RNA sequencing. Additionally, organoids were cultured from PDXs, enhancing our preclinical study capabilities. Employing a 1x1x1 design, we quickly identified tumors with responses to combination therapies. To manage the distribution of PDXs, we established the Melbourne Urological Research Alliance (MURAL). This PDX collection significantly enhances our ability to test and prioritize effective treatments for future clinical trials in prostate cancer.6. Prostate Cancer Associated Fibroblasts Have Distinct Morpho-Mechanical Features That Are Associated With Patient Outcome.The tumor stroma, including cancer-associated fibroblasts (CAFs), has a crucial role in tumor progression. This study focused on the morphological and mechanical properties of CAFs and normal prostatic fibroblasts. The findings revealed that CAFs had distinct morphological and mechanical characteristics compared to normal fibroblasts, such as differences in nuclear size, shape, F-actin arrangement, cellular volumes, and elasticity. Additionally, the study correlated these biophysical properties with transcriptomic data, identifying pathways and cellular components linked to the observed changes. Overall, high-throughput assessments of biophysical properties in prostate cancer cells and stromal components may serve as predictive tools for patient outcomes and help identify new therapeutic approaches targeting the tumor stroma.

  Study phs003369

• Genome-Wide Association Studies of Prematurity and Its Complications

  Preterm labor resulting in the delivery of a premature child is a complex problem with an enormous impact on individuals, families and society. An estimated 500,000 children are born prematurely in the U.S. each year, and 5 million worldwide die annually of prematurity and its complications. Prematurity is also the single largest contributor to disability-adjusted life years, a measure of the lifetime impact of a disease. Despite the importance of the problem and its disproportionate occurrence in poor and minority populations, its underlying etiology (or etiologies) remains unknown; the single best predictor for preterm delivery is a previous preterm birth. The largest single cause of prematurity is spontaneous preterm labor, and suspected triggers for this include infection, stress, poor nutrition and genetic factors. Family and twin studies provide strong evidence that genetic factors underlie about 40% of the risk for prematurity. A major challenge in studying genetic factors in prematurity is maternal/uterine factors, fetal/placental factors, or both may influence risk. Thus, any approach to studying preterm birth should account for both infant and maternal risk, environmental covariates and interactions. The Danish National Birth Cohort (DNBC) is a well-established, prospective cohort that enrolled women early in pregnancy, prior to any adverse pregnancy outcomes, to minimize bias in data collection and sampling. See details at: http://www.ssi.dk/English. The DNBC followed over 100,000 pregnancies beginning in the first trimester and has extensive biological material and epidemiologic data on health outcomes in both mother and child. The current study posted on dbGaP contains data from a genome-wide case/control study using approximately 1,000 preterm mother-child pairs from the DNBC most with spontaneous onset of labor or preterm premature rupture of membranes (PPROM), along with 1,000 control pairs where the child was born at ~40 weeks' gestation. After data cleaning some small changes in case/control status and other variables resulted in minor changes in numbers of cases or controls in certain categories. Environmental variables are being used as covariates in the analysis. To replicate positive findings, we are using additional mother-child pairs from the DNBC and from the general Danish population, as well as 2200 samples coming primarily from an African-American population known to have high rates of preterm labor and delivery. This group includes over 1000 mostly very low birthweight infants, over 500 infant term controls, 326 term mother/baby pairs and 180 preterm mother/baby pairs. The data from these additional cohorts will be available in separate dbGaP postings. The study is expected to yield a better understanding of the biology of parturition, identify common genetic factors that play a role in preterm birth and its complications and suggest environmental modifications that can prolong gestation, with the goal of improving both neonatal and adult outcomes. This study is part of the Gene Environment Association Studies initiative (GENEVA, http://www.genevastudy.org) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to prematurity and its complications through large-scale genome-wide association studies of a well-characterized cohort of Danish mothers and babies. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington.

  Study phs000103

• A Genomic Approach to Warfarin Dose Prescription in Admixed Caribbean Hispanics

  Warfarin is an oral anticoagulant and one of the most used drugs in the world accounting for up to 1.5% of prescriptions globally. Warfarin inhibits vitamin K epoxide reductase complex 1 (VKORC1), an enzyme responsible for the vitamin K recycling that is required for the activation of clotting factors. Warfarin is prescribed at an average dose of 5 mg/day for most of the indications but significant inter-patient variability has been observed. Single nucleotide variations at the VKORC1 (GeneID: 79001) and CYP2C9 (GeneID: 1559) genes alone explain from 28 to 35% of variability in warfarin dose requirements and up to 56% when clinical factors (age, gender, body surface area, diabetes and heart valve) are incorporated into regression analysis. However, genetic-guided dosing algorithms are mostly derived from studies in Europeans. The objective of the present study was to identify genetic polymorphisms that can explain variability in warfarin dose requirements among Caribbean Hispanics of Puerto Rico. VKORC1 (GeneID: 79001) and CYP2C9 (GeneID: 1559), the most important genetic predictors of warfarin response, were sequenced using Next Generation sequencing. Other candidate genes in DMET Plus Assay were assessed to identify genetic variants with relevance in warfarin dose requirements among Puerto Ricans. Our study used the Extreme Discordant Phenotype approach to perform a case-control association analysis that were confirmed with univariate and conditioned regressions. Accordingly, patients were stratified based on stable warfarin doses as sensitive (<4 mg/day), control (4-6 mg/day) and resistant (>6 mg/day). Genetic variants associated with warfarin response among the study cohort were used to perform a multivariate regression analyses to develop a genetic-guided dosing algorithm tailored for Puerto Ricans. The CYP2C9rs2860905 SNP was found to be strongly associated with warfarin dose requirements in Puerto Ricans. The CYP2C9 rs2860905 SNP tags four haplotypes that represent the trihybrid admixture of Puerto Ricans. Therefore, haplotypes harboring the rs2860905 variant are more informative in predicting warfarin dose among Puerto Ricans than the common single segregating SNPs (i.e., CYP2C9*2 and CYP2C9*3) relevant to Europeans. DMET Plus array confirmed the strong association of VKORC1 (GeneID: 79001) and CYP2C9 (GeneID: 1559) with warfarin dose requirements, but also identified other polymorphisms in CES2 (GeneID: 8824) and ABCB1 (GeneID: 5243) associated with warfarin resistance (>6 mg/day). Ancestry analysis showed that Puerto Ricans from Veteran Affairs Caribbean Healthcare System (VACHS) using warfarin had higher Native American proportions than Puerto Ricans from the 1000 Genomes project; however, this difference was not significant. Incorporation of rs2860905 in a regression model (R2=0.60 MSE=0.38) that also included additional genetic predictors (i.e., VKORC1-1639G>A; CYP2C9 rs1856908; ABCB1 rs10276036; CES2 rs4783745) and non-genetic factors (i.e., hypertension, diabetes and age) showed better prediction of warfarin dose requirements than CYP2C9*2 and CYP2C9*3 combined (partial R2=0.132 versus 0.023 and 0.007, respectively, p<0.001). Interestingly, deep vein thrombosis and diabetes were found associated with high warfarin dose requirements among Puerto Ricans. Our results support the use of CYP2C9 rs2860905 along with other genetic markers [e.g., VKORC1(GeneID: 79001 )] and clinical covariates to predict warfarin dose in Puerto Ricans. Although our findings need further replication, this study contributes to the field of Pharmacogenetics and to improve anticoagulation therapy among Puerto Ricans.

  Study phs001496

• Small molecule inhibitors of LOXL synergize with 5-AZA to restore erythropoiesis in myeloid neoplasms

  Objectives: Bone marrow (BM) stroma and microenvironmental factors in the BM milieu of myeloid neoplasms are increasingly being recognized as novel perspective therapeutic targets. Lysyl oxidases (LOX/LOXL) are crucial enzymes that cross-link collagen and contribute to the deposition of aberrant stiff extracellular matrix (ECM) in the BM of patients with myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN). Here, we studied whether inhibition of LOX/LOXL enzymes produced by BM-derived MSCs favors the differentiation of MDS/MPN hematopoietic stem cell and progenitor cells (HPSCs) and enhances the effects of 5-azacytidine (5-AZA). Methods: Primary co-cultures of MSCs and HPSCs were established from n=31 MDS/MPN patients and treated with the pan-LOX/LOXL inhibitor PXS-5505, 5-AZA or the combination of both for 4 days. At the end of co-culture, HSPC differentiation was assessed by CFU assays and flow cytometry. In some of the experiments, MSCs monolayers were pre-treated or not with PXS-5505 for 6 days and decellularized using 20 mM ammonia. Subsequently, autologous HSPCs were cultured on ECM matrices in the presence of 5-AZA or PXS-5505 + 5-AZA combination with or without inhibitors of integrin signaling such as blebbistatin, Y-27632 and αvβ3-integrin blocking antibodies. Patient-derived xenografts (PDX) were established in NSG mice based on intrafemoral co-injection of HSPCs and autologous MSCs. PDX were treated with 3 cycles of 5-AZA (75 mg/m2), PXS-5505 (30 mg/kg on alternate days for the duration of 5-AZA treatment) or combination of both. Results: MSCs of MDS and MPN patients displayed significant overexpression of LOX/LOXL transcripts as compared to healthy age-matched controls. Remarkably, LOX/LOXL inhibition in MSCs/HSPCs co-cultures increased erythroid differentiation of patient HSPCs that had suboptimal or no response to 5-AZA alone. From a total of n=31 advanced stage MDS/MPN patients, n=11 (35.5%) responded to the combination treatment, which was evidenced by a significant increase of CD235a+CD45- erythroid cell production compared to 5-AZA/PXS/untreated arms (p<0.05). Of note, combination treatment with 5-AZA + PXS-5505 facilitated differentiation of CD235+ erythroid progenitors from HSPCs sub-clones with low mutational VAFs. The presence of MSCs was necessary for the effects of the combination treatment and required direct cell contacts between MSCs and HSPCs. Moreover, PXS-5505-mediated alterations of the ECM composition alone were sufficient to induce erythroid differentiation. Inhibition of integrin-mediated signaling using blebbistatin, Y-27632 and αvβ3-integrin antibodies completely abrogated the effects of PXS-5505 induced erythroid differentiation. In vivo, the combination of PXS-5505 + 5-AZA favored erythroid differentiation of HSPCs and confirmed the in-vitro results. The combination treatment of 5-AZA + PXS-5505 induced the greatest reduction of disease burden as assessed by decrease of spleen indexes, total engraftment rates, BM fibrosis and mutational VAF profiles. Conclusions: The combination of 5-AZA + LOX/LOXL inhibitor PXS-5505 in MDS and MPN synergistically restores erythropoietic differentiation of primary HSPCs. The effect is dependent of contact interaction between HSPCs and niche components, such as MSCs and MSCs-derived ECM. Our data propose a strong rationale for a BM niche targeted combination treatment with 5-AZA + PXS-5505 in transfusion dependent MDS and MPN, which will be assessed in forthcoming clinical trials.

  Study EGAS00001006174

• Center for Common Disease Genomics [CCDG] - Cardiovascular ATVB: Atherosclerosis Thrombosis and Vascular Biology

  Italian Atherosclerosis Thrombosis and Vascular Biology study is a prospective, nationwide, case-control study involving 125 coronary care units in Italy. The cases were patients who were hospitalised for a first MI before the age of 45 years and underwent coronary angiography. Acute MI was defined as resting chest pain lasting more than 30 minutes, accompanied by persistent electrocardiographic changes, and confirmed by an increase in total creatine kinase or in the MB fraction to more than twice the upper normal limits. The controls were healthy subjects without a history of thromboembolic disease who were unrelated to the patients, but individually matched with them by age, gender and geographical origin. They were enrolled from among the blood donors or staff of the same participating hospitals. Recruitment of cases and controls took place between 1994 and 2007. This site hosts data from ~60 whole exomes.

  Study phs001592

• Rapid Acceleration of Diagnostics - Digital Health Technologies (RADx-DHT): NIH Digital Health Solutions for COVID-19: IBM Covid19 Contact Tracing and Data Exchange Tools

  The goal of this project is to develop both contact tracing and secure data exchange tools. The contact tracing solution securely combines data from a variety of sources (including manual self-report data and mobile device surveys) to enable tracing of contacts with individuals that have tested positive for COVID-19 or have been exposed to COVID-19. The data exchange solution is a secure mechanism that empowers users to control the data they share in the course of their return to work, including the ability to provide a verifiable health status claim. These tools are being used by an employer to evaluate the risk of allowing individuals to return to normal activities, and also the ability to trace user contact with individuals diagnosed with or suspected of having contracted COVID-19. DOI: https://rapids.ll.mit.edu/10.57895/h0an-m559

  Study phs002516

• Rapid Acceleration of Diagnostics - Digital Health Technologies (RADx-DHT): Covidseeker and COVID-19 Citizen Science: Leveraging Citizen Science and Real-Time Geospatial Temporal Mobile Data for Digital Contact Tracing and SARS-CoV-2 Hotspotting

  The Covidseeker and COVID-19 Citizen Science Study integrates a retrospectively-determined geolocation digital program into an established digital infrastructure housed within the NIH-funded Eureka platform to enroll SARS-CoV-2 positive and negative individuals. The solution also leverages the ongoing COVID-19 Citizen Science Study cohort both in-person and remotely to test and implement existing technology to enhance readily accessible contact tracing methods and identify “hot spots” of transmission of SARS-CoV-2. The tools are designed to alert users regarding overlap with SARS-CoV-2 infected individuals, identifying businesses that were visited by someone who later tested positive for COVID-19, and working with those businesses and public health departments on strategies to reduce the spread of the virus. DOI: https://rapids.ll.mit.edu/10.57895/me7r-vp06

  Study phs002519