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• Spatial genomic heterogeneity in multiple myeloma

  Paired end Whole Exome Sequencing of fine-needle aspirates from 51 Mutliple Myeloma patients.

  Dataset EGAD00001003988

• Stability of gut microbiome after COVID-19 vaccination in healthy and immuno-compromised individuals

  Bidirectional interactions between the immune system and the gut microbiota are key contributors to various physiological functions. Immune-associated diseases such as cancer and auto- immunity, and efficacy of immunomodulatory therapies, have been linked to microbiome variation. Although COVID-19 infection has been shown to cause microbial dysbiosis, it remains understudied whether the inflammatory response associated with vaccination also impacts the microbiota. Here, we investigate the temporal impact of COVID-19 vaccination on the gut microbiome in healthy and immuno-compromised individuals; the latter included patients with primary immunodeficiency and cancer patients on immuno- modulating therapies. We find that the gut microbiome remained remarkably stable postvaccination irrespective of diverse immune status, vaccine response, and microbial composition spanned by the cohort. The stability is evident at all evaluated levels including diversity, phylum, species, and functional capacity. Our results in- dicate the resilience of the gut microbiome to host immune changes triggered by COVID-19 vaccination and suggest minimal, if any, impact on microbiome-mediated processes. These findings en- courage vaccine acceptance, particularly when contrasted with the significant microbiome shifts observed during COVID-19 infection.

  Study EGAS50000000179

• Temporal Evolution Reveals Bifurcated Lineages in Aggressive Neuroendocrine Small Cell Prostate Cancer Trans-Differentiation

  Trans-differentiation from adenocarcinoma to small cell neuroendocrine (SCN) cancer is an adverse consequence of treatment escape in various cancers, including prostate, lung, and bladder cancers (Balanis and Sheu et al., PMID 31287989). Expression of dominant negative p53 (TP53DN), myrAkt1, RB1-shRNA, c-Myc, and Bcl2(PARCB forward transformation) using human naïve prostate basal epithelial cells recapitulated both transcriptional and histological characteristics of small cell neuroendocrine prostate cancer (NEPC) (Park et al., PMID 30287662). To study the temporal transcriptional landscape during this trans-differentiation process, we conducted a time course study using a PARCB model by integrating multi-omics sequencing, including bulk RNA-sequencing and ATAC-sequencing on samples taken at different time point, as well as single cell RNA sequencing on serial xenograft tumors. We found a common SCN pathway that resulted in two distinct end states defined by mutually exclusive expression of ASCL1 and ASCL2. Further investigation using CUT&RUN sequencing identified TFAP4 as a potential epigenetic regulator of both proteins. Our study reveals temporal and transcriptional changes from prostate adenocarcinoma to NEPC trans-differentiation.

  Study phs003230

• Genetic coupling of enhancer activity and connectivity in gene expression control

  In this study, we investigated whether the genetic effects of eQTLs on enhancer activity and enhancer-promoter contacts (connectivity) are inherently coupled or distinct. To address this, we performed Capture Hi-C targeting ~1100 eQTL loci, along with ATAC-seq and RNA-seq, in monocytes from 34 healthy male donors. Using single-modality and multi-modality Bayesian statistical approaches, we demonstrated that eQTL effects are predominantly shared across enhancer activity, connectivity, and gene expression. However, we also identified a locus where an eQTL disrupts a CTCF binding site at a putative insulator, facilitating contacts between the PCK2 gene promoter and downstream enhancers. To validate these findings, we used 4C-seq to confirm the allelic effects of eQTLs on enhancer-promoter connectivity at the PCK2 locus and another eQTL region associated with THBS1 expression, both of which showed consistent eQTL effects across all three modalities. Additionally, we conducted Hi-C on monocytes from two donors to map reference TADs and performed ChIP-seq to confirm the allelic effects of the PCK2 eQTL on CTCF binding. Together, these data provide comprehensive insights into the genetic coupling of enhancer activity, connectivity, and gene expression.

  Study EGAS50000000756

• Identifying transcriptional programs underlying anti-EGFR small molecule response and resistance with TraCe-seq

  To QC the TraCe-seq strategy, single-cell RNA-seq libraries were generated from a variety of human cancer cell lines transduced with the TraCe-seq library to validate the TraCe-seq strategy. Specifically, 5 different cell lines (PC9, MCF-10A, MDA-MB-231, NCI-H358, and NCI-H1373) were each transduced with a unique TraCe-seq barcode. The transduced cells were selected with puromycin only, dissociated to single cell suspensions, and then mixed together. The complex mixture of the 5 cell lines was profiled by 10X scRNA-seq. Furthermore, transduced NCI-H1373 cells were sorted by FACS to enrich for the top 50% of eGFP positive cells, and sorted cells were cultured briefly and used to construct scRNA-seq libraries and profiled by 10x scRNA-seq. To carry out the full TraCe-seq experiment, ~600 PC9 cells carrying unique TraCe-seq barcodes were expanded over 12 doublings to establish the barcoded population. A subset of the barcoded PC9 population was used to generate scRNA-seq libraries and profiled by 10x scRNA-seq prior to treatment to establish a baseline transcription profile for each barcoded clone. The rest of the cells were then treated for four days with 1 µM erlotinib, 1 µM GNE-069, or 1 µM GNE-104 respectively. scRNA-seq libraries were then generated form the treated cells and profiled by 10x scRNA-seq.

  Dataset EGAD00001007872

• RNAseq and ATACseq on HGSC lines, pre- and post-treatment with an epigenetic drug

  This study looked to determine changes in gene expression and chromatin accessibility of five HGSC cell lines, following treatment with a novel epigenetic drug. The epigenetic drug, HKMTi-1-005, is a compound with dual activity against H3K27 and H3K9 methylation. The cell lines used were PEO1, PEO4, PEA2, OVCAR5, OVCAR8.

  Study EGAS50000000047

• Nasopharyngeal RNASeq Comparing SARS-CoV-2+ Patients and SARS-CoV-2 Negative Control Subjects

  The goal of this analysis was to compare RNAs enriched in the upper respiratory tract of SARS-CoV-2 patients and SARS-CoV-2 negative controls. RNA-sequencing of RNA isolated from the viral transport medium associated with nasopharyngeal swab samples from SARS-CoV-2+ patients and SARS-COV-2 negative controls.

  Study phs002433

• Autosomal Recessive CD55 Deficiency is Associated with Protein Losing Enteropathy, Thrombosis, and Complement Dysregulation

  We describe 11 patients from 8 families with homozygous LOF mutations in the complement regulatory protein CD55. Loss of CD55 is associated with increased complement activation, severe protein losing enteropathy accompanying a primary intestinal lymphangiectasia, and deep vein thrombotic events. We have named this disease CHAPLE after the principle components of the disease.

  Study phs001376

• Somatic Mutational Analysis by Exome Sequencing Late-Stage Endometrioid Endometrial Carcinoma

  The purpose of this study was to identify somatic (tumor-specific) mutations in advanced stage endometrioid endometrial carcinoma tumor exomes. The dataset was generated at the NIH Intramural Sequencing Center (NISC) and NHGRI by next generation sequencing the exomes of 19 de-identified primary tumor DNAs, from advanced stage tumors, and matched non-tumor DNAs.

  Study phs001153

• Single cell transcriptomic profiles of advanced melanoma patients treated with checkpoint inhibitor immunotherapy

  Little is known about the resistant clones within the tumour ecosystem treated with immunotherapy. This work provides a comprehensive and integrative analysis of each individual non-responding melanoma patients, including clinical features integrated with single cell analysis, which is critical to understand features of resistance in order to improve cancer patients’ outcomes.

  Study EGAS50000000339