scholarly journals Developmental programming in human umbilical cord vein endothelial cells following fetal growth restriction

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Fieke Terstappen ◽  
Jorg J. A. Calis ◽  
Nina D. Paauw ◽  
Jaap A. Joles ◽  
Bas B. van Rijn ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Endothelial Cells ◽  
Rna Sequencing ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Enrichment Analysis ◽  
Growth Restriction ◽  
Gene Set Enrichment Analysis ◽  
Gene Set Enrichment ◽  
Gene Sets

Abstract Background Fetal growth restriction (FGR) is associated with an increased susceptibility for various noncommunicable diseases in adulthood, including cardiovascular and renal disease. During FGR, reduced uteroplacental blood flow, oxygen and nutrient supply to the fetus are hypothesized to detrimentally influence cardiovascular and renal programming. This study examined whether developmental programming profiles, especially related to the cardiovascular and renal system, differ in human umbilical vein endothelial cells (HUVECs) collected from pregnancies complicated by placental insufficiency-induced FGR compared to normal growth pregnancies. Our approach, involving transcriptomic profiling by RNA-sequencing and gene set enrichment analysis focused on cardiovascular and renal gene sets and targeted DNA methylation assays, contributes to the identification of targets underlying long-term cardiovascular and renal diseases. Results Gene set enrichment analysis showed several downregulated gene sets, most of them involved in immune or inflammatory pathways or cell cycle pathways. seven of the 22 significantly upregulated gene sets related to kidney development and four gene sets involved with cardiovascular health and function were downregulated in FGR (n = 11) versus control (n = 8). Transcriptomic profiling by RNA-sequencing revealed downregulated expression of LGALS1, FPR3 and NRM and upregulation of lincRNA RP5-855F14.1 in FGR compared to controls. DNA methylation was similar for LGALS1 between study groups, but relative hypomethylation of FPR3 and hypermethylation of NRM were present in FGR, especially in male offspring. Absolute differences in methylation were, however, small. Conclusion This study showed upregulation of gene sets related to renal development in HUVECs collected from pregnancies complicated by FGR compared to control donors. The differentially expressed gene sets related to cardiovascular function and health might be in line with the downregulated expression of NRM and upregulated expression of lincRNA RP5-855F14.1 in FGR samples; NRM is involved in cardiac remodeling, and lincRNAs are correlated with cardiovascular diseases. Future studies should elucidate whether the downregulated LGALS1 and FPR3 expressions in FGR are angiogenesis-modulating regulators leading to placental insufficiency-induced FGR or whether the expression of these genes can be used as a biomarker for increased cardiovascular risk. Altered DNA methylation might partly underlie FPR3 and NRM differential gene expression differences in a sex-dependent manner.

scholarly journals Higher Acid-Base Imbalance Associated with Respiratory Failure Could Decrease the Survival of Patients with Scrub Typhus during Intensive Care Unit Stay: A Gene Set Enrichment Analysis

2019 ◽  
Vol 8 (10) ◽  
pp. 1580 ◽  
Author(s):  
Kyoung Min Moon ◽  
Kyueng-Whan Min ◽  
Mi-Hye Kim ◽  
Dong-Hoon Kim ◽  
Byoung Kwan Son ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Respiratory Failure ◽  
Scrub Typhus ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Acid Base ◽  
Gene Set Enrichment ◽  
Gene Set ◽  
Gene Sets

Ninety percent of patients with scrub typhus (SC) with vasculitis-like syndrome recover after mild symptoms; however, 10% can suffer serious complications, such as acute respiratory failure (ARF) and admission to the intensive care unit (ICU). Predictors for the progression of SC have not yet been established, and conventional scoring systems for ICU patients are insufficient to predict severity. We aimed to identify simple and robust indicators to predict aggressive behaviors of SC. We evaluated 91 patients with SC and 81 non-SC patients who were admitted to the ICU, and 32 cases from the public functional genomics data repository for gene expression analysis. We analyzed the relationships between several predictors and clinicopathological characteristics in patients with SC. We performed gene set enrichment analysis (GSEA) to identify SC-specific gene sets. The acid-base imbalance (ABI), measured 24 h before serious complications, was higher in patients with SC than in non-SC patients. A high ABI was associated with an increased incidence of ARF, leading to mechanical ventilation and worse survival. GSEA revealed that SC correlated to gene sets reflecting inflammation/apoptotic response and airway inflammation. ABI can be used to indicate ARF in patients with SC and assist with early detection.

scholarly journals Drug perturbation gene set enrichment analysis (dpGSEA): a new transcriptomic drug screening approach

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Mike Fang ◽  
Brian Richardson ◽  
Cheryl M. Cameron ◽  
Jean-Eudes Dazard ◽  
Mark J. Cameron
Keyword(s):  
Drug Targets ◽  
T Regulatory Cells ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Regulatory Cells ◽  
Gene Set Enrichment ◽  
Gene Set ◽  
Gene Sets ◽  
Gastroenteropancreatic Neuroendocrine Tumor ◽  
Public Datasets

Abstract Background In this study, we demonstrate that our modified Gene Set Enrichment Analysis (GSEA) method, drug perturbation GSEA (dpGSEA), can detect phenotypically relevant drug targets through a unique transcriptomic enrichment that emphasizes biological directionality of drug-derived gene sets. Results We detail our dpGSEA method and show its effectiveness in detecting specific perturbation of drugs in independent public datasets by confirming fluvastatin, paclitaxel, and rosiglitazone perturbation in gastroenteropancreatic neuroendocrine tumor cells. In drug discovery experiments, we found that dpGSEA was able to detect phenotypically relevant drug targets in previously published differentially expressed genes of CD4+T regulatory cells from immune responders and non-responders to antiviral therapy in HIV-infected individuals, such as those involved with virion replication, cell cycle dysfunction, and mitochondrial dysfunction. dpGSEA is publicly available at https://github.com/sxf296/drug_targeting. Conclusions dpGSEA is an approach that uniquely enriches on drug-defined gene sets while considering directionality of gene modulation. We recommend dpGSEA as an exploratory tool to screen for possible drug targeting molecules.

scholarly journals Weighted Kolmogorov Smirnov testing: an alternative for Gene Set Enrichment Analysis

2015 ◽  
Vol 14 (3) ◽  
Author(s):  
Konstantina Charmpi ◽  
Bernard Ycart
Keyword(s):  
Weight Function ◽  
Null Hypothesis ◽  
Computing Time ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Test Statistic ◽  
Gene Set Enrichment ◽  
Gene Set ◽  
Gene Sets ◽  
Kolmogorov Smirnov

AbstractGene Set Enrichment Analysis (GSEA) is a basic tool for genomic data treatment. Its test statistic is based on a cumulated weight function, and its distribution under the null hypothesis is evaluated by Monte-Carlo simulation. Here, it is proposed to subtract to the cumulated weight function its asymptotic expectation, then scale it. Under the null hypothesis, the convergence in distribution of the new test statistic is proved, using the theory of empirical processes. The limiting distribution needs to be computed only once, and can then be used for many different gene sets. This results in large savings in computing time. The test defined in this way has been called Weighted Kolmogorov Smirnov (WKS) test. Using expression data from the GEO repository, tested against the MSig Database C2, a comparison between the classical GSEA test and the new procedure has been conducted. Our conclusion is that, beyond its mathematical and algorithmic advantages, the WKS test could be more informative in many cases, than the classical GSEA test.

scholarly journals Gastroesophageal reflux activates the NF-κB pathway and impairs esophageal barrier function in mice

2013 ◽  
Vol 305 (1) ◽  
pp. G58-G65 ◽  
Author(s):  
Yu Fang ◽  
Hao Chen ◽  
Yuhui Hu ◽  
Zorka Djukic ◽  
Whitney Tevebaugh ◽  
...  
Keyword(s):  
Gastroesophageal Reflux ◽  
Barrier Function ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Esophageal Epithelium ◽  
Gene Set Enrichment ◽  
Gene Sets ◽  
Epithelial Resistance

The barrier function of the esophageal epithelium is a major defense against gastroesophageal reflux disease. Previous studies have shown that reflux damage is reflected in a decrease in transepithelial electrical resistance associated with tight junction alterations in the esophageal epithelium. To develop novel therapies, it is critical to understand the molecular mechanisms whereby contact with a refluxate impairs esophageal barrier function. In this study, surgical models of duodenal and mixed reflux were developed in mice. Mouse esophageal epithelium was analyzed by gene microarray. Gene set enrichment analysis showed upregulation of inflammation-related gene sets and the NF-κB pathway due to reflux. Significance analysis of microarrays revealed upregulation of NF-κB target genes. Overexpression of NF-κB subunits (p50 and p65) and NF-κB target genes (matrix metalloproteinases-3 and -9, IL-1β, IL-6, and IL-8) confirmed activation of the NF-κB pathway in the esophageal epithelium. In addition, real-time PCR, Western blotting, and immunohistochemical staining also showed downregulation and mislocalization of claudins-1 and -4. In a second animal experiment, treatment with an NF-κB inhibitor, BAY 11-7085 (20 mg·kg−1·day−1 ip for 10 days), counteracted the effects of duodenal and mixed reflux on epithelial resistance and NF-κB-regulated cytokines. We conclude that gastroesophageal reflux activates the NF-κB pathway and impairs esophageal barrier function in mice and that targeting the NF-κB pathway may strengthen esophageal barrier function against reflux.

Differential gene expression in prostate tissue according to vasectomy.

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 298-298
Author(s):  
Kathryn M Wilson ◽  
Travis Gerke ◽  
Ericka Ebot ◽  
Jennifer A Sinnott ◽  
Jennifer R. Rider ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Cancer Diagnosis ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Prostate Tissue ◽  
Gene Set Enrichment ◽  
Normal Prostate ◽  
Gene Sets ◽  
Normal Prostate Tissue

298 Background: We previously found that vasectomy was associated with an increased risk of prostate cancer, and particularly, risk of lethal prostate cancer in the Health Professionals Follow-up Study (HPFS). However, the possible biological basis for this finding is unclear. In this study, we explored possible biological mechanisms by assessing differences in gene expression in the prostate tissue of men with and without a history of vasectomy prostate cancer diagnosis. Methods: Within the HPFS, vasectomy data and gene expression data (20,254 genes) was available from archival tumor tissue from 263 cases, 124 of whom also had data for adjacent normal tissue. To relate expression of individual genes to vasectomy we used linear regression adjusting for age and year at diagnosis. We ran gene set enrichment analysis to identify pathways of genes associated with vasectomy. Results: Among 263 cases, 67 (25%) reported a vasectomy prior to cancer diagnosis. Mean age at diagnosis was 66 years among men without and 65 years among men with vasectomy. Median time between vasectomy and prostate cancer diagnosis was 25 years. Gene expression in tumor tissue was not associated with vasectomy status. In adjacent normal tissue, three individual genes were associated with vasectomy with Bonferroni-corrected p-values of < 0.10: RAPGEF6, OR4C3, and SLC35F4. Gene set enrichment analysis found five pathways upregulated and seven pathways downregulated in men with vasectomy compared to those without in normal prostate tissue with a FDR < 0.05. Upregulated pathways included several immune-related gene sets and G-protein-coupled receptor gene sets. Conclusions: We identified significant differences in gene expression profiles in normal prostate tissue according to vasectomy status among men treated for prostate cancer. The fact that such differences existed several decades after vasectomy provides support for the idea that vasectomy may play a role in the etiology of prostate cancer.

Decreased expression of indoleamine 2, 3-dioxygenase in villous stromal endothelial cells of placentas with preeclampsia and/or fetal growth restriction

Placenta ◽  
2016 ◽  
Vol 45 ◽  
pp. 121
Author(s):  
Naoyuki Iwahashi ◽  
Madoka Yamamoto ◽  
Tamaki Yahata ◽  
Mika Mizoguchi ◽  
Sakiko Nanjo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Indoleamine 2

scholarly journals GSEA-InContext Explorer: An interactive visualization tool for putting gene set enrichment analysis results into biological context

2019 ◽  
Author(s):  
Rani K. Powers ◽  
Anthony Sun ◽  
James C. Costello
Keyword(s):  
Statistical Significance ◽  
Null Distribution ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Gene Set Enrichment ◽  
Gene Set ◽  
Link Type ◽  
Interactive Interface ◽  
Gene Sets ◽  
Shiny App

AbstractSummaryGSEA-InContext Explorer is a Shiny app that allows users to perform two methods of gene set enrichment analysis (GSEA). The first, GSEAPreranked, applies the GSEA algorithm in which statistical significance is estimated from a null distribution of enrichment scores generated for randomly permuted gene sets. The second, GSEA-InContext, incorporates a user-defined set of background experiments to define the null distribution and calculate statistical significance. GSEA-InContext Explorer allows the user to build custom background sets from a compendium of over 5,700 curated experiments, run both GSEAPreranked and GSEA-InContext on their own uploaded experiment, and explore the results using an interactive interface. This tool will allow researchers to visualize gene sets that are commonly enriched across experiments and identify gene sets that are uniquely significant in their experiment, thus complementing current methods for interpreting gene set enrichment results.Availability and implementationThe code for GSEA-InContext Explorer is available at: https://github.com/CostelloLab/GSEA-InContext_Explorer and the interactive tool is at: http://gsea-incontext_explorer.ngrok.io

scholarly journals Identification and Characterization of Extrachromosomal Circular DNA in Human Placentas With Fetal Growth Restriction

2021 ◽  
Vol 12 ◽  
Author(s):  
Huan Yang ◽  
Jie He ◽  
Shuai Huang ◽  
Hongbing Yang ◽  
Qingjie Yi ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Enrichment Analysis ◽  
Maternal Plasma ◽  
Growth Restriction ◽  
Formation Mechanisms ◽  
Pathway Enrichment Analysis ◽  
Circular Dnas ◽  
New Biomarkers ◽  
Host Genes

Many studies have confirmed that extrachromosomal circular DNAs (eccDNAs/ecDNAs) exist in tumor and normal cells independently of the chromosome and are essential for oncogene plasticity and drug resistance. Studies have confirmed that there are many eccDNAs/ecDNAs in maternal plasma derived from the fetus. Fetal growth restriction (FGR) is a pregnancy-related disease associated with high newborn morbidity and mortality. However, the characteristics and nature of eccDNAs/ecDNAs in FGR are poorly understood. This study aims to deconstruct the properties and potential functions of eccDNAs/ecDNAs in FGR. We performed circle-seq to identify the expression profile of eccDNAs/ecDNAs, analyzed by bioinformatics, and verified by real-time Polymerase Chain Reaction (PCR) combined with southern blot in FGR compared with the normal groups. A total of 45,131 eccDNAs/ecDNAs (including 2,118 unique ones) were identified, which had significantly higher abundance in FRG group than in normal group, and was bimodal in length, peaking at ~146bp and ~340bp, respectively. Gestational age may be one independent factor affecting the production of eccDNAs/ecDNAs, most of which come from genomic regions with high gene density, with a 4~12bp repeat around the junction, and their origin had a certain genetic preference. In addition, some of the host-genes overlapped with non-coding RNAs (ncRNAs) partially or even completely. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that host-genes on the differentially expressed eccDNAs/ecDNAs (DEEECs/DEECs) were mainly enriched in immune-related functions and pathways. The presence of some ecDNAs were verified, and whose variability were consistent with the circle-seq results. We identified and characterized eccDNAs/ecDNAs in placentas with FGR, and elucidated the formation mechanisms and the networks with ncRNAs, which provide a new vision for the screening of new biomarkers and therapeutic targets for FGR.

Next Generation Sequencing reveals profound transcriptomic differences between reticulated and non-reticulated platelets from healthy donors, CCS- and STEMI patients

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
L Hille ◽  
T.G Nuehrenberg ◽  
L Hein ◽  
F.J Neumann ◽  
D Trenk
Keyword(s):  
Healthy Subjects ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Differentially Expressed ◽  
Gene Set Enrichment ◽  
Reticulated Platelets ◽  
Gene Sets ◽  
Healthy Donors ◽  
Go Terms ◽  
Generation Sequencing

Abstract Background The youngest circulating platelets – so called reticulated platelets (RP) – represent a highly prothrombotic platelet subpopulation. Previous studies showed that patients with chronic coronary syndrome (CCS) as well as patients with ST-elevation myocardial infarction (STEMI) have higher amounts of RP compared to healthy subjects. It has been suggested that intrinsic properties of RP impact on cardiovascular risk. However, it is unknown if transcriptomic alterations contribute to the prothrombotic properties of RP. Purpose This study sought to investigate differences in the transcriptomic landscape of sorted RP versus non-RP, i.e. young and old platelets, in healthy subjects, CCS- and STEMI-patients. Methods Blood samples were obtained from healthy subjects as well as from patients with CCS/STEMI (n=8 each) the day after PCI. After staining with SYTO 13, platelets from each donor were sorted into a RP and a non-RP fraction based on their RNA-content. Next Generation Sequencing (NGS) was applied to generate sequencing reads for sorted RP and non-RP from the 3 cohorts. Data was analyzed by use of the Freiburg bioinformatics platform “Galaxy”. Results Investigation of transcriptomic alterations in non-RP versus RP by differential gene expression analysis revealed a total number of 2,476 transcripts that were differentially expressed in platelets from healthy donors, 2,075 in CCS-patients and 1,852 in STEMI patients, respectively (adj. p&lt;0.05 in all analyses). Comparison of these transcripts revealed a large overlap of 500 mRNAs which were downregulated and 660 mRNAs which were upregulated in RP in all 3 cohorts. However, there are also distinct groups of transcripts that are differentially expressed in only one of the 3 cohorts. Gene ontology (GO)-analysis of the 500 uniformly enriched transcripts in RP yielded 38 overrepresented GO-terms. A large group was related to cytoskeleton and shape change. Furthermore, GO-terms associated to the platelet activation cascade were overrepresented. Upregulated transcripts included well-known examples like GP6 and GP9, P-selectin, integrin β3, integrin a-IIb, and tubulin α4a. GO-analysis of enriched transcripts in non-RP showed a large group associated to mitosis and cell nucleus/DNA which is surprising since platelets neither contain DNA nor a nucleus. Gene set enrichment analysis (GSEA) determined higher normalized enrichment scores for several gene sets associated to platelet degranulation, aggregation and activation in the STEMI-cohort. Gene sets affecting cell adhesion and platelet calcium homeostasis were overexpressed in particular in CCS-patients. Conclusion NGS-results indicate a highly prothrombotic transcriptome of RP from each cohort with high amounts of differentially expressed transcripts overlapping. However, GSEA identified gene sets that are particularly overexpressed in CCS- or STEMI-patients which might contribute to platelet hyperreactivity in these cohorts. Gene set enrichment analysis Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): PharmCompNet Baden-Wuerttemberg: Kompetenznetzwerk Pharmakologie Baden-Wuerttemberg - Wirkstoffnetzwerke als Grundlagen der individualisierten Arzneistofftherapie

Gene Set Enrichment Analysis of Ki-67high CLL Clones Suggests Complex Interactions of B-Cell Receptor Signaling and Normal Cell Interactions in the Disease

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2833-2833
Author(s):  
Xiao J. Yan ◽  
Daniel Kalenscher ◽  
Erin Boyle ◽  
Sophia Yancopoulos ◽  
Rajendra N Damle ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Gene Set Enrichment ◽  
Ki 67 ◽  
Mutation Status ◽  
Gene Set ◽  
Gene Sets ◽  
Bcr Signaling

Abstract Abstract 2833 Introduction: In chronic lymphocytic leukemia (CLL), clonally expanded CD5+ B lymphocytes eventually overwhelm healthy immune cells, hindering normal immune function. To determine mechanisms fueling this expansion, gene expression data were gathered by microarray analysis of cells from CLL patients. Samples were grouped based on Ki-67 expression, an indicator of proliferation. To determine mechanisms correlating with B-cell proliferation and impacting on CLL B-cell biology, microarray profiles were compared using Gene Set Enrichment Analysis (GSEA) [Subramanian A, et al. PNAS 2005]. Methods: Samples were analyzed for intracellular expression of Ki-67 by flow cytometry and divided into 2 groups based on Ki-67 expression (cutoff at 5%). RNA was then purified from CD5+CD19+ CLL cells and gene expression microarray assays were performed using Illumina HumanHT12 beadchips. GSEA was carried out using a library of signatures by Dr. Louis Staudt [Shaffer AL, et al. Immunol Rev 2006] containing 305 gene sets encompassing 13, 564 genes biased towards hematopoietic signatures. Results: Of 61 cases, 14 were Ki-67high and 47 were Ki-67low. When time-to-first-treatment (TTFT) was compared between the groups, Ki67high patients had significantly shorter TTFT (2.76 yrs) compared to Ki-67low patients (23.46 yrs; P<0.0001). By GSEA, we determined 255/285 gene sets were upregulated in the Ki-67high group with 50 gene sets significantly enriched at a false discovery rate (FDR) <25%. For the Ki-67low group, 30/285 gene sets were upregulated with only one significant at FDR <25%. IGHV unmutated CLL (U-CLL) was enriched in only one gene set, termed CLLUNMUT-1, while mutated CLL (M-CLL) was only enriched in CLLMUT-1. CD38high and CD38low subsets were similarly enriched in these two gene sets, with 4 additional gene sets in the CD38high group, including MYD88UP-4 and IFN-2. Of the 50 significantly enriched gene sets in the Ki-67high group, 17 relate to signaling pathways, 16 to cellular differentiation, 6 to cellular processes, 4 to transcription factor targets, and the remaining 7 relate to cancer. Of these, the percentage of the signaling component is up 13% from its representation in the original Staudt library. The top 5 gene sets enriched in the Ki-67high group are: upregulated U-CLL compared to M-CLL (CLLUNMUT-1), myeloid tissue compared to other tissues (MYELOID-1), T cell cytokine induced proliferation (TCYTUP-8), BCR crosslinking CLL B cells (CLLBCRUP-1) and BDCA4+ dendritic cells compared to other hematopoietic cells (DC-1). The total number of genes enriched in these 50 sets is 769, with 217 genes shared in two or more gene sets. Twenty genes were enriched in the CLL BCR signature, CLLBCRUP-1 [Herishanu Y, et al. Blood 2011]. Of these, WARS, IRF4, MX1, OAS1, and NAMPT are also enriched in the T cell cytokine induced and T cell activation signatures. Only one gene set was enriched in the Ki-67low group, CLLMUT-1, upregulated in M-CLL compared to U-CLL. CD274 (PD-L1) was consistently elevated in the Ki-67low group in all the patients, irrespective of IGHV mutation status. Discussion: The observed GSEA profiles in Ki-67high patients correlated with gene signatures biased towards BCR signaling, signal transduction, and hematopoietic cancer, consistent with the Ki-67high group containing more (recently) proliferating cells influenced at least in part by BCR signaling. The profiles also suggest that additional cells (T lymphocytes and dendritic cells) may be involved. It is notable these gene sets were not observed for CLL patients subgrouped by IGHV mutation status or by CD38, and that these other subsets did not show as pronounced a distinction by GSEA profiling. Disclosures: No relevant conflicts of interest to declare.

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