{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["Yasmine LABIAD"],"study_type":["transcription profiling by array"],"organism":["Homo sapiens"],"species":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-15172"],"description":["Diffuse Large B-Cell Lymphoma (DLBCL) is a clinically and molecularly heterogeneous disease typically classified into subtypes based on gene expression patterns -most notably the Germinal Center B-cell (GCB) and Activated B-cell-like (ABC) subtypes. However, these classifications have been developed using samples from immunocompetent patients. In contrast, individuals living with HIV present with unique immunological and virological contexts, such as chronic immune activation, viral co-infections (e.g., EBV, KSHV), and a disrupted lymphoid microenvironment. These factors may fundamentally alter the biology of lymphomagenesis. The aim of this study was to explore whether the established molecular classification of DLBCL applies to HIV-positive patients or if distinct transcriptional subgroups exist within this specific population. By doing so, the study seeks to better characterize the molecular pathology of HIV-associated DLBCL and uncover potential targets for personalized therapeutic strategies adapted to this high-risk group."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Nucleic Acid Extraction - RNA was extracted using the RNeasy FFPE kit from Qiagen. The process began with deparaffinization, achieved by immersing the samples in xylene to remove paraffin, followed by ethanol washes to rehydrate the tissue. After rehydration, the tissue underwent lysis with proteinase K at 56°C for 15 minutes, followed by a heat-induced crosslink reversal step at 80°C for 15 minutes. This step ensures the recovery of high-quality RNA suitable for downstream analysis. RNA was then purified using on-column DNase treatment to eliminate any contaminating DNA, followed by several washing steps to remove impurities. RNA was eluted in RNase-free water and quantified using an Agilent NanoDrop spectrophotometer. The integrity of RNA was assessed using the Agilent Bioanalyzer, with samples exhibiting a RNA integrity number (RIN) ≥3 being considered of sufficient quality for transcriptomic analysis. Samples with suboptimal RIN scores were excluded from further processing.","Labeling - For transcriptomic analysis, Agilent's SurePrint G3 Human GE 8x60K v2 chip was used. The chip provides high gene and transcript coverage with high sensitivity. The chip has eight arrays, each with 62,976 probes. Sample preparation, labeling, and hybridization were performed according to the Agilent Gene Expression FFPE Workflow protocol, optimized for formalin-fixed, paraffin-embedded samples to ensure accurate and reproducible data. The FFPE workflow begins with an RNA input repair step to address RNA fragmentation caused by the fixation process. RNA is reverse-transcribed into complementary DNA (cDNA) using a T7-oligo(dT) primer. This cDNA is amplified by in vitro transcription with T7 RNA polymerase, generating amplified complementary RNA (aRNA). The aRNA is then fluorescently labeled with Cy3 dye, purified to remove unincorporated dye, and quantified to ensure labeling efficiency.","Sample Collection - The tumor library of the ANRS (Agence Nationale de la Recherche sur le Sida et les hépatites virales) provided us with seven paraffin-embedded samples as well as clinical and biological data (ANRS CO16 Lympho-VIR cohort). Five other samples were provided by Pr. H Lepidi (CHU de la Timone, Marseille). All samples were collected following ethical guidelines and with informed consent from the patients. We used two technical replicates per biological sample to ensure the reliability of our findings.","Hybridization - Hybridization of labeled aRNA to the microarray is performed under stringent conditions at 65°C for 17 hours to ensure specific binding of probes to their target sequences.","Scaning - Arrays are washed to remove non-specifically bound material, scanned using the Agilent SureScan Microarray Scanner, and fluorescence intensities are extracted using Agilent Feature Extraction software."],"figure_sub":["MIAME Score","Raw Data","Organization","Assays and Data","Processed Data","MAGE-TAB Files","Array Designs"],"pubmed_authors":["Yasmine LABIAD"],"data_protocol":["Data Transformation - The AgiND library, implemented in the R software environment, was utilized for data analysis and visualization. AgiND, based on the Bioconductor framework, provides robust diagnostic tools for assessing microarray data quality and normalization. To ensure consistency across samples, quantile normalization was employed, homogenizing intensity distributions to minimize technical variations. The AgiND library used in this study was version 1.12.0, compatible with R version 4.2.2. Two filters were applied to preprocess the raw data: (1) control probes were removed to eliminate noise introduced by non-informative probes, and (2) genes expressed below the background level in 100% of samples were excluded to focus on biologically relevant signals. The background level was defined based on negative control probes included in the microarray platform."],"additional_accession":[]},"is_claimable":false,"name":"Transcriptomic Study of Diffuse Large B-Cell Lymphoma Associated with HIV Infection: Identification of Novel Molecular Subtypes","description":"Diffuse Large B-Cell Lymphoma (DLBCL) is a clinically and molecularly heterogeneous disease typically classified into subtypes based on gene expression patterns -most notably the Germinal Center B-cell (GCB) and Activated B-cell-like (ABC) subtypes. However, these classifications have been developed using samples from immunocompetent patients. In contrast, individuals living with HIV present with unique immunological and virological contexts, such as chronic immune activation, viral co-infections (e.g., EBV, KSHV), and a disrupted lymphoid microenvironment. These factors may fundamentally alter the biology of lymphomagenesis. The aim of this study was to explore whether the established molecular classification of DLBCL applies to HIV-positive patients or if distinct transcriptional subgroups exist within this specific population. By doing so, the study seeks to better characterize the molecular pathology of HIV-associated DLBCL and uncover potential targets for personalized therapeutic strategies adapted to this high-risk group.","dates":{"release":"2025-06-20T00:00:00Z","modification":"2025-05-28T11:01:03.477Z","creation":"2025-05-28T11:01:03.477Z"},"accession":"E-MTAB-15172","cross_references":{"EFO":["EFO_0002768","EFO_0002944","EFO_0003814","EFO_0003813","EFO_0005518","EFO_0003816","EFO_0003815"]}}