en Medical Genetics Medical Genetics Original Research Original Research <span style="font-size:13pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="text-autospace:none"><span new="" roman="" style="font-family:" times=""><span style="font-style:italic"><b>&nbsp;&nbsp;</b><b><span style="font-size:9.0pt"><span style="font-style:normal">&nbsp; Background: </span></span></b><span style="font-size:9.0pt"><span style="font-style:normal">Diffuse large B-cell lymphoma (DLBL) and systemic lupus erythematosus (SLE) are complex autoimmune disorders that present unique clinical challenges. These conditions may share underlying genetic and signaling pathways despite their distinct manifestations. Uncovering these commonalities could offer invaluable insights into disease pathogenesis, paving the way for more targeted and effective therapeutic interventions. This study embarks on a comprehensive investigation of the common genes and signaling pathways between SLE and DLBL.</span></span></span></span></span></span></span></span><br> <span style="font-size:13pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="text-autospace:none"><span new="" roman="" style="font-family:" times=""><span style="font-style:italic"><span style="font-size:9.0pt"><span style="font-style:normal">&nbsp;&nbsp; <b>Methods:</b> The researchers scoured the Gene Expression Omnibus database, meticulously gathering microarray datasets for SLE (GSE61635) and DLBL (GSE56315). Differential expression analysis was performed, allowing the team to identify the genes that were commonly dysregulated across these 2 autoimmune conditions. To delve deeper into the biological significance of these shared genes, the researchers conducted functional enrichment analysis, network analysis, and core gene identification. Notably, the diagnostic potential of the identified hub genes was assessed using a cutting-edge neural network model.</span></span></span></span></span></span></span></span><br> <span style="font-size:13pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="text-autospace:none"><span new="" roman="" style="font-family:" times=""><span style="font-style:italic"><span style="font-size:9.0pt"><span style="font-style:normal">&nbsp;&nbsp; <b>Results: </b>The data analysis revealed a remarkable 146 genes that were shared between SLE and DLBL, of which 111 were upregulated and 45 downregulated. Functional enrichment analysis unveiled the involvement of these shared genes in vital immune system-related processes&mdash;such as defense response to viruses, interferon signaling, and broader immune system pathways. Network analysis pinpointed 5 hub genes (IFIT3, IFIT1, DDX58, CCL2, and OASL) that emerged as central players, exhibiting a high degree of centrality and predicted to hold crucial roles in the underlying molecular mechanisms. Remarkably, the neural network model demonstrated exceptional diagnostic accuracy in distinguishing between the disease states (DLBL and SLE) based solely on the expression patterns of these hub genes.</span></span></span></span></span></span></span></span><br> <span style="font-size:13pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="text-autospace:none"><span new="" roman="" style="font-family:" times=""><span style="font-style:italic"><b><span style="font-size:9.0pt"><span style="font-style:normal">&nbsp;&nbsp; Conclusion: </span></span></b><span style="font-size:9.0pt"><span style="font-style:normal">The identified hub genes and their associated pathways hold immense potential as diagnostic biomarkers and may serve as valuable targets for future therapeutic explorations. </span></span></span></span></span></span></span></span><br> <br> <span style="font-family:Calibri"><span style="font-family:'Times New Roman'"></span></span> Diffuse Large B-cell Lymphoma, Systemic Lupus Erythematous, Interferons, OASL, DDX58, CCL2, IFIT1, IFIT3 934 941 http://mjiri.iums.ac.ir/browse.php?a_code=A-10-8947-1&slc_lang=en&sid=1 Alireza Hejrati hejrati.a@iums.ac.ir 200319475328460089683 200319475328460089683 No Department of Internal Medicine, School of Medicine, Hazrat-e Rasool General Hospital, Iran University of Medical Sciences, Tehran, Iran Reza Maddah rmadah733@gmail.com 200319475328460089684 200319475328460089684 No Department of Bioprocess Engineering, Institute of Industrial and Environmental Biotechnology, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran Sadaf Parvin sadafprv@gmail.com 200319475328460089685 200319475328460089685 No School of Medicine, Hazrat-e Rasool General Hospital, Iran University of Medical Sciences, Tehran, Iran Abbas Gholami gholami.ab@iums.ac.ir 200319475328460089686 200319475328460089686 No Department of Rheumatology, Hazrat Rasool-e-Akram Hospital, School of Medicine, Iran University of Medical Sciences, Tehran, Iran Lina Hejrati Lina1381@gmail.com 200319475328460089687 200319475328460089687 No School of Medicine, Hazrat-e Rasool General Hospital, Iran University of Medical Sciences, Tehran, Iran Bahareh Shateri Amiri shateri.b@iums.ac.ir 200319475328460089688 0009-1145-1145-6154 Yes Department of Internal Medicine, School of Medicine, Hazrat-e Rasool General Hospital, Iran University of Medical Sciences, Tehran, Iran Anousheh Haghighi haghighi.a@iums.ac.ir 200319475328460089689 200319475328460089689 No Department of Rheumatology, Hazrat Rasool-e-Akram Hospital, School of Medicine, Iran University of Medical Sciences, Tehran, Iran