Bioinformatics Analysis of the Molecular Effects of Felzartamab on Antibody-Mediated Rejection in Kidney Transplant Patients

Bioinformatics Analysis of the Molecular Effects of Felzartamab on Antibody-Mediated Rejection in Kidney Transplant Patients


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نویسندگان: یلدا رهبرسعادت , سپیده زنونی واحد , محمد رضا اردلان

عنوان کنگره / همایش: Eurasian-Iranian Organ Transplant Congress , Iran (Islamic Republic) , Shiraz , 2025

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نویسنده ثبت کننده مقاله یلدا رهبرسعادت
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه مرکز تحقیقات کلیه
کد مقاله 88097
عنوان فارسی مقاله Bioinformatics Analysis of the Molecular Effects of Felzartamab on Antibody-Mediated Rejection in Kidney Transplant Patients
عنوان لاتین مقاله Bioinformatics Analysis of the Molecular Effects of Felzartamab on Antibody-Mediated Rejection in Kidney Transplant Patients
نوع ارائه سخنرانی
عنوان کنگره / همایش Eurasian-Iranian Organ Transplant Congress
نوع کنگره / همایش بین المللی
کشور محل برگزاری کنگره/ همایش Iran (Islamic Republic)
شهر محل برگزاری کنگره/ همایش Shiraz
سال انتشار/ ارائه شمسی 1404
سال انتشار/ارائه میلادی 2025
تاریخ شمسی شروع و خاتمه کنگره/همایش 1404/02/23 الی 1404/02/25
آدرس لینک مقاله/ همایش در شبکه اینترنت
آدرس علمی (Affiliation) نویسنده متقاضی Kidney Research Center, Tabriz University of Medical Sciences, Tabriz Iran

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نویسنده نفر چندم مقاله
یلدا رهبرسعادتاول
سپیده زنونی واحدچهارم
محمد رضا اردلانپنجم

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عنوان متن
کلمات کلیدیBioinformatics, Felzartamab, Kidney transplant
خلاصه مقالهFelzartamab, a CD38 monoclonal antibody, suppresses antibody-mediated rejection (ABMR) in kidney transplant patients but often leads to recurrence post-treatment. It reduces ABMR molecular activity, primarily targeting interferon gamma-inducible and NK cell transcripts, with minimal effect on endothelial transcripts. Suppression is incomplete in severe cases, and molecular recurrence is common by week 52. However, felzartamab shows parenchymal benefits, slowing kidney injury progression beyond treatment, suggesting potential long-term protective effects. To determine the molecular effects of 6 months of felzartamab treatment, genome-wide microarray analysis was performed on trial biopsies, comparing pre-treatment, end-of-treatment (week 24), and post-treatment (week 52) samples from 10 felzartamab and 10 placebo patients. Data no. GSE275824 were obtained from the GEO database, and the expression dataset was downloaded from pre-treatment, end-of-treatment (week 24), and post-treatment (week 52) samples. The data were analyzed with the GEO2R analysis program. As a result, differentially expressed genes that play roles were excluded. Gene ontology and pathway analysis of these genes were carried out with DAVID software. For the analysis of prominent genes, STRING software was used. In the validation of hub genes, genes were determined using the mcode and cytohubba attachments of the CYTOSCAPE software. We investigated significant downregulated DEGs (1031 baseline, 592 24week and 717 52 weeks down-regulated) and upregulated DEGs (900 baseline, 653 24week and 1428 52 weeks down-regulated). In gene ontology, it was observed that genes were collected in endoplasmic reticulum membrane, membrane, RNA polymerase II cis-regulatory region sequence-specific DNA binding, Golgi membrane, regulation of transcription by RNA polymerase II, DNA-binding transcription factor activity, RNA polymerase II-specific, plasma membrane, adaptive immune response, extracellular region, collagen-containing extracellular matrix. Based on the Cytoscape analysis, HLA-A, HLA-B, HLA-C, HLA-E, HLA-F, PPAPDC1A, PPAPDC1B, UQCRH, UQCRC2, COX5A, CYP4A22, RPL30, RPS20 and HIST1H3E genes were defined as hub genes. The findings suggest that felzartamab modulates critical pathways, providing insights into its molecular effects. Understanding these mechanisms may help identify biomarkers for treatment response and guide the development of alternative strategies to improve long-term kidney transplant outcomes.

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