{"entity": "researcher", "timestamp": "2026-08-20T20:43:08.209Z", "family": "Kaynar", "given": "Ali", "initials": "A", "orcid": "0000-0002-8507-744X", "affiliations": ["Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King's College London, London SE1 9RT, UK."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/afaea854b1ad44ec8c6efc6323f516cd.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/afaea854b1ad44ec8c6efc6323f516cd"}}, "publications": [{"entity": "publication", "iuid": "35ef6915c3e84674815a2bc5d9f9e404", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/35ef6915c3e84674815a2bc5d9f9e404.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/35ef6915c3e84674815a2bc5d9f9e404"}}, "title": "Identifying Hub Genes and Metabolic Pathways in Collagen VI-Related Dystrophies: A Roadmap to Therapeutic Intervention.", "authors": [{"family": "Ceyhan", "given": "Atakan Burak", "initials": "AB", "orcid": "0009-0004-7279-7482", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a7b1d40cd1ec4d4aa75f133db6d2ff1a.json"}}, {"family": "Kaynar", "given": "Ali", "initials": "A", "orcid": "0000-0002-8507-744X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/afaea854b1ad44ec8c6efc6323f516cd.json"}}, {"family": "Altay", "given": "Ozlem", "initials": "O"}, {"family": "Zhang", "given": "Cheng", "initials": "C", "orcid": "0000-0002-3721-8586", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f46e4161be08458994efddb75ed75874.json"}}, {"family": "Temel", "given": "Sehime Gulsun", "initials": "SG", "orcid": "0000-0002-9802-0880", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e08a9741204744e78b62958e0bf94794.json"}}, {"family": "Turkez", "given": "Hasan", "initials": "H", "orcid": "0000-0002-7046-8990", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cf2f1748757d45cabfe56fdfaccead6a.json"}}, {"family": "Mardinoglu", "given": "Adil", "initials": "A", "orcid": "0000-0002-4254-6090", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ca58bf2d214047e0ae5e38a42a0f2808.json"}}], "type": "journal article", "published": "2024-10-29", "journal": {"title": "Biomolecules", "issn": "2218-273X", "volume": "14", "issue": "11", "issn-l": null}, "abstract": "Collagen VI-related dystrophies (COL6RD) are a group of rare muscle disorders caused by mutations in specific genes responsible for type VI collagen production. It affects muscles, joints, and connective tissues, leading to weakness, joint problems, and structural issues. Currently, there is no effective treatment for COL6RD; its management typically addresses symptoms and complications. Therefore, it is essential to decipher the disease's molecular mechanisms, identify drug targets, and develop effective treatment strategies to treat COL6RD. In this study, we employed differential gene expression analysis, weighted gene co-expression network analysis, and genome-scale metabolic modeling to investigate gene expression patterns in COL6RD patients, uncovering key genes, significant metabolites, and disease-related pathophysiological pathways. First, we performed differential gene expression and weighted gene co-expression network analyses, which led to the identification of 12 genes (CHCHD10, MRPS24, TRIP10, RNF123, MRPS15, NDUFB4, COX10, FUNDC2, MDH2, RPL3L, NDUFB11, PARVB) as potential hub genes involved in the disease. Second, we utilized a drug repurposing strategy to identify pharmaceutical candidates that could potentially modulate these genes and be effective in the treatment. Next, we utilized context-specific genome-scale metabolic models to compare metabolic variations between healthy individuals and COL6RD patients. Finally, we conducted reporter metabolite analysis to identify reporter metabolites (e.g., phosphatidates, nicotinate ribonucleotide, ubiquinol, ferricytochrome C). In summary, our analysis revealed critical genes and pathways associated with COL6RD and identified potential targets, reporter metabolites, and candidate drugs for therapeutic interventions.", "doi": "10.3390/biom14111376", "pmid": "39595553", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11592009"}, {"db": "pii", "key": "biom14111376"}, {"db": "GEO", "key": "GSE103608"}], "notes": [], "created": "2026-08-20T13:38:48.538Z", "modified": "2026-08-20T13:38:48.796Z"}, {"entity": "publication", "iuid": "01c3e943e14c4367bb8fd9cc7c8d2bba", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/01c3e943e14c4367bb8fd9cc7c8d2bba.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/01c3e943e14c4367bb8fd9cc7c8d2bba"}}, "title": "Unveiling the Molecular Mechanisms of Glioblastoma through an Integrated Network-Based Approach.", "authors": [{"family": "Kaynar", "given": "Ali", "initials": "A", "orcid": "0000-0002-8507-744X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/afaea854b1ad44ec8c6efc6323f516cd.json"}}, {"family": "Kim", "given": "Woonghee", "initials": "W"}, {"family": "Ceyhan", "given": "Atakan Burak", "initials": "AB", "orcid": "0009-0004-7279-7482", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a7b1d40cd1ec4d4aa75f133db6d2ff1a.json"}}, {"family": "Zhang", "given": "Cheng", "initials": "C", "orcid": "0000-0002-3721-8586", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f46e4161be08458994efddb75ed75874.json"}}, {"family": "Uhl\u00e9n", "given": "Mathias", "initials": "M", "orcid": "0000-0002-4858-8056", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9ea446aa574042a295d5f69437402f76.json"}}, {"family": "Turkez", "given": "Hasan", "initials": "H", "orcid": "0000-0002-7046-8990", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cf2f1748757d45cabfe56fdfaccead6a.json"}}, {"family": "Shoaie", "given": "Saeed", "initials": "S"}, {"family": "Mardinoglu", "given": "Adil", "initials": "A", "orcid": "0000-0002-4254-6090", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ca58bf2d214047e0ae5e38a42a0f2808.json"}}], "type": "journal article", "published": "2024-10-01", "journal": {"title": "Biomedicines", "issn": "2227-9059", "volume": "12", "issue": "10", "issn-l": null}, "abstract": "Background/Objectives: Despite current treatments extending the lifespan of Glioblastoma (GBM) patients, the average survival time is around 15-18 months, underscoring the fatality of GBM. This study aims to investigate the impact of sample heterogeneity on gene expression in GBM, identify key metabolic pathways and gene modules, and explore potential therapeutic targets. Methods: In this study, we analysed GBM transcriptome data derived from The Cancer Genome Atlas (TCGA) using genome-scale metabolic models (GEMs) and co-expression networks. We examine transcriptome data incorporating tumour purity scores (TPSs), allowing us to assess the impact of sample heterogeneity on gene expression profiles. We analysed the metabolic profile of GBM by generating condition-specific GEMs based on the TPS group. Results: Our findings revealed that over 90% of genes showing brain and glioma specificity in RNA expression demonstrate a high positive correlation, underscoring their expression is dominated by glioma cells. Conversely, negatively correlated genes are strongly associated with immune responses, indicating a complex interaction between glioma and immune pathways and non-tumorigenic cell dominance on gene expression. TPS-based metabolic profile analysis was supported by reporter metabolite analysis, highlighting several metabolic pathways, including arachidonic acid, kynurenine and NAD pathway. Through co-expression network analysis, we identified modules that significantly overlap with TPS-correlated genes. Notably, SOX11 and GSX1 are upregulated in High TPS, show a high correlation with TPS, and emerged as promising therapeutic targets. Additionally, NCAM1 exhibits a high centrality score within the co-expression module, which shows a positive correlation with TPS. Moreover, LILRB4, an immune-related gene expressed in the brain, showed a negative correlation and upregulated in Low TPS, highlighting the importance of modulating immune responses in the GBM mechanism. Conclusions: Our study uncovers sample heterogeneity's impact on gene expression and the molecular mechanisms driving GBM, and it identifies potential therapeutic targets for developing effective treatments for GBM patients.", "doi": "10.3390/biomedicines12102237", "pmid": "39457550", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11504402"}, {"db": "pii", "key": "biomedicines12102237"}], "notes": [], "created": "2026-08-20T13:38:56.812Z", "modified": "2026-08-20T13:38:56.909Z"}, {"entity": "publication", "iuid": "6110ae28b294411ab4245240c5608b87", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/6110ae28b294411ab4245240c5608b87.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/6110ae28b294411ab4245240c5608b87"}}, "title": "Discovery of a Therapeutic Agent for Glioblastoma Using a Systems Biology-Based Drug Repositioning Approach.", "authors": [{"family": "Kaynar", "given": "Ali", "initials": "A", "orcid": "0000-0002-8507-744X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/afaea854b1ad44ec8c6efc6323f516cd.json"}}, {"family": "Ozcan", "given": "Mehmet", "initials": "M", "orcid": "0000-0002-1222-2802", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e690dbebe4144d72b97aad264290fd72.json"}}, {"family": "Li", "given": "Xiangyu", "initials": "X", "orcid": "0000-0002-8301-9959", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5c452ad4e8bb4302a572693103742047.json"}}, {"family": "Turkez", "given": "Hasan", "initials": "H", "orcid": "0000-0002-7046-8990", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cf2f1748757d45cabfe56fdfaccead6a.json"}}, {"family": "Zhang", "given": "Cheng", "initials": "C", "orcid": "0000-0002-3721-8586", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f46e4161be08458994efddb75ed75874.json"}}, {"family": "Uhl\u00e9n", "given": "Mathias", "initials": "M", "orcid": "0000-0002-4858-8056", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9ea446aa574042a295d5f69437402f76.json"}}, {"family": "Shoaie", "given": "Saeed", "initials": "S"}, {"family": "Mardinoglu", "given": "Adil", "initials": "A", "orcid": "0000-0002-4254-6090", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ca58bf2d214047e0ae5e38a42a0f2808.json"}}], "type": "journal article", "published": "2024-07-18", "journal": {"title": "Int J Mol Sci", "issn": "1422-0067", "volume": "25", "issue": "14", "issn-l": null}, "abstract": "Glioblastoma (GBM), a highly malignant tumour of the central nervous system, presents with a dire prognosis and low survival rates. The heterogeneous and recurrent nature of GBM renders current treatments relatively ineffective. In our study, we utilized an integrative systems biology approach to uncover the molecular mechanisms driving GBM progression and identify viable therapeutic drug targets for developing more effective GBM treatment strategies. Our integrative analysis revealed an elevated expression of CHST2 in GBM tumours, designating it as an unfavourable prognostic gene in GBM, as supported by data from two independent GBM cohorts. Further, we pinpointed WZ-4002 as a potential drug candidate to modulate CHST2 through computational drug repositioning. WZ-4002 directly targeted EGFR (ERBB1) and ERBB2, affecting their dimerization and influencing the activity of adjacent genes, including CHST2. We validated our findings by treating U-138 MG cells with WZ-4002, observing a decrease in CHST2 protein levels and a reduction in cell viability. In summary, our research suggests that the WZ-4002 drug candidate may effectively modulate CHST2 and adjacent genes, offering a promising avenue for developing efficient treatment strategies for GBM patients.", "doi": "10.3390/ijms25147868", "pmid": "39063109", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11277330"}, {"db": "pii", "key": "ijms25147868"}], "notes": [], "created": "2026-08-20T13:41:54.695Z", "modified": "2026-08-20T13:41:54.766Z"}]}