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    A comprehensive analysis of the angiogenesis-related genes in glioblastoma multiforme vs. brain lower grade glioma
    (Assoc Arquivos Neuro- Psiquiatria, 2020) Sut, Burcu Biterge
    Brain tumors are one of the most common causes of cancer-related deaths around the world. Angiogenesis is critical in high-grade malignant gliomas, such as glioblastoma multiforme. Objective: The aim of this study is to comparatively analyze the angiogenesis-related genes, namely VEGFA, VEGFB, KDR, CXCL8, CXCR1 and CXCR2 in LGG vs. GBM to identify molecular distinctions using datasets available on The Cancer Genome Atlas (TCGA). Methods: DNA sequencing and mRNA expression data for 514 brain lower grade glioma (LGG) and 592 glioblastoma multiforme (GBM) patients were acquired from The Cancer Genome Atlas (TCGA), and the genetic alterations and expression levels of the selected genes were analyzed. Results: We identified six distinct KDR mutations in the LGG patients and 18 distinct KDR mutations in the GBM patients, including missense and nonsense mutations, frame shift deletion and altered splice region. Furthermore, VEGFA and CXCL8 were significantly overexpressed within GBM patients. Conclusions: VEGFA and CXCL8 are important factors for angiogenesis, which are suggested to have significant roles during tumorigenesis. Our results provide further evidence that VEGFA and CXCL8 could induce angiogenesis and promote LGG to progress into GBM. These findings could be useful in developing novel targeted therapeutics approaches in the future.
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    Computational analysis of TP53 vs. CTNNB1 mutations in hepatocellular carcinoma suggests distinct cancer subtypes with differential gene expression profiles and chromatin states
    (Elsevier Sci Ltd, 2020) Sut, Burcu Biterge
    Genetic variations are important drivers of carcinogenesis. It is extremely important to identify molecular distinctions between patients of the same disease for effective cancer treatment. This study aims to understand cellular and molecular differences between hepatocellular carcinoma patients carrying TP53 or CTNNB1 mutations, which could possess clinical significance. For this purpose, DNA sequencing and mRNA expression data for hepatocellular carcinoma patients were analyzed. Differentially expressed genes and the cellular processes that they are involved in were determined for TP53/CTNNB1-altered patient groups. We found that the mutations of TP53/CTNNB1 genes in the patient cohort was almost mutually exclusive and gene expression profiling in these subgroups were unique. Gene Ontology (GO) enrichment analysis of the differentially expressed genes identified several important cellular processes. In line with this, selected histone variants, histone chaperons, as well as the binding partners of TP53/CTNNB1 showed distinct enrichment levels. TP53/CTNNB1-altered patient groups laso showed different prognostic outcomes and tumor infiltration levels. In conclusion, our results strongly imply differential chromatin states and transcriptional regulation in relation to the mutational status of TP53 vs. CTNNB1, suggesting that these genes might be inducing different cellular pathways involving distinct chromatin environments during the course of carcinogenesis.
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    Data article on genes that share similar expression patterns with EEF1 complex proteins in hepatocellular carcinoma
    (Elsevier, 2020) Sut, Burcu Biterge
    Eukaryotic Elongation Factor complex 1 (EEF1) consists of six subunits namely EEF1A1, EEF1A2, EEF1B2, EEF1D, EEF1E1 and EEF1G. Recently we showed that EEF1 complex proteins might play critical roles in cancer [1]. This article provides data on genes that share similar expression patterns with EEF1 complex proteins in cancer by analyzing RNA expression data using GEPIA online tool. Correlation analysis was performed on selected genes in a pairwise manner and the Pearson coefficients were automatically calculated by the GEPIA online tool. These data can be useful for future studies directed towards understanding the mechanisms by (C) 2020 The Author(s). Published by Elsevier Inc.
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    Histopathological and epigenetic alterations in the spinal cord due to prenatal electromagnetic field exposure: An H3K27me3-related mechanism
    (Sage Publications Inc, 2021) Keles, Ayse Ikinci; Sut, Burcu Biterge
    Neural system development is one of the most important stages of embryogenesis. Perturbations in this crucial process due to genetic and environmental risk factors cause neural tube defects and other central nervous system diseases. We investigated the effects of prenatal exposure to 900-MHz electromagnetic field (EMF) on the spinal cord. Pregnant rats were exposed to 900-MHz EMF for 1 h/day from E13.5 until birth. Six pups from the control and EMF groups were sacrificed at postnatal day 32, and the upper thoracic region of the spine was removed and processed for histological procedures. For histopathological analyses, hematoxylin&eosin staining and, for stereological analyses and the quantitation of motor neurons, cresyl violet staining was performed. H3K27me3 levels were determined via immunofluorescence staining. Histopathological analysis identified structural alterations of ependymal cells, enlarged central canals, as well as degenerated and shrunken motor neurons in the EMF group, while the control group tissues had normal appearances. We also observed enrichment of H3K27me3 in the ependymal cells and the motor neurons in the spinal cord of the control group rats, while the EMF group had low levels of H3K27me3 staining. Our results suggest that the loss of H3K27me3 signals might correlate with reduced neuronal stem cell potential in the EMF group and result in anatomical and structural differences in the spinal cord. This study provided a comprehensive histopathological analysis of the spinal cord after prenatal EMF exposure and offered an H3K27me3-dependent molecular explanation for the detrimental effects of EMF exposure on the spine.
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    Molecular profiling of immune cell-enriched Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) interacting protein USP13
    (Pergamon-Elsevier Science Ltd, 2020) Sut, Burcu Biterge
    Aims: Coronavirus disease 2019 (COVID-19), which is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), is a major health concern worldwide. Due to the lack of specific medication and vaccination, drug-repurposing attempts has emerged as a promising approach and identified several human proteins interacting with the virus. This study aims to provide a comprehensive molecular profiling of the immune cell-enriched SARS-CoV-2 interacting protein USP13. Materials and methods: The list of immune cell-enriched proteins interacting with SARS-CoV-2 was retrieved from The Human Protein Atlas. Genomic alterations were identified using cBioPortal. Survival analysis was performed via Kaplan-Meier Plotter. Analyses of protein expression and tumor infiltration levels were carried out by TIMER. Key findings: 14 human proteins that interact with SARS-CoV-2 were enriched in immune cells. Among these proteins, USP13 had the highest frequency of genomic alterations. Higher USP13 levels were correlated with improved survival in breast and lung cancers, while resulting in poor prognosis in ovarian and gastric cancers. Furthermore, copy number variations of USP13 significantly affected the infiltration levels of distinct subtypes of immune cells in head & neck, lung, ovarian and stomach cancers. Although our results suggested a tumor suppressor role for USP13 in lung cancer, in other cancers, its role seemed to be context-dependent. Significance: It is critical to identify and characterize human proteins that interact with SARS-CoV-2 in order to have a better understanding of the disease and to develop better therapies/vaccines. Here, we provided a comprehensive molecular profiling the immune cell-enriched SARS-CoV-2 interacting protein USP13, which will be useful for future studies.
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    Somatic Missense Mutations of Histone Variant H3.3 in Central Nervous System Cancers
    (Istanbul University Press, 2020) Sut, Burcu Biterge
    Objective: Histone variants are important modulators of chromatin functions. Studies have pointed out that epigenetic factors are often dysregulated in carcinogenesis. Although some cancer-Associated mutations of the histone variant H3.3 have been identified previously, a complete list of H3.3 mutations and their potential effects is yet to be uncovered. Therefore, this study aims to identify the missense mutations of the histone variant H3.3 in central nervous system (CNS) cancers and to computationally predict their functional consequences on pathogenicity, protein stability and structure. Materials and Methods: A complete set of human H3.3 mutations was acquired from the COSMIC v90 database and missense mutations were selected. The potential effects of these mutations were assessed using PredictSNP2 and FATHMMXF. Structural outcomes were predicted using MUpro and HOPE servers. Results: We identified 45 unique missense H3.3 substitutions in several tissues including CNS. PredictSNP2 and FATHMM-XF predicted 17 and 42 mutations as deleterious respectively, most of which caused decreased protein stability. Amino acid alterations in CNS cancers were predicted to cause alterations of the 3D structure. Conclusion: Histone variants play significant roles in epigenetic regulation and are often mutated in cancers. Our results showed that H3.3 mutations detected in CNS cancers could affect the genomic distribution of post-Translational modifications and histone variants, hence dramatically alter the gene expression profile and contribute to carcinogenesis. © Istanbul University Press. All rights reserved.