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Spyrou, G. M.

Publications and source records attributed to Spyrou, G. M..

11 recordsLinked to original sources

Multi-omics dissection of Parkinson's patient subgroups associated with motor and cognitive severity

Heterogeneity in the severity of Parkinsons disease (PD) inhibits the effective interpretation of clinical trial outcomes. Multi-omics analysis may help explain the pathological mechanisms underlying disease progression and reveal biomarkers of clinical severity. We performed Multi-Omics Factor Analysis (MOFA) on whole blood RNA, miRNA and Cerebrospinal fluid (CSF) and blood plasma proteomics from the Parkinsons Progression Marker Initiative (PPMI), to identify molecular factors correlated with motor (MDS-UPDRS3) and cognitive (Semantic Fluency Test, SFT) function. Three molecular factors significantly correlated with the MDS-UPDRS3 score and two with SFT, which remained significant after adjusting for age, sex, and medication dose. We used the identified factors to stratify patients into subgroups with distinct motor and cognitive severity. The severe motor clusters showed deregulation of cytotoxic natural killer cell mechanisms in peripheral blood, and changes to proteins associated with the endoplasmic reticulum in CSF. The severe cognitive clusters showed changes in complement and synaptic dysfunction. Our analysis capitalizes on multi-omics data integration to enrich our understanding of the mechanisms driving motor and cognitive decline in PD, to support precision medicine.

bioinformatics↗

Machine Learning Models for Predicting Multiple Myeloma Staging and MGUS Progression Using Gene Expression Data

In this study, we developed and evaluated Machine Learning (ML) models aimed at predicting the stage of multiple myeloma (MM) and the progression of monoclonal gammopathy of undetermined significance (MGUS) to MM. Accurate staging of MM is critical for determining appropriate treatment strategies, and our models, employing algorithms such as ElasticNet, Random Forest, Boosting, and Support Vector Machines, demonstrated high efficacy in capturing the biological differences across disease stages. Among these, the ElasticNet model exhibited strong generalizability, achieving consistent multiclass AUC values across various datasets and data transformations. Predicting MGUS progression to MM presents a significant challenge due to the scarcity of MGUS cases that have progressed. We employed a two-pronged approach to address this: developing models using a limited dataset containing progressing MGUS patients and training models on combined MGUS and MM datasets. The models achieved AUC values slightly above 0.8, particularly with ElasticNet, Boosting and Support Vector Machines, indicating their potential in stratifying MGUS patients by progression risk. This study is original in integrating MM data with MGUS cases to enhance the predictive accuracy of MGUS progression, offering a novel methodology with potential clinical applications in patient monitoring and early intervention. Our feature selection and enrichment analyses further revealed that the identified genes are involved in key signaling pathways, including PI3K-Akt, MAPK, Wnt, and mTOR, all of which play crucial roles in MM pathogenesis. These findings align with established biological knowledge, suggest possible therapeutic targets and increase the explainability of our models.

bioinformatics↗

Stage-specific gene ratios highlight genes and mechanisms related to presymptomatic and symptomatic Multiple Myeloma

Background/aimMultiple Myeloma is the second most common blood cancer, characterised by the accumulation of malignant plasma cells and the production of large amounts of a monoclonal immunoglobulin protein, in the bone marrow. The identification and progression/behaviour of molecular markers across stages remains a scientific challenge. This work aims to provide a holistic approach to the understanding of the disease progression, providing specific methodologies and candidate biomarkers, able to characterise and distinguish the disease state across stages. Materials and methodsTwo large bulk RNA datasets were used to collect and integrate stage-specific information at the gene level by means of: (a) differential expression analysis to obtain differential expressed genes (DEGs), (b) a recently introduced computational methodology able to detect monotonically expressed genes (MEGs), (c) a proposed computational methodology that uses pairs of MEGs at sample level, to classify and discriminate different stages of Multiple Myeloma. Additional numerical metrics were applied to rank the performance of these pairs across samples, facilitating the characterization and differentiation of disease stages. Validation was conducted using five additional external datasets, which were then utilised to enrich the final selection of top-rated genes identified from the two bulk RNA datasets under study. The final top-ranked genes were further used for pathway enrichment analysis in order to provide candidate pathways per stage. ResultsWe first show that MEGs provide better statistics than DEGs, both at gene and pathway level analysis. Secondly, we show that the proposed computational methodology by means of MEGs reveals short lists of high discriminative genes across stages, which in turn highlight significant groups of pathways. ConclusionWe integrated traditional analysis of DEGs with a recently introduced methodology for identifying MEGs, creating a novel computational approach capable of identifying highly discriminative genes and pathways that can serve as candidate markers for stage identification in a single sample. HighlightsO_LIA novel computational approach was used to identify Monotonically Expressed Genes (MEGs) whose expression was constantly increasing or decreasing. Genes such as RB1, CD27, TP53, and MCL1, previously highlighted in Multiple Myeloma, showed a consistent monotonic pattern, providing potential indicators for tracking the progression from the pre-malignant stages to active Multiple Myeloma. C_LIO_LIThe study calculated gene pair ratios using MEGs characterised by normal distribution and low dispersion. These ratios effectively distinguished healthy from disease samples, although the discrimination between disease stages (MGUS, SMM, MM) was less clear due to their overlapping molecular profiles. C_LIO_LIEnrichment analysis of significant gene pairs identified critical pathways affected during Multiple Myeloma progression, such as bone disease-related calcium pathways, glucocorticoid-regulated functions, and cardiac and neurological systems. These findings align with known clinical manifestations in MM patients, such as bone disease and amyloid cardiomyopathy. C_LIO_LIThe gene lists generated from our computational approach were validated against internal and external datasets, confirming their applicability. The methodology showed promise in identifying candidate genes for disease progression and could be applied to other diseases to uncover novel gene pairs not highlighted by traditional analyses. C_LI

bioinformatics↗

Immediate-Early Genes as Influencers in Genetic Networks and their Role in Alzheimer's Disease

Abstract/SummaryImmediate-early genes (IEGs) are a class of activity-regulated genes (ARGs) that are transiently and rapidly activated in the absence of de novo protein synthesis in response to neuronal activity. We explored the role of IEGs in genetic networks to pinpoint potential drug targets for Alzheimers disease (AD). Using a combination of network analysis and genome-wide association study (GWAS) summary statistics we show that (1) IEGs exert greater topological influence across different human and mouse gene networks compared to other ARGs, (2) ARGs are sparsely involved in diseases and significantly more mutational constrained compared to non-ARGs, (3) Many AD-linked variants are in ARGs gene regions, mainly in MARK4 near FOSB, with an AD risk eQTL that increases MARK4 expression in cortical areas, (4) MARK4 holds an influential place in a dense AD multi-omic network and a high AD druggability score. Our work on IEGs influential network role is a valuable contribution to guiding interventions for diseases marked by dysregulation of their downstream targets and highlights MARK4 as a promising underexplored AD-target. HighlightsO_LIImmediate-early genes are topologically influential in brain genetic networks in mouse and human. C_LIO_LIActivity-regulated Genes (ARGs) are highly constrained with sparse gene-disease relevance. C_LIO_LIThere are several AD-associated variants in ARGs gene regions, mainly in MARK4 near FOSB. C_LIO_LIGWAS and network analysis of ARGs pinpoint MARK4 as a promising underexplored AD target. C_LI

bioinformatics↗

Ranking of cell clusters in a single-cell RNA-sequencing analysis framework using prior knowledge

Prioritization or ranking of different cell types in a scRNA-Seq framework can be performed in a variety of ways, some of these include: i) obtaining an indication of the proportion of cell types between the different conditions under study, ii) counting the number of differentially expressed genes (DEGs) between cell types and conditions in the experiment or, iii) prioritizing cell types based on prior knowledge about the conditions under study (i.e., a specific disease). These methods have drawbacks and limitations thus novel methods for improving cell ranking are required. Here we present a novel methodology that exploits prior knowledge in combination with expert-user information to accentuate cell types from a scRNA-seq analysis that yield the most biologically meaningful results. Prior knowledge is incorporated in a standardized, structured manner, whereby a checklist is attained by querying MalaCards human disease database with a disease of interest. The checklist is comprised of pathways and drugs and, optionally, drug mode of actions (MOAs), associated with the disease. The user is prompted to "edit" this checklist by removing or adding terms (in the form of keywords) from the list of predefined terms. Our methodology has substantial advantages to more traditional cell ranking techniques and provides an informative complementary methodology that utilizes prior knowledge in a rapid and automated manner, that has previously not been attempted by other studies. The current methodology is also implemented as an R package entitled Single Cell Ranking Analysis Toolkit (scRANK) and is available for download and installation via GitHub (https://#hub.com/aoulas/scRANK) Author SummarySingle-cell RNA Sequencing (scRNA-Seq) provides an additive resolution down to the cellular level that was previously not available from traditional "Bulk" RNA sequencing experiments. However, it is often difficult to prioritize the specific cell-types which are primarily responsible for the cause of a disease. This work presents a novel methodology that exploits prior knowledge for a disease in combination with expert-user information to accentuate cell types from a scRNA-seq analysis that are most closely related to the molecular mechanism of a disease of interest. Prior knowledge is incorporated in a standardized, structured manner, whereby a checklist is attained by querying a human disease database called MalaCards. This checklist comes in the form of pathways and drugs and, optionally, drug mode of actions (MOAs), associated with the disease. The expert-user is prompted to "edit" the prior knowledge checklist by removing or adding terms from the list of predefined terms. This methodology has substantial advantages to more traditional cell prioritizing or ranking techniques and provides an informative complementary methodology that utilizes prior knowledge in a rapid and automated manner.

bioinformatics↗

Oct4 is a gatekeeper of epithelial identity by regulating cytoskeletal dynamics in skin keratinocytes

Oct4 is a pioneer transcription factor regulating pluripotency. However, it is poorly known whether Oct4 has an impact on epidermal cells. We generated OCT4 knockout clonal cell lines using immortalized human skin keratinocytes to identify a functional role for the protein. Here we report that Oct4-deficient cells transitioned into a mesenchymal-like phenotype with enlarged size and shape, exhibited accelerated migratory behavior, decreased adhesion and appeared arrested at G2/M cell cycle checkpoint. Oct4 absence had a profound impact on cortical actin organization, with loss of microfilaments from cell membrane, increased puncta deposition in the cytoplasm and stress fiber formation. E-cadherin, {beta}-catenin and ZO1 were almost absent from cell-cell contacts while fibronectin deposition was markedly increased in ECM. Mapping of the transcriptional and chromatin profiles of Oct4-deficient cells revealed that Oct4 controls the levels of cytoskeletal, ECM and differentiation related genes, whereas epithelial identity is preserved through transcriptional and non-transcriptional mechanisms.

cell biology↗

DReAmocracy: A Method to Capitalize on Prior Drug Discovery Efforts to Highlight Candidate Drugs for Repurposing

In the area of drug research, several computational drug repurposing studies have highlighted candidate repurposed drugs, as well as drugs from clinical trial studies in different phases. To our knowledge, the aggregation of the proposed lists of drugs by previous studies has not been extensively exploited towards the generation of a dynamic reference matrix regarding the disease-related frequencies of drug features such as the modes of action, the initial indications and the targeted pathways. To fill this knowledge gap, we performed a weight-modulated majority voting of the modes of action, initial indications and targeted pathways of the drugs in a well-known repository, namely the Drug Repurposing Hub. Our method, DReAmocracy, exploits this pile of information and creates frequency tables and finally a disease suitability score for each drug. As a testbed, we applied this method to a group of neurodegenerative diseases (Alzheimers, Parkinsons, Huntingtons and Multiple Sclerosis). A super-reference table with drug suitability scores has been created for all four neurodegenerative diseases and can be queried for any drug candidate against them. Top-scored drugs for Alzheimers disease include agomelatine and mirtazapine, for Parkinsons disease apomorphine and pramipexole, for Huntingtons fluphezine and perphezine, and for Multiple Sclerosis zonisamide and disopyramide. Overall, DReAmocracy is a methodology that leverages the existing experimental and/or computational knowledge (1) to reveal trends in selected tracks of drug discovery research that includes modes of action, targeted pathways and initial indications for the investigated drugs and (2) to score new candidate drugs for repurposing against a selected disease.

bioinformatics↗

In depth analysis of Cyprus-specific mutations of SARS-CoV-2 strains using computational approaches

This study aims to characterize SARS-CoV-2 mutations which are primarily prevalent in the Cypriot population. Moreover, using computational approaches, we assess whether these mutations are associated with changes in viral virulence. We utilize genetic data from 144 sequences of SARS-CoV-2 strains from the Cypriot population obtained between March 2020 and January 2021, as well as all data available from GISAID. We combine this with countries regional information, such as deaths and cases per million, as well as COVID-19-related public health austerity measure response times. Initial indications of selective advantage of Cyprus-specific mutations are obtained by mutation tracking analysis. This entails calculating specific mutation frequencies within the Cypriot population and comparing these with their prevalence world-wide throughout the course of the pandemic. We further make use of linear regression models to extrapolate additional information that may be missed through standard statistical analysis. We report a single mutation found in the ORF1ab gene (S6059F) that appears to be significantly enriched within the Cypriot population. We further analyse this mutation using regression models to investigate possible associations with increased deaths and cases per million. Moreover, protein structure prediction tools show that the mutation infers a conformational change to the protein that significantly alters its structure when compared to the reference protein. Investigating Cyprus-specific mutations for SARS-CoV-2 can not only lead to important findings from which to battle the pandemic on a national level, but also provide insights into viral virulence worldwide.

bioinformatics↗

Identification of viral-mediated pathogenic mechanisms in neurodegenerative diseases using network-based approaches

During the course of a viral infection, virus-host protein-protein interactions (PPIs) play a critical role in allowing viruses to evade host immune responses, replicate and hence survive within the host. These interspecies molecular interactions can lead to viral-mediated perturbations of the human interactome causing the generation of various complex diseases, from cancer to neurodegenerative diseases (NDs). There are evidences suggesting that viral-mediated perturbations are a possible pathogenic aetiology in several NDs such as Amyloid Later Sclerosis, Parkinsons disease, Alzheimers disease and Multiple Sclerosis (MS), as they can cause degeneration of neurons via both direct and/or indirect actions. These diseases share several common pathological mechanisms, as well as unique disease mechanisms that reflect disease phenotype. NDs are chronic degenerative diseases of the central nervous system and current therapeutic approaches provide only mild symptomatic relief rather than treating the disease at heart, therefore there is unmet need for the discovery of novel therapeutic targets and pharmacotherapies. In this paper we initially review databases and tools that can be utilized to investigate viral-mediated perturbations in complex NDs using network-based analysis by examining the interaction between the ND-related PPI disease networks and the virus-host PPI network. Afterwards we present our integrative network-based bioinformatics approach that accounts for pathogen-genes-disease related PPIs with the aim to identify viral-mediated pathogenic mechanisms focusing in MS disease. We identified 7 high centrality nodes that can act as disease communicator nodes and exert systemic effects in the MS enriched KEGG pathways network. In addition, we identified 12 KEGG pathways targeted by 67 viral proteins from 8 viral species that might exert viral-mediated pathogenic mechanisms in MS by interacting with the disease communicator nodes. Finally, our analysis highlighted the Th17 differentiation pathway, a hub-bottleneck disease communicator node and part of the 12 underlined KEGG pathways, as a key viral-mediated pathogenic mechanism and a possible therapeutic target for MS disease.

bioinformatics↗

Generalized linear models provide a measure of virulence for specific mutations in SARS-CoV-2 strains

This study aims to highlight SARS-COV-2 mutations which are associated with increased or decreased viral virulence. We utilize, genetic data from all strains available from GISAID and countries regional information such as deaths and cases per million as well as covid-19-related public health austerity measure response times. Initial indications of selective advantage of specific mutations can be obtained from calculating their frequencies across viral strains. By applying modelling approaches, we provide additional information that is not evident from standard statistics or mutation frequencies alone. We therefore, propose a more precise way of selecting informative mutations. We highlight two interesting mutations found in genes N (P13L) and ORF3a (Q57H). The former appears to be significantly associated with decreased deaths and cases per million according to our models, while the latter shows an opposing association with decreased deaths and increased cases per million. Moreover, protein structure prediction tools show that the mutations infer conformational changes to the protein that significantly alter its structure when compared to the reference protein.

bioinformatics↗

Drug repurposing through a bioinformatics pipeline applied on IPF and other fibrotic diseases

Subject Fibrotic diseases cover a spectrum of systemic and organ-specific maladies that affect a large portion of the population, currently without cure. The shared characteristic these diseases feature is their uncontrollable fibrogenesis deemed responsible for the accumulated damage in the susceptible tissues. Idiopathic Pulmonary Fibrosis (IPF), an interstitial lung disease, is one of the most common and studied fibrotic diseases and still remains an active research target.Objective We highlight unique and common (i) genes, (ii) biological pathways and (iii) candidate repurposed drugs among nine fibrotic diseases. We bibliographically explore the resulting candidate substances for potential anti-fibrotic mode of action and focus on diseases that appear to be more similar to IPF so as to jointly examine potential treatments.Methodology We identify key genes for the 9 fibrotic diseases by analyzing transcriptomics datasets. We construct gene-to-gene networks for each disease and examine these networks to explore functional communities of biological pathways. We also use the most significant genes as input in Drug Repurposing (DR) tools and re-rank the resulting candidates according to their structural properties and functional relationship to each investigated disease.Results We identify 7 biological pathways involved in all 9 fibrotic diseases as well as pathways unique to some of these diseases. Based on our DR results, we suggest captopril and ibuprofen that both appear to slow the progression of fibrotic diseases according to existing bibliography. We also recommend nafcillin and memantine, which haven’t been studied against fibrosis yet, for further wet-lab experimentation. We also observe a group of cardiomyopathy-related pathways that are exclusively highlighted for Oral Submucous Fibrosis (OSF). We suggest digoxin to be tested against OSF, since we observe cardiomyopathy-related pathways implicated in OSF and there is bibliographic evidence that digoxin may potentially clear myocardial fibrosis. Finally, we establish that IPF shares several involved genes, biological pathways and candidate inhibiting-drugs with Dupuytren’s Disease, IgG4-related Disease, SSc and Cystic Fibrosis. We propose that treatments for these fibrotic diseases should be jointly pursued.Competing Interest StatementThe authors have declared no competing interest.View Full Text

bioinformatics↗