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Biology subjects

Krivonosov, M.

Publications and source records attributed to Krivonosov, M..

4 recordsLinked to original sources

Explainable machine learning models for glioma subtype classification and survival prediction

Gliomas are complex and heterogeneous brain tumors characterized by an unfavorable clinical course and a fatal prognosis, which can be improved by an early determination of tumor kind. Here, we develop explainable machine learning (ML) models for classifying three major glioma subtypes (astrocytoma, oligodendroglioma, and glioblastoma) and predicting survival rates based on RNA-seq data. Thirteen key genes (TERT, NOX4, MMP9, TRIM67, ZDHHC18, HDAC1, TUBB6, ADM, NOG, CHEK2, KCNJ11, KCNIP2, and VEGFA) proved to be closely associated with glioma subtypes as well as survival. The Support Vector Machine (SVM) turned out to be the optimal classification model with the balanced accuracy of 0.816 and the area under the receiver operating characteristic curve (AUC) of 0.896 for the test datasets. The Case-Control Cox regression model (CoxCC) proved best for predicting survival with the Harrells C-index of 0.809 and 0.8 for the test datasets. Using SHapley Additive exPlanations (SHAP) we reveal the gene expression influence on the outputs of both models, thus enhancing the transparency of the prediction generation process. The results indicate that the developed models could serve as a valuable practical tool for clinicians, assisting them in diagnosing and determining optimal treatment strategies for patients with glioma. Simple SummaryDistinguishing glioma subtypes and assessing patient survival is a non-trivial task due to the high heterogeneity of these brain tumors. Accurate diagnosis is a critical step in developing treatment tactics. In this study, using publicly available RNA sequencing data, we identified a set of key genes and built explainable AI models to classify the major glioma subtypes (astrocytoma, oligodendroglioma, and glioblastoma) and predict patient survival. Experiments evaluating the models demonstrated their ability to generate highly accurate predictions. At the same time, the explainable artificial intelligence approach allowed us to identify relationships between the expression levels of the selected genes and the predictions of the models. Taken together, the obtained results indicate the potential of our predictive models for glioma diagnosis.

bioinformatics↗

Accelerated epigenetic aging and inflammatory/immunological profile (ipAGE) in patients with chronic kidney disease

Chronic kidney disease (CKD) is defined by reduced estimated glomerular filtration rate (eGFR). This failure can be related to a phenotype of accelerated aging. In this work we considered 76 subjects with end-stage renal disease (ESRD) and 83 healthy controls. We evaluated two measures that can be informative of the rate of aging, i.e. whole blood DNA methylation using the Illumina Infinium EPIC array and plasma levels of a selection of inflammatory/immunological proteins using Multiplex Immunoassays. We demonstrated accelerated aging in terms of the most common epigenetic age estimators in CKD patients. We developed a new predictor of age based on inflammatory/immunological profile (ipAGE) and confirmed age acceleration in CKD patients. Finally, we evaluated the relationship between epigenetic age predictors and ipAGE and further identified the inflammatory/immunological biomarkers differentially expressed between cases and controls. In summary, our data show an accelerated aging phenotype in CKD patients sustained by inflammatory processes.

bioinformatics↗

Age-dependent DNA methylation Parenclitic Networks in family-based cohort patients with Down Syndrome

Despite the fact that the cause of Down Syndrome (DS) is well established, the underlying molecular mechanisms that contribute to the syndrome and the phenotype of accelerated aging remain largely unknown. DNA methylation profiles are largely altered in DS, but it remains unclear how different methylation regions and probes are structured into a network of interactions. We develop and generalize the Parenclitic Networks approach that enables finding correlations between distant CpG probes (which are not pronounced as stand-alone biomarkers) and quantifies hidden network changes in DNA methylation. DS and a familybased cohort (including healthy siblings and mothers of persons with DS) are used as a case study. Following this approach, we constructed parenclitic networks and obtained different signatures that indicate (i) differences between individuals with DS and healthy individuals; (ii) differences between young and old healthy individuals; (iii) differences between DS individuals and their age-matched siblings, and (iv) difference between DS and the adult population (their mothers). The Gene Ontology analysis showed that the CpG network approach is more powerful than the single CpG approach in identifying biological processes related to DS phenotype. This includes the processes occurring in the central nervous system, skeletal muscles, disorders in carbohydrate metabolism, cardiopathology, and oncogenes. Our open-source software implementation is accessible to all researchers. The software includes a complete workflow, which can be used to construct Parenclitic Networks with any machine learning algorithm as a kernel to build edges. We anticipate a broad applicability of the approach to other diseases.

bioinformatics↗

Complex sex-specific age-related changes in DNA methylation including variability, epimutations and entropy

In humans, females live longer than males but experience a worse longevity, as genome-wide autosomal DNA methylation differences between males and females have been reported. So far, few studies have investigated if DNA methylation is differently affected by aging in males and females. We performed a meta-analysis of 4 large whole blood datasets, comparing 4 aspects of epigenetic age-dependent remodeling between the two sexes: differential methylation, variability, epimutations and entropy. We reported that a large fraction (43%) of sex-associated probes undergoes age-associated DNA methylation changes, and that a limited number of probes shows age-by-sex interaction. We experimentally validated 2 regions mapping in FIGN and PRR4 genes, and showed sex-specific deviations of their methylation patterns in models of decelerated (centenarians) and accelerated (Down syndrome) aging. While we did not find sex differences in the age-associated increase in epimutations and in entropy, we showed that the number of probes showing age-related increase in methylation variability is 15 times higher in males compared to females. Our results can offer new epigenetic tools to study the interaction between aging and sex and can pave the way to the identification of molecular triggers of sex differences in longevity and age-related diseases prevalence.

genomics↗