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Esteban-Medina, M.

Publications and source records attributed to Esteban-Medina, M..

3 recordsLinked to original sources

Domain-adaptation deep learning models do not outperform simple baseline models in single-cell anti-cancer drug sensitivity prediction

Tumor drug response is profoundly shaped by cellular heterogeneity, making single-cell resolution essential for precision oncology. While drug-response labels are abundant for cell lines at bulk resolution, translating these predictive models to the single-cell level requires effective domain adaptation strategies. Motivated by advances in computer vision, recent deep-learning domain adaptation methods promise to transfer knowledge from bulk (source) to single-cell (target) data with-out the need for target labels. However, their true translational utility remains unclear due to a lack of rigorous evaluation against non-adaptive baselines across diverse biological and technical contexts. Here, we present a comprehensive benchmark comparing four representative domain adaptation methods against two simple gradient boosting baseline methods. Through systematic evaluation across 19 single-cell datasets and 10 drugs, we show that none of the complex adaptation methods outperforms the simpler baselines. By analyzing the drivers of model performance, we find that target-informed hyperparameter tuning and sparse label supervision are the principal sources of prediction gain. Our study reveals that current approaches fail to bridge the bulk-to-single-cell conceptual shift and provides a unified codebase and comprehensive data collection to facilitate robust model comparisons. By enabling transparent evaluation and robust benchmarking against simple models, this resource aims to accelerate future developments in translational pharmacogenomics.

cancer biology↗

A versatile and interoperable computational framework for the analysis and modeling of COVID-19 disease mechanisms

The COVID-19 Disease Map project is a large-scale community effort uniting 277 scientists from 130 Institutions around the globe. We use high-quality, mechanistic content describing SARS-CoV-2-host interactions and develop interoperable bioinformatic pipelines for novel target identification and drug repurposing. Community-driven and highly interdisciplinary, the project is collaborative and supports community standards, open access, and the FAIR data principles. The coordination of community work allowed for an impressive step forward in building interfaces between Systems Biology tools and platforms. Our framework links key molecules highlighted from broad omics data analysis and computational modeling to dysregulated pathways in a cell-, tissue- or patient-specific manner. We also employ text mining and AI-assisted analysis to identify potential drugs and drug targets and use topological analysis to reveal interesting structural features of the map. The proposed framework is versatile and expandable, offering a significant upgrade in the arsenal used to understand virus-host interactions and other complex pathologies.

systems biology↗

Mechanistic modeling of the SARS-CoV-2 disease map

Here we present a web interface that implements a comprehensive mechanistic model of the SARS-CoV-2 disease map in which the detailed activity of the human signaling circuits related to the viral infection and the different antiviral responses, including immune and inflammatory activities, can be inferred from gene expression experiments. Moreover, given to the mechanistic properties of the model, the effect of potential interventions, such as knock-downs, over-expression or drug effects (currently the system models the effect of more than 8000 DrugBank drugs) can be studied in specific conditions. By providing a holistic, systems biology approach to the understanding of the complexities of the viral infection process, this tool will become an important asset in the search for efficient antiviral treatments. The tool is freely available at: http://hipathia.babelomics.org/covid19/

systems biology↗