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Carbonell-Caballero, J.

Publications and source records attributed to Carbonell-Caballero, J..

5 recordsLinked to original sources

EBEx: an Ensemble-Based Explainable Framework for Gene Calling in Heterogeneous Diseases

Complex and clinically heterogeneous diseases pose significant challenges for gene prioritisation and patient stratification, as relevant genes often show weak or context-specific signals and transcriptomic datasets are limited in size. These limitations hinder the discovery of robust molecular signatures using traditional case-control approaches and motivate computational pipelines capable of capturing molecular diversity. Here, we present an explainable ensemble-based AI pipeline to prioritise disease-relevant genes from transcriptomic data, using Chronic Obstructive Pulmonary Disease (COPD) as a use case. To retain biologically relevant interactors obscured by molecular heterogeneity, the framework integrates data-driven signals with curated COPD-related gene sets, further expanded through network-based prioritisation and supported by molecular interactions. Gene relevance is evaluated via aggregated explainability scores across multiple classifier configurations to ensure robust candidate selection. The final set comprised < 8% of evaluated genes, [~] 62% arising from network-based expansion, substantially reducing dimensionality while preserving biological heterogeneity. Beyond case-control classification, the approach identified candidate genes and molecular subgroups associated with specific clinical features, capturing patient-level heterogeneity. The prioritised genes recapitulated key disease-related processes, including immune responses and extracellular matrix degradation, and highlighted additional associations like the enrichment of the IL-4 and IL-13 signalling pathway, which is of clinical interest given ongoing biologic developments targeting these axes. Our pipeline outperformed existing methods in discriminating COPD from controls, and the final gene list was validated in independent cohorts. Implemented as a scalable and reusable R package, this framework facilitates the study of molecular heterogeneity in complex diseases like COPD, supporting advances in diagnosis and precision medicine. Availability and implementationEBEx code and tutorials can be found in: https://iposelag.github.io/EBEx/

bioinformatics↗

PARP1 Regulates 3D Structure and Function of Super-Enhancers and Hormone-Control Regions in Breast Cancer Cells

Poly (ADP-ribose) polymerase 1 (PARP1) has been linked to various genomic pathways and in the maintenance of genomic stability. PARP1 has also been postulated to regulate cis-regulatory elements, but the mechanisms remain largely unknown. Here, we employed genomic approaches to show how PARP1 occupies Super-Enhancers (SEs) of luminal A T47D breast cancer cells and how some PARP1 is dynamically relodged by progesterone at hormone-control regions (HCRs). Disruption of PARP1 causes transcriptome reprogramming, altering the expression of both SE-associated and HCRs-regulated genes. This is achieved through a dual coordinated action in the establishment of long-range and intra-TADs chromatin loops, which are lost upon PARP1 ablation, but enforced by its catalytic inhibition. We show that PARP1 also plays a role in regulation of chromatin compartments. Our results reveal PARP1, as a new chromatin looper and compartments organizer controlling SEs and HCRs genes linked to cell identity and hormonal response in breast cancer cells via 3D genome organization. Highlights (Separate document)O_LIPARP1 occupies cell specific super-enhancers and hormone-control regions. C_LIO_LILoss of PARP1 alters the cell identity and progestin-induced gene expression signature. C_LIO_LIGene expression changes upon PARP1 loss relay on altered 3D chromatin looping and compartments. C_LI eTOC blurbWe have discovered that the nuclear repair protein and cancer drug target; PARP1 is preferentially bound at super-enhancers. The binding of PARP1 is essential for the underlying, cell specific gene expression program and the 3D structure of the chromatin surrounding the super-enhancer regions. Graphical abstractSeparate document O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=198 SRC="FIGDIR/small/668155v1_ufig1.gif" ALT="Figure 1"> View larger version (81K): org.highwire.dtl.DTLVardef@1da9027org.highwire.dtl.DTLVardef@2e1966org.highwire.dtl.DTLVardef@8582eaorg.highwire.dtl.DTLVardef@155e77b_HPS_FORMAT_FIGEXP M_FIG C_FIG

genomics↗

Open Benchmarking for Cell-Based Multiscale Models: Lessons from a Community Initiative

The emergence of virtual human twins (VHT) in biomedical research has sparked interest in multiscale in silico modelling frameworks, particularly in their application bridging cellular to tissue levels. Among the diverse array of multiscale modelling tools, off-lattice center-based agent-based models (CBM) offer a promising approach due to their depiction of cells in 3D space, closely resembling biological reality. Despite the proliferation of CBM tools addressing various biomedical challenges, a comprehensive and systematic comparison among them has been elusive. This paper presents a community-driven benchmark initiative aimed at evaluating and comparing CBM for biomedical applications, akin to successful efforts in other scientific domains such as the Critical Assessment of Protein Structure Prediction (CASP). Enlisting developers from leading tools like BioDynaMo, Chaste, PhysiCell,TiSim, and CompuTiX, we devised a benchmark scope, defined metrics, and established reference datasets to ensure a meaningful and equitable evaluation. Unit tests targeting different solvers within these tools were designed, ranging from diffusion and mechanics to cell cycle simulations and growth scenarios. Results from these tests demonstrate varying tool implementations in handling diffusion, mechanics, and cell cycle equations, emphasising the need for standardised benchmarks and interoperability. Discussions among the community underscore the necessity for defining gold standards, fostering interoperability, and drawing lessons from analogous benchmarking experiences. The outcomes, disseminated through a public platform in collaboration with OpenEBench, aim to catalyse advancements in computational biology, offering a comprehensive resource for tool evaluation and guiding future developments in cell-level simulations. This initiative endeavours to strengthen and expand the computational biology simulation community through continued dissemination and performance-oriented benchmarking efforts to enable the use of VHT in biomedicine.

systems biology↗

Sex-specific transcriptome similarity networks elucidate comorbidity relationships

Humans present sex-driven biological differences. Consequently, the prevalence of analyzing specific diseases and comorbidities differs between the sexes, directly impacting patients management and treatment. Despite its relevance and the growing evidence of said differences across numerous diseases (with 4,370 PubMed results published within the past year), knowledge at the comorbidity level remains limited. In fact, to date, no study has attempted to identify the biological processes altered differently in women and men, promoting differences in comorbidities. To shed light on this problem, we analyze expression data for more than 100 diseases from public repositories, analyzing each sex independently. We calculate similarities between differential expression profiles by disease pairs and find that 13-16% of transcriptomically similar disease pairs are sex-specific. By comparing these results with epidemiological evidence, we recapitulate 53-60% of known comorbidities distinctly described for men and women, finding sex-specific transcriptomic similarities between sex-specific comorbid diseases. The analysis of shared underlying pathways shows that diseases can co-occur in men and women by altering alternative biological processes. Finally, we identify different drugs differentially associated with comorbid diseases depending on patients sex, highlighting the need to consider this relevant variable in the administration of drugs due to their possible influence on comorbidities.

bioinformatics↗

Signaling Pathway Activities Improve Prognosis for Breast Cancer

With the advent of high-throughput technologies for genome-wide expression profiling, a large number of methods have been proposed to discover gene-based signatures as biomarkers to guide cancer prognosis. However, it is often difficult to interpret the list of genes in a prognostic signature regarding the underlying biological processes responsible for disease progression or therapeutic response. A particularly interesting alternative to gene-based biomarkers is mechanistic biomarkers, derived from signaling pathway activities, which are known to play a key role in cancer progression and thus provide more informative insights into cellular functions involved in cancer mechanism. In this study, we demonstrate that pathway-level features, such as the activity of signaling circuits, outperform conventional gene-level features in prediction performance in breast cancer prognosis. We also show that the proposed classification scheme can even suggest, in addition to relevant signaling circuits related to disease outcome, a list of genes that do not code for signaling proteins whose contribution to cancer prognosis potentially supplements the mechanisms detected by pathway analysis.

bioinformatics↗