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Biology subjects

Torres-Moral, T.

Publications and source records attributed to Torres-Moral, T..

2 recordsLinked to original sources

Spatially resolved diversity in molecular states underlies congenital melanocytic nevi and associated tumors

The congenital melanocytic nevus (CMN) is a developmental skin disorder characterized by prenatal melanocyte overgrowth, exhibiting heterogeneity in surface size, depth, and clinical behavior. Large/giant CMN carry an elevated, anticipatory melanoma risk relative to more common, small CMN. However, deeper insights into melanocytic states, genomic and epigenomic alterations, and microenvironmental cues governing disease progression are needed to predict lesions disposed to transformation. Although large/giant CMN melanocyte heterogeneity was recently established, spatial organization of these states and their niche interactions are unknown. Using advanced spatial and single-cell transcriptomics and bulk methylomics, we characterized ten CMN, seven CMN-associated proliferative nodules and three clinically diagnosed melanomas arising in CMN from children, integrating data from healthy skin references to contextualize melanocyte states in situ. CMN-specific melanocytic states, distinct in differentiation and proliferation, were spatially stratified, with immature melanocytes in deep dermis and more differentiated melanocytes approaching the epidermis. We then constructed a robust atlas of CMN cellular states by integrating single-cell transcriptomic data from five new large/giant CMN with published datasets, using it to deconvolute the spatial information. Cell-cell communication inference uncovered enhanced signaling (e.g. pleiotrophin, IGF1, periostin, semaphorin pathways) between CMN melanocytes, fibroblasts, and hair follicle-associated cells. Analysis of CMN-derived tumors, including longitudinal cases with [≥]2 samples, revealed divergent spatial melanocytic transcription distinguishing immune-enriched lesions from tumors with oncogenic/pro-invasive signatures. Collectively, these findings establish a spatially resolved framework linking melanocyte heterogeneity, signaling, and genomic instability in CMN, providing mechanistic insights to refine risk stratification and prognosis for CMN-associated tumors.

genetics↗

Transcriptomic meta-analysis in plaque psoriasis: an integrative bioinformatic approach to deciphering the genetic landscape and molecular pathways

Psoriasis is a chronic inflammatory skin disease influenced by both genetic and environmental factors. Despite extensive research, its precise etiology remains unclear, posing significant challenges to understanding and treatment. The disease pathogenesis involves self-reactive T cells and immune-related cytokines. Genome-wide association studies have identified various susceptibility loci for immune-related diseases, but the underlying mechanisms remain only partially understood. Recent discoveries of critical signaling pathways, biological processes, and immune cell involvement have expanded our knowledge and offer hope for improved therapeutic strategies. This study aimed to enhance our understanding of psoriasis and proposes novel therapeutic approaches by employing integrated bioinformatics to identify signaling pathways and biological processes as potential disease markers. Presenting a systematic review and taking a meta-analytical approach to transcriptomic profiles, this investigation examined differential gene expression patterns across 44 studies involving 975 samples comparing lesional psoriasis, non-lesional psoriasis, and healthy controls. Consensus transcriptome signatures revealed a significant association between immune-related genes and psoriasis pathogenesis. Functional enrichment analysis identified several enriched pathways related to immunity and immune system processes. Comparison of these findings with the existing literature indicated that some immune-related genes were already known, while others are novel in the context of psoriasis. Additionally, novel gene analysis demonstrated psoriasis involvement in pathways such as gluconeogenesis, the FoxO signaling pathway, and mitophagy. This integrative approach confirmed classic genetic associations while uncovering novel gene expression patterns and pathways relevant to psoriasis. Notably, the disruption of the gluconeogenesis pathway emerged as a critical finding. These insights enhance our understanding of psoriasis pathophysiology and pave the way for targeted therapies, offering improved management options for affected individuals.

molecular biology↗