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Pintard, D.

Publications and source records attributed to Pintard, D..

3 recordsLinked to original sources

A trustworthy semantic knowledge network linking data-driven cell phenotypes to diseases and drugs

Genome-wide association and other genetic studies have identified genes involved in disease pathogenesis, and their encoded proteins have provided therapeutic targets. However, little is known about which cells are the functional home of these disease-associated genes and proteins. Single-cell technologies are enabling high-resolution profiling of cell phenotypes and revealing cellular contexts of disease, yet much of the resulting knowledge remains embedded in individual datasets and scientific literature. To address these gaps, the National Library of Medicine has developed Cell Knowledge Network (NLM-CKN, https://nlm-ckn.org). Reproducible computational workflows have generated cell phenotype knowledge for 2,585 cell sets and 5,139 selectively expressed genes from 88 datasets covering 10 human organs. Mapping of these cell sets to cell types grounds Cell Ontology terms in experimental evidence. This experimental knowledge is integrated with external knowledge of anatomical and cell-type hierarchies, gene-disease associations, and therapeutic interventions. A semantic schema defines node types and relations, enabling knowledge to be transformed into triple assertions and loaded into an ArangoDB database with provenance and quantitative evidence. The NLM-CKN interface supports graphical exploration of the cellular constituents of healthy human tissues. Finally, topological analyses generate insights into cellular contributions to disease pathogenesis, cellular contexts for therapeutic intervention, and drug-repurposing hypotheses.

bioinformatics↗

Limitations of differential expression for cell-type marker discovery in single-cell RNA sequencing atlases

Cell-type marker genes are definitional characteristics of a cell type, and in single-cell RNA sequencing atlases they are commonly nominated through differential expression (DE) testing. The Wilcoxon rank-sum test is the default method for marker gene discovery in Seurat and a recommended method in Scanpy, two widely used computational software packages for scRNA-seq analysis. Structurally, Wilcoxon's standardized statistic grows with sample size at a fixed underlying effect, meaning computed rankings across clusters of unequal size are incomparable. We quantified this effect across three atlas datasets - lung, kidney, and brain. Mean Wilcoxon score scaled with log cluster size at Pearson correlation r = 0.90-0.95 in each organ. In contrast, a classification-based comparator, NS-Forest, showed low correlation with cluster size (r = 0.10-0.28). This DE-cluster size relationship remained essentially unchanged after controlling for classification performance through partial correlation, decayed monotonically under cluster size downsampling, and was reproduced in simulation with marker quality fixed. The Wilcoxon rank-sum test can be transformed into a rank-based effect size by normalizing by the target-background pair count, removing the positive size dependence. However, this effect size nominates an identical set of candidate genes as the original statistic, indicating the cluster size dependence and poor specificity of DE nominated genes are separate problems. Genes nominated under default settings were substantially less specific to their target clusters, with median on-target fractions of 0.204 (lung), 0.166 (kidney), and 0.083 (brain), compared to NS-Forest's marker genes (0.580, 0.687, 0.364), revealing the relatively poor specificity that highly scoring DE genes exhibit.

bioinformatics↗

Spatially resolved transcriptional programs link fallopian tube precursor lesions to immune activation and stromal reorganization

Despite its name, high-grade serous ovarian carcinoma (HGSC) originates in the fallopian tube, not the ovary, arising from a morphologically recognizable precursor lesion, serous tubal intraepithelial carcinoma (STIC). Yet the early cellular and microenvironmental changes driving this transformation remain poorly understood, limiting progress in early detection, interception, and prevention. Here, we generated a Visium HD spatial transcriptomic atlas of fallopian tube carcinogenesis spanning histologically unremarkable fallopian tube epithelium (FTE), STIC, and invasive HGSC. This approach enabled unbiased, tissue-wide, whole-transcriptome mapping at single-cell-level resolution within preserved histologic architecture, providing spatial granularity beyond prior region-of-interest-based platforms. STIC lesions displayed a coordinated epithelial transformation program marked by proliferation, replication stress, DNA repair activation, chromatin remodeling, and induction of tumor-associated antigens, including PRAME and CLDN6, which are emerging targets for vaccine and antigen-directed therapeutic strategies. In contrast, histologically unremarkable FTE contained spatially restricted epithelial defense programs marked by SCGB1A1 and MUC6, suggesting localized protective states that may influence susceptibility to malignant transformation. Using distance- and density-aware spatial analyses, we found that precursor lesions were embedded within immune-enriched, stromal-depleted microenvironments characterized by interferon-dominant immune activation, attenuation of TNF/NF-{kappa}B signaling, macrophage and lymphoid remodeling, and extracellular matrix-associated fibroblast interactions. Computational pathology analysis of collagen architecture confirmed reduced collagen fiber density in STIC-adjacent stroma, linking transcriptomic evidence of stromal remodeling to structural extracellular matrix changes. Together, these data define early epithelial, immune, and stromal programs associated with STIC and identify tumor-associated antigens, epithelial defense states, and immune-stromal niches as candidate targets for HGSC prevention and early interception.

cancer biology↗