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Gaskins, G.

Publications and source records attributed to Gaskins, G..

3 recordsLinked to original sources

Virtual phenotypic screening discovers novel scaffolds inhibiting the PI3K/mTOR pathway

Phenotypic drug discovery has yielded many first-in-class small-molecule drugs by discovering modulators of disease phenotypes in physiologically relevant cellular systems. However, high-content phenotypic assays lack the ultra-high-throughput scalability of target-based screens. Recent advances in virtual screening present an opportunity to address this bottleneck, but have been limited to simple phenotypes like viability, restricted to small repurposing libraries, or lack in-depth biological validation. Here, we present PhenoCompass, a multimodal co-embedding model that aligns compound structures and high-content phenotypic imaging to enable virtual phenotypic screening over billion-compound libraries. Following training on the Joint Undertaking in Morphology dataset with more than 100,000 Cell Painting compound profiles, retrospective validation with historical biochemical high-throughput screening data demonstrates that PhenoCompass ranks compounds according to their biochemical target engagement. Leveraging PhenoCompass, we performed a prospective screen of 3.8 billion Enamine REAL compounds for inhibitors of PI3K/mTOR pathway, a critical signaling cascade whose aberrant activation is a common tumor driver. This search identified 11 novel compounds with pathway-consistent Cell Painting readout and diverse scaffolds, a 54-fold enrichment over the training set. Orthogonal validation experiments using a FOXO3A reporter assay and direct kinase inhibition confirmed seven structurally novel inhibitors with distinct mechanisms of action. These results highlight the convergence of diverse molecular target profiles onto a shared morphological pathway signature and establish PhenoCompass as a robust framework for high-content phenotypic virtual screening.

bioinformatics↗

Machine-learning convergent melanocytic morphology despite noisy archival slides

Melanocytic atypia, ranging from benign to malignant, often leads to diagnostic discordance, complicating its prediction by machine learning models. To overcome this, we paired H&E-stained histology images with contiguous or serial sections immunohistochemically (IHC) stained for melanocytic cells via antibodies for MelanA, MelPro, or SOX10. We developed a deep-learning pipeline to identify melanocytic atypia by digitizing a real-world archival dataset of 122 paired whole slide images from 61 confirmed melanoma in situ (MIS) cases at two institutions. Only 37.7% of the cases contained tissue pairs that matched well enough for deep learning. Nonetheless, the MelanA+MelPro models achieved an average area under the receiver-operating characteristic (AUROC) of 0.948 and an average area under the precision-recall curve (AUPRC) of 0.611, while the SOX10 models had an average of 0.867 AUROC and 0.433 AUPRC. Despite learning from biologically different IHC stains, the convolutional neural network (CNN) models independently exhibited an intuitive convergent rationale by explainable AI saliency calculations. Different antibodies, with nuclear versus cytoplasmic staining, provided complementary yet consistent information, which the CNNs integrated effectively. The resulting multi-antibody virtual stains identified morphologic cytologic and small-scale architectural features directly from H&E-stained histology images, which can assist pathologists in assessing cutaneous MIS.

pathology↗

Evolutionarily Conserved Roles For Blood-Brain Barrier Xenobiotic Transporters In Endogenous Steroid Partitioning And Behavior

Optimal brain function depends upon efficient control over the brain entry of blood components; this is provided by the blood-brain barrier (BBB). Curiously, some brain-impermeable drugs can still cause behavioral side effects.\n\nTo investigate this phenomenon, we asked whether the promiscuous drug efflux transporter Mdr1 has dual functions in transporting drugs and endogenous molecules. If this is true, brain-impermeable drugs may cause behavioral side effects by affecting brain levels of endogenous molecules.\n\nUsing computational, genetic and pharmacologic approaches across diverse organisms we demonstrate that BBB-localized efflux transporters are critical for regulating brain levels of endogenous steroids, and steroid-regulated behaviors (sleep in Drosophila and anxiety in mice). Furthermore, we show that Mdr1-interacting drugs are associated with anxiety-related behaviors in humans.\n\nWe propose a general mechanism for common behavioral side effects of prescription drugs: pharmacologically challenging BBB efflux transporters disrupts brain levels of endogenous substrates, and implicates the BBB in behavioral regulation.\n\nAbbreviations

neuroscience↗