bioRxiv Science⌕ Search

Biology subjects

Crouch, A. C.

Publications and source records attributed to Crouch, A. C..

2 recordsLinked to original sources

A Multi-Objective Scoring (MOS) Framework for Detecting Cross-Modal Spatial Similarity: Conceptual and Direct Formulations

Spatial multi-omics methods allow researchers to study complex biological systems by integrating multiple molecular layers while preserving their spatial organization. However, integrating spatial transcriptomics and mass spectrometry imaging (MSI) remains challenging due to the differences between the two modalities, including sampling geometry, spatial resolution, signal scaling, and measurement principles. For example, 10x Genomics Visium captures transcriptomic data on a discrete hexagonal grid of spots; however, matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) produces dense Cartesian pixel maps of molecular distributions. These differences make exact spatial co-registration difficult and limit the effectiveness of single-metric similarity approaches. Here, we introduce a Multi-Objective Scoring (MOS) framework designed to detect cross-modal spatial similarity without requiring exact pixel-to-pixel alignment. The MOS framework integrates multiple complementary spatial descriptors into a unified similarity score, including coordinate-based metrics (value correlation, importance-based Intersection-over-Union (IoU), and importance-map correlation) and descriptor-based metrics that capture higher-order spatial organization, such as spatial histograms, radial profiles, quadrant statistics, and Morans I spatial autocorrelation. These metrics are combined through a weighted ensemble model. This model calculates the weights using synthetic spatial datasets that simulate realistic tissue geometry, sampling differences, and spatial distortions. The framework was applied to a spatial multi-omics dataset from murine brain tissue, integrating spatial transcriptomics with MALDI-MSI lipidomics across young and aged control and Alzheimers disease (AD) models. Synthetic data validation results demonstrated strong pattern-matching performance (96.14% accuracy), and application to experimental data identified several MSI analyte features whose spatial distributions closely matched transcriptomic patterns. In particular, strong and reproducible associations were observed between myelin-related genes (Mbp and Plp1) and multiple analyte features enriched in white matter regions. Overall, whether applied conceptually or directly, the MOS framework provides a strong strategy for cross-modal spatial integration and offers a scalable tool for discovering spatial relationships across diverse multi-omics datasets and facilitating hypothesis generation.

biochemistry↗

Targeting de novo lipogenesis and the Lands cycle induces ferroptosis in KRAS-mutant lung cancer

Mutant KRAS (KM) is the most common oncogene in lung cancer (LC). KM regulates several metabolic networks, but their role in tumorigenesis is still not sufficiently characterized to be exploited in cancer therapy. To identify metabolic networks specifically deregulated in KMLC, we characterized the lipidome of genetically engineered LC mice, cell lines, patient derived xenografts and primary human samples. We also determined that KMLC, but not EGFR-mutant (EGFR-MUT) LC, is enriched in triacylglycerides (TAG) and phosphatidylcholines (PC). We also found that KM upregulates fatty acid synthase (FASN), a rate-limiting enzyme in fatty acid (FA) synthesis promoting the synthesis of palmitate and PC. We determined that FASN is specifically required for the viability of KMLC, but not of LC harboring EGFR-MUT or wild type KRAS. Functional experiments revealed that FASN inhibition leads to ferroptosis, a reactive oxygen species (ROS)-and iron-dependent cell death. Consistently, lipidomic analysis demonstrated that FASN inhibition in KMLC leads to accumulation of PC with polyunsaturated FA (PUFA) chains, which are the substrate of ferroptosis. Integrating lipidomic, transcriptome and functional analyses, we demonstrated that FASN provides saturated (SFA) and monounsaturated FA (MUFA) that feed the Lands cycle, the main process remodeling oxidized phospholipids (PL), such as PC. Accordingly, either inhibition of FASN or suppression of the Lands cycle enzymes PLA2 and LPCAT3, promotes the intracellular accumulation of lipid peroxides and ferroptosis in KMLC both in vitro and in vivo. Our work supports a model whereby the high oxidative stress caused by KM dictates a dependency on newly synthesized FA to repair oxidated phospholipids, establishing a targetable vulnerability. These results connect KM oncogenic signaling, FASN induction and ferroptosis, indicating that FASN inhibitors already in clinical trial in KMLC patients (NCT03808558) may be rapidly deployed as therapy for KMLC.

cancer biology↗