Pradipta Ghosh

The paper identifies and characterizes Schwann cell-derived extracellular vesicles in chemotherapy-induced neuropathy, showing changes in their proteome and function.

The paper identifies GIV as a macrophage checkpoint suppressing reverse cholesterol transport and shows its inhibition restores cholesterol efflux, reducing plaque burden and systemic lipid overload.

The paper introduces COMPASS, a method to quantify pathway activity from gene expression without reference cohorts, showing improved consistency and robustness compared to existing methods.

This paper identifies two stromal states in IBD that predict clinical outcomes and shows that targeting one state can reverse disease pathology.

This paper identifies GIV as a macrophage-intrinsic factor that controls PD1 endocytosis, determining durable response versus hyperprogressive disease to PD1 blockade.

This paper identifies a host-encoded toggle switch involving NOD2 and GIV that controls cAMP levels in macrophages, converting tolerant cells into microbicidal machines to restore microbial clearance and gut barrier integrity.

The paper identifies niColAMs as critical for IBD recovery and shows GIV-NOD2 interaction is essential for microbial sensing and gut homeostasis.

F.O.R.W.A.R.D is a network-based target prioritization framework that uses clinical outcomes and transcriptomic data to predict drug efficacy in IBD, achieving 100% predictive accuracy in benchmarking.

The paper identifies a Microbe-Associated Colorectal Cancer Signature (MACS) induced by Fusobacterium nucleatum in genetically predisposed hosts, linking microbial infection to early CRC initiation.

The paper identifies a 338-gene signature of macrophage reactivity and tolerance that predicts disease outcomes across diverse conditions and species.

The paper develops predictive models of gastric cancer progression using Boolean implication networks and identifies gene clusters associated with different stages of the disease.

This paper investigates design principles for dose-response alignment in signaling motifs with negative feedback loops, showing how kinetic parameters and activation levels affect performance.

The paper uses BoNE to identify dual PPARα/γ agonism as a therapeutic strategy for IBD, validated in preclinical models and patient-derived cells.

The paper identifies a conserved 166-gene host immune signature across viral pandemics, with a 20-gene subset predicting disease severity and guiding therapeutic strategies.

The paper identifies a GTPase circuit that enables secretion-coupled cellular autonomy in cancer cells through feedback loops and dose response alignment of growth factor sensing and secretion.

The paper presents a network-based model of GIV/Girdin-dependent cAMP signaling, revealing its role as a tunable control valve distinct from GPCRs and PDEs.

This study shows that ELMO1 dysregulation in the gut epithelium and macrophages contributes to IBD by promoting bacterial internalization and pro-inflammatory cytokine production.