Epithelial transformation induces prompt responses in surrounding microenvironment. This research line aims to characterize the molecular crosstalk between intestinal epithelial cells and fibroblasts during tumorigenesis, with the goal of identifying novel tumor vulnerabilities and potential therapeutic targets within the stromal compartment. Using single-cell transcriptomics, organoid–fibroblast co-cultures, and mouse models, we resolve fibroblast heterogeneity and test causal interactions via genetic and pharmacological perturbations. Our goal is to uncover tumor vulnerabilities and therapeutic targets within the stromal compartment.

The developing tumor releases circulating factors and extracellular vesicles that condition distant tissues. This project charts how colorectal cancer–derived signals prime liver fibroblasts to establish a pre-metastatic niche that supports organ-specific colonization. We combine proteomics of tumor secretomes, profiling of liver-resident and recruited fibroblast subsets by single-cell and bulk transcriptomics, and mouse model perturbations to define causal pathways. By identifying fibroblast programs that remodel the hepatic microenvironment, we aim to uncover biomarkers and therapeutic strategies that prevent or reverse metastatic seeding.

Tumor development releases factors that reprogram pre-adipocytes, alters differentiation, lipid metabolism, and inflammatory outputs with consequences for tumor growth and systemic physiology. This project investigates how colorectal cancer secretomes influence adipose progenitors across depots. We combine organoid–preadipocyte co-cultures, single-cell and bulk profiling, and in vivo models to map pathways (e.g., IL-6, TGF-β, catecholamine signaling) driving adipose remodeling. By defining tumor-educated pre-adipocyte states and regulatory nodes, we aim to therapeutically disrupt tumor–adipose crosstalk and improve patient outcomes.