Peter ten Dijke

This paper develops a microfluidic platform using insulator-based dielectrophoresis to isolate breast cancer cells from blood with high recovery and purity.

This study identifies ECM1 as a gatekeeper that transiently suppresses HGF activity during liver regeneration, enabling tissue repair through c-MET-ERK-MYC signaling.

This paper identifies co-receptors for a parasite TGFβ antagonist, uses structural data to design cell-type-specific TGFβ modulators, and demonstrates their selective antagonistic effects.

This paper improves the folding and targeting of an engineered TGF-β monomer for gene-based delivery by modifying its pro-domain and adding a CD44 binding domain.

This study investigates how CAFs drive cancer cell invasion through matrix remodeling and inter-spheroid proximity in a 3D in vitro model of Luminal A breast cancer.

The paper develops a high-throughput 3D ECM remodeling assay to identify MEK as a key driver of fibrotic fibroblast activity, showing that MEK-ERK signaling, not TGFβ signaling, drives ECM remodeling.

This paper develops an automated microinjection robot for zebrafish xenograft models, achieving 60% success rate and 70% survival rate, with twice the speed of manual injections.

This paper shows TGM6, a helminth protein, mimics TGF-β binding to TβRII to inhibit TGF-β signaling in fibroblasts but not T cells.

This paper identifies TGM4, a helminth TGF-beta mimic, as a modular ligand that selectively targets myeloid cells through specific receptor interactions, differing from TGM1's broader T cell targeting.

This study investigates how EMT-dependent cell-matrix interactions influence unjamming transitions in cancer spheroid invasion using 3D invasion assays and quantitative image analysis.

This study shows ECM1 prevents hepatic fibrosis by inhibiting TGF-β1 activation, with implications for developing safe anti-fibrotic therapies.

This study identifies EGF/STAT1 and IFNγ/NRF2 signaling pathways regulating ECM1 expression, showing their role in maintaining liver homeostasis versus promoting chronic liver disease.