EMT | Medical University of Gdańsk

About the Unit

We investigate how phenotypic plasticity enables cancer cells to leave the primary tumour, survive during dissemination and establish metastatic lesions. Our research focuses particularly on epithelial–mesenchymal transition (EMT) and circulating tumour cells (CTCs) in breast cancer, combining patient-derived material, single-cell molecular profiling and experimental models to understand tumour heterogeneity and identify clinically relevant vulnerabilities.

We are part of the Division of Translational Oncology at the Institute of Medical Biotechnology and Experimental Oncology, Medical University of Gdańsk.

Nothing in life is to be feared, it is only to be understood. Now is the time to understand more, so that we may fear less.
Maria Skłodowska-Curie

Research at a glance

Cancer cell plasticity & EMT

We study epithelial–mesenchymal transition (EMT) and epithelial-mesenchymal plasticity (EMP) as a source of tumour-cell heterogeneity and ask how different phenotypic states influence properties of cancer cells, their ability to disseminate, metastatic competence and interaction with the microenvironment.

Liquid biopsy for detecting cancer

We investigate DNA released from cancer cells (ctDNA) and rare circulating tumour cells (CTCs) in the bloodstream, with emphasis on the biological diversity of epithelial, hybrid and mesenchymal CTC states and their relationship to tumour aggressiveness.

Single-cell translational oncology

We use single-cell genomic and transcriptomic approaches to resolve heterogeneity that is obscured by bulk analysis and to connect molecular profiles of individual CTCs with mechanism of survival and clinically relevant tumour biology.

From in vitro models to patient samples

Our translational strategy links molecular analysis of in vitro models, murine models, clinical samples and computational strategies to understand mechanisms of cancer progression.

Research overwiew

Metastasis is not driven by a uniform population of cancer cells. Tumour cells can change their phenotype in response to intrinsic and microenvironmental signals, generating states with different capacities to migrate, survive, interact with host cells and respond to treatment. We investigate this plasticity across the metastatic cascade, from the primary tumour to cells detected in the circulation and metastatic sites.

Learn more