“Our goal is to understand the cause and consequence of cellular heterogeneity during tumor evolution and therapy response”

The context to which we apply our interest is the transitioning from pre-cancerous conditions to malignant cancer.

We employ colon cancer as our prototype cancer model to study tumor progression, with well-characterized signaling pathways affected by driver mutations. These drivers are typically acquired early during tumor progression, while genetic drivers of malignant growth and metastasis formation have not been identified. A dominant role is attributed for the tumor microenvironment in the acquisition of malignant growth behavior, which includes the induction of cellular plasticity.

The so-called malignant transformation that demarcates the transitioning from pre-malignancy to cancer, is a bottleneck in the evolutionary timeline of tumors. The Snippert lab is particularly interested in changes of cellular behavior and phenotypes that underly that critical moment. Experimentally, these early stages remain largely unexplored territory as there is strong study bias towards late-stage cancers. The Snippert lab uses an integrated approach of descriptive (spatial) single-cell atlases of early cancers, with experimental explorations using functional organoid models.

“Ultimately, we aim to utilize our new insights to prevent, rather than cure, metastatic disease”

Hugo Snippert – Group leader

Genetic heterogeneity

Cellular plasticity

(Single-cell) drug response