Cancer-on-a-chip model shows that the adenomatous polyposis coli mutation impairs T cell engagement and killing of cancer spheroids.

Evaluating the ability of cytotoxic T lymphocytes (CTLs) to eliminate tumor cells is crucial, for instance, to predict the efficiency of cell therapy in personalized medicine. However, the destruction of a tumor by CTLs involves CTL migration in the extra-tumoral environment, accumulation on the tumor, antigen recognition, and cooperation in killing the cancer cells. Therefore, identifying the limiting steps in this complex process requires spatio-temporal measurements of different cellular events over long periods.

The adhesion capability of cells is heterogeneously distributed over the cell envelope.

Understanding and controlling microbial adhesion is a critical challenge in biomedical research, given the profound impact of bacterial infections on global health. Many facets of bacterial adhesion, including the distribution of adhesion forces across the cell wall, remain poorly understood. While a recent 'patchy colloid' model has shed light on adhesion in Gram-negative cells, a corresponding model for Gram-positive cells has been elusive.

Different binding mechanisms of Staphylococcus aureus to hydrophobic and hydrophilic surfaces.

Bacterial adhesion to surfaces is a crucial step in initial biofilm formation. In a combined experimental and computational approach, we studied the adhesion of the pathogenic bacterium Staphylococcus aureus to hydrophilic and hydrophobic surfaces. We used atomic force microscopy-based single-cell force spectroscopy and Monte Carlo simulations to investigate the similarities and differences of adhesion to hydrophilic and hydrophobic surfaces.