An original method is presented to study single-colloid interaction with a substrate in liquid environment. Colloids, either in solution or adsorbed on a surface, are fixed by suction against the aperture of a microchanneled atomic force microscopy cantilever. Their adhesion to the substrate is measured, followed by their release via a short overpressure surge. Such colloid exchange procedure allows for 1), the quick variation of differently functionalized colloids within the same experiment; 2), the investigation of long-term interactions by leaving the colloids on a surface for a defined time before detaching them; and 3), the inspection of irreversible interactions. After validation of the method by reproducing literature results obtained with traditional colloidal atomic force microscopy, the serial use of colloids with different surface functionalization was shown on a micropatterned surface. Finally, concanavalin A-coated colloids were allowed to adsorb on human embryonic kidney cells and then detached one by one. The adhesion between cells and colloids was up to 60 nN, whereas individual cells adhered with 20 nN to the glass substrate. A cellular elastic modulus of 0.8 kPa was determined using the attached colloid as indenter.
Atypical teratoid/rhabdoid tumors (ATRT) are known for their heterogeneity concerning pathophysiology and outcome. However, predictive factors within distinct subgroups still need to be uncovered. Using multiplex immunofluorescent staining and single-cell RNA sequencing we unraveled distinct compositions of the immunological tumor microenvironment (TME) across ATRT subgroups. CD68 + cells predominantly infiltrate ATRT-SHH and ATRT-MYC and are a negative prognostic factor for patients' survival. Within the murine ATRT-MYC and ATRT-SHH TME, Cd68 + macrophages are core to intercellular communication with tumor cells. In ATRT-MYC distinct tumor cell phenotypes express macrophage marker genes. These cells are involved in the acquisition of chemotherapy resistance in our relapse xenograft mouse model. In conclusion, the tumor cell-macrophage interaction contributes to ATRT-MYC heterogeneity and potentially to tumor recurrence.
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