Standard genomic and proteomic profiling methods for colorectal tumors do not always translate into reliable precision medicine outcomes. Tumor plasticity mechanisms can result in nongenetic responses to targeted therapies, calling for a functional approach using dynamic and physiologically relevant patient models.

This study establishes a functional precision medicine workflow by combining the application of kinase inhibitors with quantitative and spatial proteomics to reveal both intrinsic and extrinsic signaling crosstalk in a living biobank of patient-derived colorectal cancer organoid models.

The data and methods used here provide a framework for a better understanding of colorectal cancers that accounts for off-target effects of kinase inhibitors and patient-specific plasticity mechanisms that influence downstream cell signaling responses.

This preprint has been assigned the following badges: New Methods, New Materials, Open Data, Open Software.

Read the preprint on bioRxiv (Plattner et al., 2022): https://doi.org/10.1101/2022.09.16.508204.