Somatic mutations accumulate in the genome of dividing cells, occasionally leading to a cellular fitness advantage and positive selection. This fitness advantage results in small clones, driven by point mutations in common cancer-related genes such as TP53 and NOTCH1, similar to those seen in malignant tumors. Determining the role of these clones in human carcinogenesis requires the direct visualization of their mutations in the spatial context.
Existing technologies are restricted to gene expression profiles (spatial transcriptomics), lacking the exact genetic sequence.