"We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply. Colorectal cancer Computational models Tumour heterogeneity Cancer is generally thought to be caused by expansion of a single mutant cell1. However, analyses of early colorectal cancer lesions suggest that tumors may instead originate from multiple, genetically distinct cell populations2,3."
"Cancer is generally thought to be caused by expansion of a single mutant cell1. However, analyses of early colorectal cancer lesions suggest that tumors may instead originate from multiple, genetically distinct cell populations2,3."
Colorectal cancer exhibits tumour heterogeneity that challenges the classical single-mutant-cell expansion model of carcinogenesis. Computational models and analyses of early colorectal lesions indicate that tumors can originate from multiple genetically distinct cell populations, implying polyclonal origins. Polyclonal founding populations create complex clonal architecture in early neoplasia, with potential consequences for progression, treatment resistance, and biomarker reliability. Recognition of multi-origin tumors motivates spatially resolved genetic characterization and refined modelling to capture inter-clonal interactions and evolutionary dynamics that shape early colorectal tumor development and clinical trajectories.
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