The study presents and validates a "Big Bang" model to explain the early growth dynamics of human colorectal tumors. The model posits that tumors grow predominantly as a single expansion, producing numerous intermixed sub-clones that are not subject to stringent selection. Both public (clonal) and detectable private (subclonal) alterations arise early during growth. Genomic profiling of 349 individual glands from 15 colorectal tumors revealed high intra-tumor heterogeneity (ITH), uniform intra-tumor heterogeneity (ITIH), and sub-clone mixing in distant regions, supporting the model's predictions. Most detectable ITH originates from early private alterations, not later clonal expansions, exposing the primordial tumor's genomic profile. Some tumors exhibit early sub-clone mixing, indicating potential malignant potential. The model explains the pervasive nature of ITH and the absence of significant clonal expansions or selective sweeps, suggesting that early private mutations dominate the genomic structure of the neoplasm. The findings have implications for understanding cancer progression, early detection, and treatment resistance.The study presents and validates a "Big Bang" model to explain the early growth dynamics of human colorectal tumors. The model posits that tumors grow predominantly as a single expansion, producing numerous intermixed sub-clones that are not subject to stringent selection. Both public (clonal) and detectable private (subclonal) alterations arise early during growth. Genomic profiling of 349 individual glands from 15 colorectal tumors revealed high intra-tumor heterogeneity (ITH), uniform intra-tumor heterogeneity (ITIH), and sub-clone mixing in distant regions, supporting the model's predictions. Most detectable ITH originates from early private alterations, not later clonal expansions, exposing the primordial tumor's genomic profile. Some tumors exhibit early sub-clone mixing, indicating potential malignant potential. The model explains the pervasive nature of ITH and the absence of significant clonal expansions or selective sweeps, suggesting that early private mutations dominate the genomic structure of the neoplasm. The findings have implications for understanding cancer progression, early detection, and treatment resistance.