Our results indicate that ETBF-induced tumors in the distal colon of Apcmin/+ mice form via Apc LOH, the same mechanism as spontaneous (sham) tumors in our mouse model, various other Apc mutant mouse models (27, 45), and approximately 50% of sporadic colorectal tumors (25, 56, 57). This evidence concerns the gene APC and colorectal neoplasm.