Fusobacterium nucleatum promotes intestinal tumorigenesis and modulates the tumor immune microenvironment. The study shows that Fusobacterium spp. are enriched in human colonic adenomas and stool samples from patients with colorectal adenomas and carcinomas. In the ApcMin/+ mouse model of intestinal tumorigenesis, F. nucleatum increases tumor multiplicity and recruits tumor-infiltrating myeloid cells, which can promote tumor progression. Tumors from ApcMin/+ mice exposed to F. nucleatum exhibit a pro-inflammatory expression signature similar to human fusobacteria-positive colorectal carcinomas. Unlike other bacteria linked to colorectal carcinoma, F. nucleatum does not exacerbate colitis or inflammation-associated intestinal carcinogenesis. These findings suggest that Fusobacterium spp. generate a pro-inflammatory microenvironment conducive to colorectal neoplasia progression. The study also shows that F. nucleatum selectively expands myeloid-derived immune cells in intestinal tumors, contributing to tumor progression. A Fusobacterium-associated human colorectal cancer gene signature was identified and validated in mice, showing enrichment of inflammatory response genes. The study highlights the role of Fusobacterium nucleatum in promoting tumor growth and modulating the tumor immune microenvironment, suggesting that targeting Fusobacterium populations may be a potential strategy for colorectal cancer prevention.Fusobacterium nucleatum promotes intestinal tumorigenesis and modulates the tumor immune microenvironment. The study shows that Fusobacterium spp. are enriched in human colonic adenomas and stool samples from patients with colorectal adenomas and carcinomas. In the ApcMin/+ mouse model of intestinal tumorigenesis, F. nucleatum increases tumor multiplicity and recruits tumor-infiltrating myeloid cells, which can promote tumor progression. Tumors from ApcMin/+ mice exposed to F. nucleatum exhibit a pro-inflammatory expression signature similar to human fusobacteria-positive colorectal carcinomas. Unlike other bacteria linked to colorectal carcinoma, F. nucleatum does not exacerbate colitis or inflammation-associated intestinal carcinogenesis. These findings suggest that Fusobacterium spp. generate a pro-inflammatory microenvironment conducive to colorectal neoplasia progression. The study also shows that F. nucleatum selectively expands myeloid-derived immune cells in intestinal tumors, contributing to tumor progression. A Fusobacterium-associated human colorectal cancer gene signature was identified and validated in mice, showing enrichment of inflammatory response genes. The study highlights the role of Fusobacterium nucleatum in promoting tumor growth and modulating the tumor immune microenvironment, suggesting that targeting Fusobacterium populations may be a potential strategy for colorectal cancer prevention.