biostudies-literatureGreen EHVeterans Administration Medical CenterBLRD VANIDDK NIH HHSNational Institute of Diabetes and Digestive and Kidney DiseasesNational Cancer InstituteNCI NIH HHSVeterans Administration Medical Center, Yale School of Medicine51-65https://www.ebi.ac.uk/biostudies/studies/S-EPMC11985286biostudies-literatureUnknown266(1)Colorectal cancer (CRC) is responsible for over 900,000 annual deaths worldwide. Emerging evidence supports pro-carcinogenic bacteria in the colonic microbiome are at least promotional in CRC development and may be causal. We previously showed toxigenic C. difficile from human CRC-associated bacterial biofilms accelerates tumorigenesis in Apc^Min/+ mice, both in specific pathogen-free mice and in gnotobiotic mice colonized with a defined consortium of bacteria. To further understand host-microbe interactions during colonic tumorigenesis, we combined single-cell RNA-sequencing (scRNA-seq), spatial transcriptomics, and immunofluorescence to define the molecular spatial organization of colonic dysplasia in our consortium model with or without C. difficile. Our data show a striking bThe Journal of pathologyMultiomic spatial atlas shows deleted in malignant brain tumors 1 (DMBT1) glycoprotein is lost in colonic dysplasia.PMC11985286BX005699IK2 BX005699P30DK058404P30CA068485P30 DK058404BX002943U54 CA274367I01 BX002943F31 CA294983R00 CA230192P50CA236733P30 CA068485P50 CA236733R00CA230192R35 CA197570Sears CLDing HCoffey RJRutherford MELunnemann HMLiu QDrewes JLLiu XWashington MKKaur HHeiser CNLau KSGreen EHShrubsole MJLacy DBKotrannavar SRMarkham NOSimmons AJfalseMultiomic spatial atlas shows deleted in malignant brain tumors 1 (DMBT1) glycoprotein is lost in colonic dysplasia.Colorectal cancer (CRC) is responsible for over 900,000 annual deaths worldwide. Emerging evidence supports pro-carcinogenic bacteria in the colonic microbiome are at least promotional in CRC development and may be causal. We previously showed toxigenic C. difficile from human CRC-associated bacterial biofilms accelerates tumorigenesis in Apc^Min/+ mice, both in specific pathogen-free mice and in gnotobiotic mice colonized with a defined consortium of bacteria. To further understand host-microbe interactions during colonic tumorigenesis, we combined single-cell RNA-sequencing (scRNA-seq), spatial transcriptomics, and immunofluorescence to define the molecular spatial organization of colonic dysplasia in our consortium model with or without C. difficile. Our data show a striking b2025-01-01T00:00:00Z2025 May2026-06-01T23:04:45.502Z2025-07-05T03:04:35.496ZS-EPMC119852864002623310.1002/path.6406