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Sestrin2 loss could be a universal mechanism of human colon carcinogenesis that allows for barrier dysfunction, mTORC1 hyperactivation, unrestricted tumor growth and chemoresistance.

The nuclear protein Sam68 plays a role in the genotoxic stress-initiated "nuclear to cytoplasmic" activation of NF-κB and is involved in the development and survival of colon cancer.

miR-34a prevents inflammation-induced colonic regeneration from oncogenesis by simultaneously targeting processes in both immune and epithelial cells, including T helper 17 cell differentiation, recruitment, and IL-17 induced epithelial proliferation.

Integrated molecular analysis demonstrated that colorectal cancer can be classified into four molecular subtypes (proliferative, immunomodulatory, immunosuppressed, and immune-excluded subtypes), providing valuable insight into the intricate relationship between tumor microenvironment heterogeneity and various clinical phenotypes.

Proper gut health depends on the balance between two naturally occurring variants of a transcription factor in the colon.

Based on benchmarking various methods and analyzing multiple real scRNA-seq datasets, a computational platform/workflow and a set of tips for best practices are developed for analyzing causal interactions or relationships in single cells.

The MYC transcription factor network member MGA is a subunit of a non-canonical Polycomb complex, which, when inactivated, accelerates tumorigenesis in mouse models of cancer and proliferation in colon organoids.

A tumor-specific regulatory region has been identified upstream of the Myc oncogene.

The tumor suppressor APC regulates a metabolic program that drives normal intestinal differentiation in zebrafish.

GrimAge acceleration may increase the risk of colorectal cancer.