Crypt density and recruited enhancers underlie intestinal tumour initiation.

ABSTRACT: Oncogenic mutations that drive colorectal cancer can be present in healthy intestines for long periods without overt consequence^1,2. Mutation of Apc, the most common initiating event in conventional adenomas³, activates Wnt signalling, thus conferring fitness on mutant intestinal stem cells (ISCs)^4,5. Apc mutations may occur in ISCs that arise by routine self-renewal or by dedifferentiation of their progeny. Although ISCs of these different origins are fundamentally similar^6,7, it is unclear whether both generate tumours equally well in uninjured intestines. It is also unknown whether cis-regulatory elements are substantively modulated upon Wnt hyperactivation or as a feature of subsequent tumours. Here we show in two mouse models that adenomas a

SUBMITTER: Gaynor L 

PROVIDER: S-EPMC12166968 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature