Polyclonality and metabolic heterogeneity in a colorectal tumor model.

ABSTRACT: The monoclonal origin of cancer is widely accepted, although numerous studies suggest that some are of polyclonal origin. Loss of checkpoints in transformed cells gives rise to carcinomas comprising a wide diversity of cell types that fulfill distinct, even complementary, metabolic functions, contrasting with a hypothetical monoclonal origin. Here, using a Drosophila intestinal tumor model, we show that, despite an identical genetic background, these tumors (1) comprise a conserved set of different metabolic-specialized clusters; (2) are always polyclonal and derive from several clones characterized by distinct metabolic specificity; (3) depend on motility of the founder clones for their growth; and (4) share metabolic needs similar to those of human cancers. In summary, our study i

SUBMITTER: Delamotte P 

PROVIDER: S-EPMC12355558 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature