Supercompetitor behavior in colorectal cancer is characterized by biased competition that favors APC-deficient cells through neighborhood suppression of wild-type intestinal stem cells.
The competition between cancer cells and wild-type intestinal stem cells in tumorigenesis reveals a complex dynamic involving cell-intrinsic behaviors and the secretion of Wnt antagonists.
Historically, cancers are thought to be clonal, but in cases like familial adenomatous polyposis, polyclonality exists, raising questions about competing cell dynamics in tumor formation.
Using the Apchet;Confetti mouse model, we explored the extent of clonal interactions in polyclonal tumors to better understand tumorigenesis in colorectal cancer.
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