Abstract
ABSTRACTAdenomatous polyposis coli (APC) mutations cause aneuploidy and are responsible for familial adenomatous polyposis characterized by chromosomal instability. PLK1 contributes to sustain an intact spindle assembly checkpoint ensuring genomic stability. In our work using independent ApcMin/+ mouse models we revealed that PLK1 functions as tumor suppressor in APC-mutated colorectal cancers.
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