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Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, with increasing incidence in early-onset patients. The tumour suppressor Adenomatous Polyposis Coli (APC) plays a key role in maintaining epithelial homeostasis, and its mutation is a hallmark of CRC. While most studies have focused on truncating APC mutations, the contribution of C-terminal missense mutations remains poorly understood.
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