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APC, also named as DP2.5, belongs to the adenomatous polyposis coli (APC) family. APC is a tumor suppressor that regulates cell division, helps ensure that the number of chromosomes in a cell is correct following cell division, and associates with other proteins involved in cell attachment and signaling. APC promotes rapid degradation of CTNNB1 and participates in Wnt signaling as a negative regulator. It plays a critical role in several cellular processes. APC regulates beta-catenin levels through Wnt-signaling and is involved in actin cytoskeletal integrity, cell-cell adhesion and cell migration. APC activity is correlated with its phosphorylation state. Defects in APC are a cause of familial adenomatous polyposis (FAP) which includes also Gardner syndrome (GS). Defects in APC are a cause of hereditary desmoid disease (HDD) which also known as familial infiltrative fibromatosis (FIF). Defects in APC are a cause of medulloblastoma (MDB) which is a malignant, invasive embryonal tumor of the cerebellum with a preferential manifestation in children. Defects in APC are a cause of mismatch repair cancer syndrome (MMRCS) which also known as Turcot syndrome or brain tumor-polyposis syndrome 1 (BTPS1).