The tumor protein p53 (TP53) gene encodes P53 oncoprotein, a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The P53 oncoprotein responds to diverse cellular stresses to regulate the expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism.

The adenomatous polyposis coli (APC) gene is a tumor suppressor gene, the protein it encodes plays a key regulatory role in the Wnt/β-catenin signaling pathway ^[1]. The APC protein can antagonize the Wnt signaling pathway, assisting in regulating cell migration, adhesion, transcriptional activation, and apoptosis. More than 10% of human tumors have mutations in the APC gene, and most colorectal cancers have mutations in the APC gene ^[2]. Defects in the APC gene lead to the occurrence of familial adenomatous polyposis (FAP), characterized by hundreds to thousands of adenomatous polyps in the rectum. This is an autosomal dominant precancerous disease, which usually develops into malignant tumors ^[1-2]. Disease-related mutations in the APC gene are highly prevalent in a small region known as the mutation cluster region (MCR), which usually leads to the production of truncated proteins ^[3-4]. In mice, either Apc gene deletion or multiple intestinal neoplasia (Min) mutations that result in the production of truncated APC proteins cause phenotypes similar to human familial adenomatous polyposis (FAP) and/or colorectal tumors ^[5-9].

Trp53 & Apc dKO mice are a double-gene knockout model obtained by mating Trp53 KO mice (catalog number: C001203) with Apc KO mice (catalog number: C001511). Homozygous knockout of the Apc gene is lethal. Trp53 & Apc dKO mice can be used for the study of the mechanisms of tumors or tumor-related diseases such as familial adenomatous polyposis (FAP) and colorectal cancer.