Trp53, the mouse ortholog of the human TP53 tumor suppressor gene, is crucial in maintaining genomic stability. It functions in regulating the cell cycle, DNA repair, apoptosis, cellular metabolism, and senescence, acting as a "guardian of the genome" [4]. Mutations in Trp53 are associated with Li-Fraumeni syndrome, a hereditary condition characterized by early-onset tumors in multiple organs [3,4]. Genetic mouse models are valuable for studying Trp53.

Trp53-deficient mice have provided insights into its role in different biological processes. For instance, BALB/c-Trp53-deficient mice showed a delayed involution phenotype and a mammary tumor phenotype, enhancing understanding of p53's role in involution, hormonal regulation of its activity, and cooperation with other oncogenic pathways in mammary tumorigenesis [2]. In the adrenal medulla, dual loss of Rb1 and Trp53 led to spontaneous pheochromocytoma, indicating Trp53 is an efficient genetic modifier of Rb1 loss in PCC development [5]. The Trp53 +/-mouse model has been used in short-term carcinogenicity testing. It responds positively to genotoxic carcinogens, negatively to non-genotoxic rodent carcinogens and non-carcinogens, and its most common spontaneous tumors are malignant thymic lymphomas and subcutaneous sarcomas [1].

In conclusion, Trp53 is essential in multiple biological processes, with its disruption leading to various diseases, especially cancer. Mouse models, such as Trp53 knockout and conditional knockout models, have significantly contributed to understanding its role in breast cancer, pheochromocytoma development, and carcinogenicity testing, providing valuable insights into disease mechanisms and potential therapeutic strategies.