Trp53, the mouse ortholog of the human TP53 gene, is a crucial tumor suppressor gene. It plays extensive roles in regulating the cell cycle, DNA repair, apoptosis, cellular metabolism, and senescence, acting as the "guardian of the genome" [2]. Mutations or deletions of Trp53 lead to loss of its normal function, which is associated with the development of many cancers. Mouse models are valuable for studying Trp53's function in vivo.

Trp53 -deficient mice have provided insights into its role in breast cancer. The original Trp53 -knockout mice showed no mammary gland phenotype, but BALB/c-Trp53 -deficient mice demonstrated a delayed involution phenotype and a mammary tumor phenotype. This indicates the importance of Trp53 in mammary gland involution and the development of breast cancer [1]. Additionally, in the adrenal medulla, dual loss of Rb1 and Trp53 led to the development of spontaneous pheochromocytomas, suggesting that Trp53 is an efficient genetic modifier of Rb1 loss in the development of this tumor type [3].

In conclusion, Trp53 is essential for maintaining normal cellular homeostasis and preventing tumorigenesis. Mouse models, especially those with Trp53 knockout or conditional knockout, have significantly contributed to our understanding of its role in diseases such as breast cancer and pheochromocytoma, providing valuable insights into the mechanisms of tumor development and potential therapeutic targets.