The p53 protein, also known as tumor protein p53, is a crucial component in the cellular response to stress and damage. Often referred to as the “guardian of the genome,” p53 plays a central role in preventing cancer by coordinating cell cycle arrest, DNA repair, senescence, and apoptosis in response to various forms of cellular stress, including DNA damage, hypoxia, and oncogene activation.

When p53 is non-functional, whether due to mutations, deletions, or other alterations, cells lose this important safeguard. As a result, cells can continue to proliferate despite DNA damage or other problems, which can lead to the accumulation of additional mutations and potentially the development of cancer. In fact, p53 is the most frequently mutated gene in human cancers; mutations in p53 are found in over half of all tumors.

The effects of it can be particularly problematic in the context of genomic instability, as cells can continue to replicate despite DNA damage. This can lead to the accumulation of additional mutations and chromosomal aberrations, promoting the development and progression of cancer.

Research into restoring the function of p53 in cancer cells is a major area of cancer research, as this could potentially halt the growth of cancer cells and induce them to undergo apoptosis. However, this is challenging due to the diverse nature of p53 mutations and the potential for p53-independent survival pathways in cancer cells. Nonetheless, several strategies are being explored, including the use of small molecules to reactivate mutant p53, gene therapy to replace mutant p53 with wild-type p53, and synthetic lethal approaches to target p53-deficient cells.