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Official Full Name
tumor protein p53
This gene encodes a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The encoded protein responds to diverse cellular stresses to regulate expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Mutations in this gene are associated with a variety of human cancers, including hereditary cancers such as Li-Fraumeni syndrome. Alternative splicing of this gene and the use of alternate promoters result in multiple transcript variants and isoforms. Additional isoforms have also been shown to result from the use of alternate translation initiation codons (PMIDs: 12032546, 20937277). [provided by RefSeq, Feb 2013]
TP53; tumor protein p53; P53; BCC7; LFS1; TRP53; cellular tumor antigen p53; antigen NY-CO-13; tumor protein 53; phosphoprotein p53; p53 tumor suppressor; mutant tumor protein 53; transformation-related protein 53; Li Fraumeni syndrome; mutant p53 protein; truncated p53 protein; tumor suppressor TP53; FLJ92943; tumor suppressor p53; brp53; drp53; fb40d06; wu:fb40d06; zgc:111919; etID22686.5

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The TP53 gene was the first tumor suppressor gene to be identified in 1979. It was originally believed to be an oncogene, but genetic and functional data obtained 10 years after its discovery considered it to be a tumor suppressor. Inactivation of TP53 function and its attendant pathway is a common feature of human tumors which usually correlates with increased malignancy, poor patient survival, and resistance to treatment.

Frequency of cancer deaths worldwide and relationship to the frequency of TP53 mutations Figure 1. Frequency of cancer deaths worldwide and relationship to the frequency of TP53 mutations (Adapted from Soussi et al. 2015).

The TP53 gene is located at the short arm of chromosome 17 (17p13). The TP53 protein includes distinct functional domains: the N-terminus transactivation domain, the oligomerization domain, the sequence-specific DNA-binding domain, and the C-terminus negative regulatory domain. The TP53 gene has been implicated in a growing number of biological processes, including DNA repair, cell-cycle arrest, autophagy, apoptosis, metabolism, and aging. The TP53 protein acts as a central hub that receives, integrates, and transmits multiple signals, generated during various stress events, to ensure cell and tissue homeostasis. Although the most important activity of TP53 is to act as a direct transcription activator for several hundred genes, it is also able to act as a transcription repressor. The transcription factor TP53 can activate the transcription of numerous downstream genes, such as p21 and MDM2, by binding to specific sequences, which often mediates their biological functions. In fact, the transcription dependent and independent of TP53 are regulated by its mRNA and protein levels, cellular localization, and ability to bind more than 100 cellular proteins and control the expression of thousands of potential target genes. Under normal conditions, TP53 is rapidly degraded and, therefore, not present at detectable levels within the cell. The TP53 pathway is activated by such cellular stresses which alter the normal cell-cycle progression or can induce mutations of the genome, resulting in the transformation of a normal cell into a cancerous cell.

Genetic variations in the tumor suppressor gene TP53 contribute to human cancers in different ways. First, somatic mutations are frequent in most cancers. The ant proliferative role of p53 protein in response to various stresses and during physiological processes such as senescence makes it a primary target for inactivation in cancer. The main modes of TP53 inactivation are single-base substitution and loss of alleles, with inactivation through viral or cellular proteins playing a major role in specific cancers. Second, the inheritance of a TP53 mutation causes predisposition to early-onset cancers including sarcomas, breast carcinomas, brain tumors, and adrenal cortical carcinomas, defining the Li-Fraumeni (LFS) and Li-Fraumeni-like (LFL) syndromes. Third, TP53 is highly polymorphic in coding and noncoding regions and some of these polymorphisms have been shown to modify cancer phenotypes and to increase cancer susceptibility in TP53 mutation carriers. Although tumor suppressors are commonly inactivated through frameshift or nonsense mutations, most TP53 mutations are missense and cause single amino-acid changes at a number of different positions. Therefore, mutations are diverse in their type, position, sequence context, and structural impact, making it likely to identify mutation patterns in relation with cancer type and etiology. The occurrence of special mutation patterns may inform on the nature of the mutagens that have caused them, making TP53 an interesting gene to analyze in the realm of molecular epidemiology.

TP53-based therapy has been in the pipeline of numerous academic and pharmaceutical laboratories. In the wake of the disappointment surrounding gene and viral therapies, a new generation of chemical drugs targeting mutant TP53 is under development and several candidates are currently in clinical trials. Drugs to inhibit the interaction between wild-type TP53 and MDM2, thereby increasing TP53 activity, are also in development. Especially, these therapies hold the promise of offering efficacy in all types of tumors, whether they express wild-type or mutant TP53.


  1. Mogi A, Kuwano H. TP53 mutations in nonsmall cell lung cancer. BioMed Research International, 2011, 2011.
  2. Olivier M, et al. TP53 mutations in human cancers: origins, consequences, and clinical use. Cold Spring Harbor perspectives in biology, 2010, 2(1): a001008.
  3. Leroy B, et al. TP 53 mutations in human cancer: database reassessment and prospects for the next decade. Human mutation, 2014, 35(6): 672-688.
  4. Soussi T. TP53 mutations in human cancer: database reassessment and prospects for the next decade. Advances in cancer research. Academic Press, 2011, 110: 107-139.

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