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Is called “guardian” or “police”, because any alteration that is in the cell, and there are many cancer associated, activates it. Crucial in preventing cancer, p53 is an anticancer gene that under normal circumstances we defend the disease. P53 blocks or kills the altered cell, prevents their proliferation or cell division (cell suicide) or because maintains blocked without leaving reproduce. Is a gene that is activated only in stressful situations, when there is damage in a cell is a detector of dangerous situations, a sensor.


So that there is a cancer p53 has to be inactive, and is at 55% of the most common cancers:

  • Breast
  • Lung
  • Bladder
  • Lymphoma
  • Ovarian
  • Esophageal
  • Colorectal
  • Head and neck
  • Sarcomas


Researcher Manuel Serrano, head of the group of tumor suppression National Cancer Research Centre (CNIO) who has worked in p53 said: “It is a key gene, so is the star of gene” it is simple: p53 is key,   because it is the gene most frequently mutated in cancer.


Tumor protein p53 also known as:

  • P53
  • Cellular tumor antigen p53
  • Phosphoprotein p53
  • Tumor suppressor p53
  • Antigen NY-CO-13
  • Transformation-related protein 53 (TRP53)

The name p53 was given in 1979 describing the apparent molecular mass: SDS-PAG analysis indicates that it is a 53-kilodalton (kDa) protein. All these p53 proteins are called the p53 isoforms (from Wikipedia).

  • It is a suppressor gene located on the short arm of chromosome 17 band 13, and encodes a nuclear protein of 53 Kd. P53 function in normal state is to regulating the cell cycle to DNA damage, which has been called “guardian of the genome”
  • Is a DNA-binding protein which belongs to the p53 family. It contains transcription activation, DNA-binding, and oligomerization domains. Activation of p53 begins through a number of mechanisms including phosphorylation by ATM, ATR, Chk1 and MAPKs.


  • When DNA is damage: the human body is always exposed to external damage, in addition to the endogenous – in our cells there are sometimes mistakes accidentals- is good to know if external agents such:
  • Alcohol
  • Snuff
  • Insecticides
  • Industrial pollution
  • Solar radiation
  • Ultraviolet radiation

Have been incriminated as potential mutagens p53.


  • P53 accumulates in the nucleus, and is able to stop the cell cycle in G1 (check point) before doubling the DNA and initiate repair. P53 will induce synthesis inhibiting proteins cyclin-CDKs complex, blocking the cell cycle.


  • If the injury is repaired the cycle continues, but if not repaired cell apoptosis is induced by gene expression as bax. Altering the P53 protein causes genomic instability, where cells unable to prevent proliferation and trigger apoptosis when DNA integrity, so that they are able to accumulate mutations to complete carcinogenesis is committed. (from BioCancer Research Journal).


Related Links p53:


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