P53 mutations and Cancer - Essay Example

The genes are codes that instruct the cell how to make many different proteins. One gene 'codes' for one protein. In a cancerous cell some of the genes have been damaged or lost. And this is termed as 'mutation'. A mutation may mean that too much protein is madeor that a protein is not made at all. There are three different types of genes that are important in making a cell cancerous genes that encourage the cell to multiply; genes that stop the cell multiplying; and genes that repair the other damaged genes.

Some genes encourage multiplication of cells. In general these genes are only activated during repair after a wound or an operation in an adult. But if these genes become abnormal, they instruct the cell to multiply all the time and are termed as oncogenes or in other words are the 'cancer genes'. There are also those genes that instruct the cells to stop multiplication and these are the tumor suppressor genes. These are genes are in the cell particularly to stop the cell multiplying or doubling.

They act as the natural brake to the oncogene's accelerator. Here again the problem is accelerated if one of these 'tumor suppressor genes' becomes damaged and stops working. As a result the cell may then carry on multiplying. In other words it becomes immortal, which is one of the properties of a cancer cell. The best known tumor suppressor gene is called p53. . Disruption of this gene is associated with approximately 50 to 55 percent of human cancers. In other words it can be said that the p53 protein acts as a checkpoint in the cell cycle, either inhibiting or initiating programmed cell death.

Hence p53's has an important role to play when in comes to cancer which is nothing but unchecked proliferation of cells. At this point of time there is another question that arises in our mind. If people have a built-in tumor suppressor then why do so many get cancer Research suggests that there are several factors that determine the p53 molecule activity as it can be inactivated in several ways. Genetics plays an important role, for instance, in some human families if p53 mutations are inherited the family members have a high incidence of cancer.

However in many cases the molecule is inactivated by an external source. For instance, DNA tumor viruses, such as the human adenovirus and the human papilloma virus, have a tendency to bind to and inactivate the p53 protein function, which invariably alter cells and initiate tumor growth. Besides, some sarcomas amplify another gene, called mdm-2, which produces a protein that binds to p53 and inactivates it, much the way the DNA tumor viruses do (Burley n. pag). Hence it can be said that there are several factors that determine the functioning of p53 molecules.

There is another way in which p53 molecule can trigger the cancerous growth in human body. In a normal cell, p53 protein binds DNA, which in turn stimulates another gene to produce p21 which is another protein molecule. The p21 protein in turn interacts with cdk2 which is another protein that stimulates cell division. If for any reason p21 binds cdk2, the cell cannot continue through the cell cycle and does not