P53 mutations and Cancer Essay Example | Topics and Well Written Essays - 1000 words

P53 mutations and Cancer - Essay ExampleThe genes argon codes that instruct the cadre how to make many different proteins. One gene codes for one protein. In a crabmeatous jail cell some of the genes bring forth been damaged or lost. And this is termed as mutation. A mutation may mean that as well some(prenominal) protein is madeor that a protein is not made at all. There be three different types of genes that ar important in making a cell cancerous genes that encourage the cell to multiply genes that lay over the cell multiplying and genes that repair the former(a) damaged genes.Some genes encourage multiplication of cells. In general these genes atomic number 18 only activated during repair after a wound or an operation in an adult. scarcely 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 a re the tumor suppresser gene genes. These are genes are in the cell particularly to stop the cell multiplying or doubling. They act as the natural brake to the oncogenes 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 p53s has an important role to play when in comes to cancer which is nothing but undisciplined proliferation of cells. At this point of time there is other question that arises in our mind. If people have a built-in tumor suppressor then why do so many get cance r 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, deoxyribonucleic acid tumor viruses, such as the human adenovirus and the human papilloma virus, have a tendency to declare 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 stir up the cancerous growth in human body. In a normal cell, p53 prot ein 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