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P53 Gene And Its Role In Cancer Biology Essay, P53 essay

P53 essay

The first indication that cells might contain genes whose loss is associated with the development of cancer came from experiments using a technique called cell fusion. In 1960, a research team in Paris headed by Georges Barski discovered that cells of two different types grown in culture will occasionally fuse together to form hybrid cells containing the chromosomes of both original cell types.

A very similar condition called Li-Fraumeni-like syndrome shares many of the features of classic Li-Fraumeni syndrome . Both conditions significantly increase the chances of developing multiple cancers beginning in childhood; however, the pattern of specific cancers seen in affected family members is different.

An adaptive evolutionary process has caused p53 to be intrinsically unstable; the protein will unfold at body temperature. This degradation might cause a folding and unfolding event, which could be linked to the amount of cancer mutations possible with this protein. This thermodynamically unstable feature might also help with the binding to other proteins.

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The discovery of unknown interactions contrasts with confirmatory studies because the research interest lies in discovering new proteins in the endogenous environment that interact with a given bait protein. The endogenous environment can entail a plethora of possible protein sources but is generally characterized as a complex protein mixture considered to be the native environment of the bait protein. Any cellular lysate in which the bait is normally expressed, or complex biological fluid (., blood, intestinal secretions, etc.) where the bait would be functional, is an appropriate prey protein source for discovery studies.

The p53 pathway is important in the G1 phase in that the p53 gene functions in detecting DNA damage within the cell. ... Under normal circumstances, p53 is unstable and short lived; in cells with DNA damage, p53 stabilizes and accumulates. ... If DNA damage is irreparable, p53 activates death genes such as Bax, inducing apoptosis. ... Rb is a tumor suppressor gene that controls gene expression necessary for DNA synthesis (S phase). ... Other research has focused on the restoration of the p53 pathway. ...

First, a little background. Humans have two copies of every gene. We inherit one from our mom and one from our dad, and each gene has a different job. One of these genes is called TP53. And TP53, as Schiffman and other scientists describe it, is the so-called “Guardian of the Genome.” That’s because the gene plays an important role in protecting us from cancer by encoding for the protein p53, which is a tumor suppressor.

In normal cells, p53 remains in a latent, standby mode stage with a very low half-life of about twenty minutes. It interacts with more than 150 other proteins, some that restrict its production and eliminates its excess. A major protein involved with it is mouse double minute-2 (MDM2). MDM2 binds to p53 as a tag for ubiquintination, or degeneration of it in the proteasome, which keeps the tumor suppressor at relatively low levels. Because MDM2 is also negatively regulated by p53, their relationship continues in a cycle, where both proteins keep one another in check. Another related protein is MDM4, which also lowers p53 but directly and not through ubiquintination.

The distinction is important, says the study's lead investigator, Professor Geoffrey M. Wahl, ., a professor in the Gene Expression Laboratory. "p53 is disarmed in more than half of all cancers, and Mdm2 and Mdm4 are over-expressed to act like cancer-causing oncogenes in much of the rest. We need to know how each of these p53 inhibitors work in normal cells before we can figure out the most effective therapeutic strategies to manipulate them in cancer cells," he says.

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The argument that size is the other factor is as follows. If there is a basal rate of mutations in every dividing cell, there is a certain probability that each cell may develop a “renegade promoting mutation”. The more cells there are, the greater the probability that some cell somewhere will go bad. The “renegade problem” then, is really a product of one of the fundamental tenets of evolution – that of mutation and evolution of size (as a function of cell number). It provided the basis of genetic diversity and at the same time a major hurdle that must have been overcome for complex multicellular organisms to evolve.

P53 plays a very crucial role in cell cycle regulation and apoptosis induction, the mutation of p53 would lead to the cancerization in cells and induce cancer. Bai and Zhu (2006) reported that the mutation or loss of p53 gene and protein can be found in over 50% of tumor cells in human all around the world. For these reasons, the application of cancer therapy through protein p53 and Tp53 gene is a very potential aspect in cancer treatment. This review will describe the structure and function of p53 protein, examine its role in natural and tumor cells and focus on the cancer therapy application through p53.

Oncogenes are "gain of function" genes. They gain the ability to drive non-stop growth. In spite of their dominant activities, a single mutated oncogene usually isn't enough to cause cancer all by itself because tumor-suppressor genes are acting to put the brakes on to keep cell growth from getting out of control.


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p53 essay
p53 essay

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