A Study On The P53

Its locus is particularly amplified in these noted tumours leading to the progression of these cancers, it can be suppressed by p53 (tumour/ proliferation suppressor) which represses the EZH2 promoter, resulting inhibition of cell proliferation and invasion (Bracken, 2003; Xiao, 2011).

level? A mutation in just one allele of proto-oncogenes can cause over production of cells tumor, and thus tumor formation, because they are dominant. Tumor suppressor genes require mutations of both alleles to inhibit function because they are recessive.

TP53 is a 20kb long gene located on the small arm of chromosome 17 [18]. It is the first tumor suppressor gene to be identified and the most extensively studied [19, 20]. First described in 1979, this gene was first believed to be an oncogene, a cell growth promoter [19]. However, data form in-vivo studies performed years later provided convincing evidence supporting its tumor suppressive activity [18, 21].

The purpose of this research was to determine the mechanisms in naked mole-rats that restricts cell proliferation and tumor formation. Contact inhibition is a mechanism observed where cell proliferation stops when two cells come in contact with one another. This process is caused by elevated levels of p27 cyclin-dependent kinase inhibitor which stops cells in the G1 phase from dividing. The cylcin-dependent kinase inhibitor p16 is also thought to regulate contact inhibition but its levels do not change in mice or human samples. Tumor-suppressor genes Rb and p53 are present in high concentration during contact inhibition to help control cell proliferation and apoptosis respectively. It was hypothesized that the naked mole-rats' cancer resistivity

Mutations in this gene are responsible for an increased incidence of melanoma in a very small amount of families. The incidence of melanoma of CDK4 is similar to the families that have mutations in the gene CDKN2A. The gene CDK4 is a proto-oncogene that makes a protein that helps control cell division. However, when the CDK4 gene is mutated, it products an abnormal CDK4 protein that is too active. This abnormal protein makes cell divide uncontrollably fast, which could lead to tumor formation. Clinically, CDK4 and CDKN2A are mostly similar.

In the book p53: The Gene That Cracked The Cancer Code by Sue Armstrong, they focus on statistics rather than a story. This book describes the change throughout time while focusing on the p53 gene. It talks about different genes that affect p53 and how cancer can happen.

Cancer occurs when cells in the human body create irregularities and start to duplicate at anomalous quick rates. The outcome is the development of tumors in or on the surface of the body and organs. Tumors might be generous (not destructive) or threatening (harmful). Since ordinary cell improvement and duplication is a moderate procedure which is well controlled, it is evident when cells duplicate so rapidly.

Cancer is a disease caused by an uncontrolled division of abnormal cells. The DNA sequence in cells can be changed as a result of copying errors during replication. If these changes whatever their cause are left uncorrected, both growing and non-growing somatic cells might gain many mutations that they could no longer function. The relevance of DNA damage and repair to the generation of cancer was obvious when it was recognized that everything that causes cancer also cause a change in the DNA sequence. Tumor suppressor genes are protective genes and normally they limit cell growth by monitoring the speed of cell division, repair mismatched DNA and control when a cell dies. When a tumor suppressor gene is mutated cells grow

Cells may experience uncontrolled growth and if they are damaged or mutated in the DNA.There are four types of genes that are responsible for the cell division process. Those four types of genes are Oncogenes, Tumor Suppressor genes, Suicide genes, and DNA-Repair genes. Oncogenes tell the cells when to divide. Tumor Suppressor genes tell the cells when not to divide. Suicide genes controls apoptosis and tell the cells to kill themselves if something goes wrong. DNA-Repair informs the cells to repair damaged DNA. Cancer can occur when the cells of genes mutation are not able to correct damaged DNA and are not able to commit cell suicide. If you have some DNA mutations of the oncogenes or tumor suppressor genes that can lead to pancreatic cancer. It is a Great chance that the mutation was a result of some factors that affected the DNA after you were born rather than you inheriting it from your parents.

Human life starts from a fertilized cell which breaks down, again and again, an adult human body is composed of the abundance of cells and each one have their own specific function to perform. During adulthood, most of the cell does not duplicate except some cells continue to divide to replace the old or damaged cell in blood, skin and intestine. This growth is very controlled and no excessive cell growth takes place. But sometimes when a mutation occurs in one or more genes which causes unnecessary cell reproduction and as a conclusion, there is no control over the growth of cells. It is called malignant transformation and this is the starting of cancer (Hosick et al., 2015). There are many different types of cancer but the early stage diagnosis

The normal process of cell division is altered in cancerous cells typically by mutations in the genes involved in the regulation of cellular division. The number of mutations normally will begin to spread because when the genes that make DNA repairing proteins become mutated, this causes the DNA that they would be repairing to become mutated as well. Some changes allow the damaged cells to divide more quickly than normal and to invade other tissues. The cancers cells can divide even where there are signals and normal cells meant to prevent the cell growth.

The ability of p53 to regulate metabolism is also associated with the ability to regulate cellular ROS levels. As previously mentioned, p53 can either remove damaged cells that have suffered sustained oxidative stress, or limit levels of ROS in order to lower oxidative stress and consequently, potential cell damage. Through the regulation of carbohydrate and lipid metabolism, p53 is able to influence the response to ROS accordingly. By driving the expression of TIGAR and promoting PPP activity, p53 can increase the production of NAPDH, which can be used to generate the cellular antioxidant GSH (Bensaad 2006). Moreover, at the expense of nucleotide synthesis, p53 can also promote GSH synthesis following serine starvation, thereby lowering ROS

Transformation-Related Protein 53, also known as TP53, is a tumor suppressor gene. It is named after its molecular mass. The gene was discovered by Arnold Levine, David Lane, and William Old in 1979 and was voted molecule of the year by science magazine in 1993. Although, it was not until 1989 that it was revealed to be a tumor suppressor gene. It was previously thought of as an oncogene. TP53 encodes for a protein, called p53 protein, that helps to regulate the cell cycle and inhibits mutations in the genome as well. Both of these functions help to conserve stability. One of the reasons for TP53’s high importance, and the extensive research on the gene, is its function to suppress cancer cells in multicellular organisms, including humans (Vijayaraj).

Being such a complex and important molecule, all of the functions of p53 are not yet understood. As such, much of the research conducted in the past few decades focuses on discovering new functions of p53 and the mechanisms behind them. Once discovered, these functions may be targeted as potential therapeutic approaches to cancer caused by p53 mutations.

Cancer occurrs by the production of multiple mutations in a single cell that causes it to proliferate out of control. Cancer cells often different from their normal neighbors by a host of specific phenotypic changes, such as rapid division rate, invasion of new cellular territories, high metabolic rate, and altered shape. Some of those mutations may be transmitted from the parents through the germ line. Others arise de novo in the somatic cell lineage of a particular cell. Cancer-promoting mutations can be identified in a variety of ways. They can be cloned and studied to learn how they can be controlled.