How Does P53 Prevents Cancer Formation

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).

In vitro: In lymphocytes, Cladribine caused accumulation of DNA strand breaks, subsequently activating the tumor suppressor p53. In MM1.S, RPMI8226 and U266 cells, Cladribine dose-dependently inhibited cell proliferation and survival [1].

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

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.

There are two important type of genes responsible for the development or cancer namely tumor suppressor because their normal function is

An ordinary human body contains approximately one trillion cells and precisely 46 chromosomes in each cell. However, the human body can be altered by a genetic mutation. Over the course of history, genetic mutations have had a large impact on the human race. They have brought harm to numerous amounts of people. Cancer, in particular, is one of the most lethal diseases. Cancer begins when a portion of DNA inside a chromosome is damaged, causing a cell to mutate. Then, the mutated cell reproduces multiple times and creates a tumor. Afterwards, cancer cells break off of the tumor, enter the bloodstream, and disperse throughout the body. If the cells break off, the tumor is considered malignant - this type of cancer is very difficult to cure.

Have you ever wondered how cancer forms? Well, cancer starts when a cell's DNA becomes

There are two key ways in which cancerous tumors form. Within the human genome, the two primary gene classes which control cell growth are proto-oncogenes which encourage cell growth, and tumor suppressers which inhibit it. Proto-oncogenes can lead to cancerous growths if mutations in the gene cause it to produce too much growth-stimulatory protein, or a hyper-active form of it. Tumor suppresser genes can also lead to cancerous cell reproduction when mutations make the gene incapable of putting the breaks on reproduction. Normal activity of a proto-oncogene can thus be cancerous if the tumor suppresor genes are rendered incapable of carrying out their function of regulation. With this classification, it is easy to see how one might use gene therapy and recombinant DNA techniques to introduce into the system a fully-functioning tumor suppresser gene. Presumably, if cells are reproducing at a normal rate and are merely incapable of being

Tumour suppressor genes: In health this family of genes usually act as a counter balance for oncogenesis. It is thought that they may be responsible for repairing gene damage in cells, or are growth inhibitor genes. In Hodgkin’s disease, there are often evidences of mutation in tumour suppressor genes as well as other genes.

Pancreatic cancer is a major disease that up to present times has a very high mortality and progression rate which is because it presents very late in its course and most has already metastasized before clinical diagnosis. This makes it difficult to treat.

| * is a common target of deletion or mutational inactivation in human tumors * an inhibitor of Cdk4-cyclin D complexes; * The loss of p16 leads to increased Cdk4-cyclin D activity

Proto-oncogenes induce cell growth and reproduction, while tumor suppressor genes inhibit it. Together, they carefully control the proliferation of cells. However, if a proto-oncogene is mutated, it can become a carcinogenic oncogene, driving excessive multiplication. Tumor suppressor genes, on the other hand, contribute to cancer when they are inactivated by mutation (Ruddon, 1995).

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

It may be possible to correct an abnormality in a tumor suppressor gene such as P53 by inserting a copy of the wild-type gene; in fact, insertion of the wild-type P53 gene into P53-deficient tumor cells has been shown to result in the death of tumor cells (3). This has significant implications, since P53 alterations are the most common genetic abnormalities in human cancers. The over expression of an oncogene such as K-RAS can be blocked at the genetic level by integration of an antisense gene whose transcript binds specifically to the oncogene RNA, disabling its capacity to produce protein. Experiments in vitro and in vivo have demonstrated that when an antisense K-RAS vector is integrated into lung cancer cells that over express K-RAS their tumorigenicity is decreased (4).