P53 Tumor Protein Analysis

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.

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

Scientists have found a number of risk factors that may influence the probability of someone getting Hodgkin’s disease, but it is still not clear how these factors increase the risk (4). For example, some researchers think that infections with the Epstein-Barr virus may sometimes cause damage to the deoxyribonucleic acid (DNA) in the B lymphocytes, which leads to the creation of Reed-Sternberg cells (4). DNA is the set of instructions sent to the genes that dictates cell functions. Some genes are responsible for controlling when cells grow, divide, and die (4). Genes that assist the cells ability to grow, divide, and stay alive are known as oncogenes (4). Genes that slow down cell division or cause cells to die at the proper

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.

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.

Moreover, it’s important to understand that gene mutation occurs in our cell all the time. Accordingly, the prevention of cancer is profoundly dependent on the p53 tumour suppressor protein, which is the process to eliminate excess, damaged or infected cells by apoptosis (Haupt 2003). But if the cell doesn’t die in the process of apoptosis, it may lead a person to developing a cancer. Oncogene are a sequence of deoxyribonucleic acid (DNA) that has been altered or mutated from its original form and induces cancer (Encyclopaedia Britannica 2017). Some people have high risk of developing cancer because they inherited mutations in certain genes (Cancer research UK 2014). Mutation are classified into two, inherited and acquired types of mutation, widely discussed below (ASCO 2017)

Over the years, evidence has proven that any mutations on chromosomes whether they are broken, missing or repositioned is not just a side effect of cancer, but can be an increasing factor for

Cancers seem to develop progressively. There will be intermediate stages between those normal cells and highly altered cells. Hyperplasia is the first stage in which cells look normal but with increased cell number. Next stage is dysplasia, characterized by more cytologically abnormal cells. Dysplasia is followed by metastasis stage, where cells can invade new tissues. During transformation from normal cells to altered cells, either inhibition of tumor suppressor gene or activation of anti-apoptotic genes happen. Almost in all cancers, cell cycles regulators are mutated. Main hallmarks of cancer include induction of angiogenesis, activation of the oncogene, suppression of apoptotic or tumor suppressor gene, activation

In the recent decade, neoplasms are incurably deleterious, formidable non-communicable diseases. A neoplasm presumably arises when a singly normal cell in a given tissue has dynamically accumulated irreversible genetic impairments and instability of such key genes. And these preposterous genes usually incurs a perversity of cell cycle, growth, proliferation, differentiation, survival as well as senescence because they have lost their regulatory functions (Hanahan and Weinberg, 2000; Kumar et al., 2013; Strayer and Rubin, 2014).

Tumor suppressor gene tells the when to die, repair the mistakes made in the DNA, and slow down cell division. If a tumor suppressor gene gets mutated the cells will grow out of control with nothing to stop them. The mutation can be caused when this gene isn’t activated. Two common example of a tumor suppressor are the p53 and NF1. Proto oncogenes codes for protein which helps with the cell cycle, prevents differentiation in cell, and programs cell death. If a proto oncogenes gets mutated there would be change in the protein sequence which would interfere normal cell regulations. The name of the proto oncogene was oncogene. DNA repair identifies incorrections and damages and fixes them. These three genes are mostly used to find cancer because

These genes cause the cell-division process to decelerate, DNA mistakes are corrected, and apoptosis occurs so mutations are limited and preventing cancer cells from forming. When the tumor suppressor genes do not function accordingly, this creates issues with cell division and mutations and then cancer can form. Tumor suppressor genes cause cancer when they are inactive, compared to the oncogene when they cause cancer because they are activated. An example of a tumor suppressor gene would be retinoblastoma, an eye cancer, mostly associated with children, that affects the retina. This disease can be inherited and inherited distortions of tumor suppressor genes have been discovered in families. These genes can sometimes cause cancer to be inherited, but not always because normally the mutations are acquired. A specific trans-activator is a part of gene regulation that raises the rate of a specific gene that can later be activated by a response, or are unnaturally expressed. These genes are needed for domains of the p53 protein, and also are needed for protein expression and protein regulation.

Cancer, also known as a malignant tumor, is a disease in which some cells in the body multiply uncontrollably leading to a mass of abnormal cells (“What is Cancer”).This is the result of damage to the DNA (deoxyribonucleic acid) of a normal healthy cell which causes the natural biological function of the cell behavior to become altered (Mandal). Normal cell behavior is directed by the DNA which regulates the growth and death of the cell among other things (Mandal). When a normal cell’s DNA is damaged, the cell tries to repair the DNA and if it is unable to

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.

In an immunoprecipitation assay, 293T cells testing wild type and mutated TQ/SQ sites in TRAF6 was utilized to determine the effect of genotoxic agents on the phosphorylation of TRAF6 at TQ/SQ motifs. The authors immunoprecipitated for flag asTRAF6 was tagged with the flag antibody. CDDP and ATM/ATR were used as our tested variables. The assay elucidated that the double mutation of S13 and T330 on TRAF6 significantly reduced phosphorylation of TRAF6 in the presence of CDDP and absence of ATM/ATR. Consequently, this data provides information for belief that mutated TRAF6 is not sufficient for phosphorylation to occur in the presence of CDDP. Finally, a cellular fractionation assay for 293T wild type and mutant TRAF6 cells with or without CDDP treatment tested whether such mutation in the presence of genotoxic stress inhibits or promotes TRAF6 expression. As in the previous fractionation studies, tubulin and laminB were loading controls. These results concluded that the mutant displayed resistance to the CDDP mediated reduction of TRAF6 in the cytosol. Overall, these studies suggest that CDDP induces phosphorylation of TRAF6 in the cytosol, which may contribute to the reduction of K63-linked ubiquitination in the cytosol. The information provided thus far suggests that K63-linked ubiquitination of p53 is accomplished by TRAF6, which is hypothesized to suppress spontaneous apoptosis. Moreover, genotoxic stress is shown to promote TRAF6