Cancerous Cells: A Case Study

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).

TP53, also called tumor protein 53 is a tumor suppressor gene that encodes p53 and acts as a control center for the cell to act on when stressed (Brachova). Human p53 is a nuclear phsophoprotein of molecular weight 53kDa located on chromosome 17 containing 11 exons and 10 introns (Ling). One of its primary roles is as a transcription factor and in its active state is a homotetramer comprised of four 393 amino acid residues (Joerger , The tumor suppressor p53). Another main role p53 plays is as a tumor suppressor and once activated, protects against cancer by “functioning as a sequence-specific transcription factor, through protein-protein interactions, activating cell cycle arrest, apoptosis, and DNA damage repair (Brachova).”

Therefore, the most notable P53-induced mechanisms in mediating this response are cell cycle arrest and apoptosis [18], which activation depends on the cellular context and the extent of damage [20].

The P53 prevents cancer formation by acting as a tumour suppressor gene. Also known as the TP53. It plays important roles in multicellular organisms by stopping genome mutations. The name p53 was established in 1979 describing the molar mass indicating that it is a 53kDa protein. It was first discovered in 1979 and was thought to be an oncogene (a gene capable of transforming regular cells into tumour cells). However in 1989 further research by Bert Vogelstein from John Hopkins School of medicine discovered that it was actually a tumour suppressor gene. The p53 protein consists of 393 amino acids. This protein can activate other proteins that have the ability to fix

This technique was shown to provide “more effective control of locoregional recurrence in diseases like NSCLC as well as systemic control of micrometastases,” the spread of cancer cells where secondary tumors are too small to be detected (Roth, Swisher, & Meyn, 1999; “Micrometastases”, n.d.). As explained previously in this paper, p53 is involved in many pathways influencing the cell cycle and apoptosis, making it a good candidate for targeting using gene therapy. Moreover, although cancer cells have mutations in many genes that regulate growth and repair, because p53 plays such a significant role in apoptosis, the restoration of its function will induce apoptosis in the cancer

An irritant, such as cigarette smoke, effects the cells of the epithelium lining. Initially the body can repair the cell, but with repeated exposure the cells of the lungs become damaged and grow uncontrollably. P53 is a gene for various downstream targets that are involved in cell progression, DNA repair and regulation of cells that undergo apoptosis. Mutations to P53 hinder its normal tumor suppressing capabilities. Therefore, DNA damage remains unchecked, faulty cells proceed through the cell cycle and apoptosis is invaded. All these factors create a genetic condition where the cell is more susceptible to further mutation. If the cancer grows large enough, it can affect the organ by closing off the aveoli, leading to shortness of

Compare and contrast tumour suppressor genes and proto-oncogenes. Discuss an example of how recent advances in our understanding of these genes have led to the development of a novel therapy that is being used in the treatment of human cancer.

The article then looks at the role, in solid tumours, of areas of low oxygen (hypoxia) in selecting for those cells that have mutations in the p53 tumour supressing gene. A common feature inside solid tumours is hypoxia and an increase of cell death. This happens because often the rate of growth in a solid tumour outstrips the supply of oxygen to the cells. The normal reaction of a group of cells, expressing the normal p53 gene, when exposed to an hypoxic region, is an increase in the rate of apoptosis. However, in a solid tumour there are many cells with many different types of mutations. In the battle against solid tumours, some tumours resistant to treatment have cropped up. The article takes a look at the role of hypoxia possibly selecting for those cells resistant to apoptosis.

Cancer is a term used for diseases in which irregular cells divide without any control and have the capability to penetrate and infect normal body tissue through the blood and lymph system. Cancer is the second leading cause of mortality in the United States, exceeded barely by heart disease. According to the CDC Cancer Statistics and Data, there were more than 1.45 million people diagnosed with various kind of cancer between 1999 and 2007 and out of those more than 562,000 people died due to cancer (cdc.gov, 2012). Currently there are more than 200 different types of cancer that have been discovered. Cancer could be

From surgery to radium exposure to such extremes as radiation therapy, as doctors’ knowledge of the varying types of cancer, and the expansion of medical research regarding cancer has changed, so has the preferred method of treatment. Doctors and researchers dedicated to studying cancer have led to a greater understanding of cancer development; consequently the development of treatments and cures that are more effective, less harmful, have fewer side effects, and in some cases serve to prevent the spread of cancer.

As the main source of death in the United States, malignancy gets a gigantic measure of consideration from analysts and research healing centers devoted to deciding the cause and hunting down cures. Around one-portion of men and 33% of ladies will build up some kind of malignancy amid their lifetime. Confidence is vital, be that as it may, as a great many individuals are presently living disease free on account of the endeavors of scientists and the donations of individuals over the world.

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.

are able to fix the mistakes in the DNA that could potentially cause cancer. Unfortunately,

Proteins are a very important part of the human body. Each of these proteins has a specific job in our body. One decides the color of hair, one decides the color of eyes, or one may keep the human body from diseases by making it immune. When some of these proteins are affected they will work in an inverse way causing harm to the human body. TP53 is an example of a protein that works in an uncontrolled way, possibly from the exposure of uranium and other materials, causing diseases such as cancer. In this paper, the radioactivity and the high chemical toxicity of uranium will be discussed. Also, when DNA and RNA become damaged, it then causes other proteins to