Cancerous Cells: A Case Study

The maximum cell density of the naked mole rat cells was found to be three times lower than the mouse sample. This result shows that naked mole-rat cells are hypersensitive to contact inhibition, also known as early contact inhibition. Researchers attempted to determine whether this early contact inhibition was caused by cell contact or secreted factors by replacing the media of naked mole-rat fibroblasts. The replacement increased the maximum cell density but not enough to reach the same level as the mouse sample showing that contact is the cause of the contact inhibition. Naked mole-rat and mouse fibroblasts were infected with oncoproteins which disable Rb and p53 in different samples to determine their role in early contact inhibition. The results showed that both Rb and p53 both played a role in preventing cell proliferation but Rb is more important in the regulation of early contact inhibition. Naked mole-rat fibroblasts were compared to human, mouse and a mutated naked mole-rat fibroblast without early contact inhibition by analyzing for p27 using Western blot. The naked mole-rat sample was the only sample that expressed little p27. When the same process was repeated for p16, the naked mole-rat sample was the only sample expressing high levels of p16. This result shows how p16 is the early contact inhibitor in the naked mole rat and p27 serves as a backup. GFP

In the context of the cell cycle, P53 is shown to have a G1 and G2/M checkpoint function [23]; in fact, upon receiving a stimulus such as DNA damage, p53 induces cell cycle arrest providing time for the cell to repair the genomic damage before being released back into the proliferating pool . The best known P53 target gene product involved in this process is the cyclin-dependent kinase (CDK) inhibitor p21 [18]. The progression through the S phase of the cell cycle is tightly controlled by CDKs [19]. P21 functions by inhibiting Cyclin-CDK complexes, therefore, hindering the cell cycle transition from G1 to S phase [23]. In addition to being implicated in the G1/S arrest of the cell cycle, it has been demonstrated that P21, alongside p53, is also essential in the G2/M phase [23,

normal cell. These extra cells form a mass of tissue that is a tumor. Cancer forms in the genes of

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

The pathophysiological mechanisms are currently unknown, however it is believed that mutations in ribosomal proteins disrupt ribosome biogenesis, leading to red cell aplasia.1,2 Defective ribosome biogenesis is believed to lead to p53 activation which may cause apoptosis and cell cycle

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

Functional studies have demonstrated that combination of primary BRAF or NRAS driver genes together with additional genetic alterations such as deletion of CDKN2A or PTEN and inactivation of tumor protein p53 (TP53) tumor suppressor gene as a necessary event to bypass OIS79–82. High frequency BRAF mutation in concert with loss of function in tumor suppressors (PTEN, p53) and cell-cycle control genes (CDKN2A) has also been observed in ~40% human melanoma and most melanoma cell lines further highlighting the importance of co-operating pathways to fully form

Dr. Charles E. Crutchfield III, a clinical professor of dermatology at the University of Minnesota Medical School, and medical director of Crutchfield Dermatology states that there are three main types of skin cancer, the most common of which is basal cell carcinoma the second most common skin cancer is squamous cell carcinoma, and the final and and the most dangerous form of skin cancer is melanoma. According to the American Academy of Dermatology every year in the United States over two million people are diagnosed with some form of skin cancer.

The cancer cells in a tumor are not all the exact same type of cancer cell. Tumors are a mix of different but similar mutated cells they won't all react the same way. Cancer cells have varying levels of sensitivity towards cancer drugs and treatments. (Fangirls crying when their favorite character dies vs the fangirl who writes the author and stalks his house at night plotting vengeance). Cancer cells mutate at a high rate, because of this, cancer cells that survive may reproduce and mutate further to become immune to that particular drug.

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.

The accompanying is a sign posting of significant causes and is not complete, for example, chemical or toxic compound exposures, ionising radiation, pathogens and genetics (MedicineNet.com 2014). Nowadays there are a number of medicine accessible to treat cancer. In this essay, I will look at the different types of treatment and the advantages and disadvantages for each type of treatment.

Tumor suppressor genes encode proteins, inhibiting excessive cell proliferation and division, through protein inhibitors for cell cycle progression or promoting differentiation and apoptosis via proteins that involved in induction of apoptosis. Mutations that cause inactivation or loss of function in these tumor suppressor genes, result in inactivation of P53, pRb, PTEN, NF1/NF2. The mutations can be deletion or insertion, nonsense or missense mutations, frame shift mutations, or epigenetic tuning events such as methylation, which lead to neoplasia. These mutations are recessive and clinically important, only when they appear as homozygous or a combination with heterozygous alteration. The

With quite one.61 million cases diagnosed annually, carcinoma is that the leading reason behind cancer connected death within the men and second leading reason behind cancer death in girls worldwide [Jemal et al. 2011]. carcinoma is morphologically divided into non-small cell carcinoma and little cell carcinoma with non-small cell carcinoma (NSCLC) accounting for eightieth of all cases. it\'s a heterogeneous clinical cancer with major microscopic anatomy subtype reminiscent of epithelial cell carcinomas (SCC), adenocarcinomas (AC) and huge cell carcinomas [Brambilla et al. 2001]. The medical accomplishment in 20 years has provided least impact on the treatment of the cancer, the general 5 year survival rate of NSCLC is roughly 15 August 1945.

“Cancer is the abnormal, uncontrolled multiplication of cells” (Fahey, 2015). There are many different kinds of cancers that affect various parts of the human body. Some of the most common types of cancer include lung cancer, breast cancer, and prostate cancer. Cancer, of all types, is one of the leading causes of death across the world today with Denmark and France being the countries with the highest rate for all cancers (World Cancer Research Fund International, 2012). “The lifetime risk of developing or dying from cancer refers to the chance a person has, over the course of his or her lifetime (from birth to death), of being diagnosed with or dying from cancer. These risk estimates, like annual incidence and mortality data, provide another measure of how widespread cancer is in the United States (American Cancer Society, 2016).” This risk for cancer is also becoming increasingly high as time goes on. According to the American Cancer Society, one in three people have a lifetime risk of being diagnosed with and/or dying from cancer (2016). The statistics of this risk varies between men and women as one gender may be more susceptible to a particular cancer than the other. Cancer can be treated in various ways and some forms are treatable whereas some are neither curable nor treatable. Here I will attempt to discuss how and/or why cancer forms, its detection, its treatment, as well as a few warning signs of some of the various forms of cancer.

Cancer cells’ ability to migrate and metastasize to other organs and tissues in the body is primarily responsible for disease mortality. Cell migration is caused by a cascade of biophysical processes that interact to give rise to metastatic behavior. Four key biophysical properties involved in cell migration are adhesion, contractility, cytoskeletal polymerization and matrix degradation. Independently a lot is known about the cross talk between each of these biophysical process and the extracellular matrix. Previous studies have shown that varying ligand density has a biphasic increase then decrease effect on the speed of cell migration. It