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Review literature on pancreatic cancer
Essay on pancreatic cancer
Essay on pancreatic cancer and reference
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The earliest discovery of Pancreatic Cancer is linked back to the 18th century by Giovanni Battista. Pancreatic cancer occurs when cells in your pancreas develop mutations in their DNA. These mutations cause cells to grow uncontrollably and to continue living after normal cells would die. These accumulating cells can form a tumor. The p53 and BRCA2 genes make a protein that slows or prevents growth of normal cells and protects the cells against cancer.The p53 tumor suppressor is one of our defenses against this type of damage. Tumor suppressor genes, a mutation (an abnormal change in the gene) of the p53 and BRCA-2 gene induces cells to produce abnormal proteins that alters the growth of the cell. Recent studies have suggested that BRCA2
genes plays a role in the development of pancreatic cancer. The p53 gene that is abnormal in 75% of all pancreatic cancer. P53 tumor suppressor is normally found at low levels, but when DNA damage is sensed, p53 levels rise and initiate protective measures, uncontrolled growth of this gene can cause cancer throughout the cells. THE BRCA2 gene proteins help repair damaged DNA and, therefore, play a role in ensuring the stability of the cell’s genetic material. As a result, cells are more likely to develop additional genetic alterations that can lead to cancer. It is difficult to determine whether or not one has Pancreatic Cancer, inherited DNA changes are thought to cause as many as 10% of pancreatic cancers.
Specifically “TP53, p16INK4A, and SMAD4. The p53 nuclear protein activates transcription of a cyclin kinase inhibitor p21WAF1/CIP1. Following genomic stress, inappropriate growth factor stimulation or expression of oncogenic ras increased expression of p53, and thus p21WAF1/CIP1 resulted in inactivation of specific CDK/cyclin complexes” (MedScape). If this transformed cell can escape internal and external fail-safe mechanisms, receive nutrients, and activate its proliferative program, it can form a mass of cancerous cells. Tumor growth can cause the loss of pancreatic functions. Another characteristic of pancreatic cancer is metastasis happens early in tumor growth, which is most likely responsible for pancreatic cancer’s aggressive
Malignant melanoma is a type of cancer arising from the melanocyte cells of the skin. The melanocytes are cells in the skin that produce the pigment melanin. Malignant melanoma develops when the melanocytes no longer respond to normal control mechanisms of cellular growth and are capable of invasion locally or spread to other organs in the body (metastasis), where again they invade and compromise the function of that organ.
Basil Cell Carcinoma is the most common form of skin cancer. It usually begins as a mole (skin melanoma) on your body; however this cancer can also begin in other areas such as your eye or intestines. This cancer is also the most dangerous type of skin cancer. If diagnosed and treated early, it is almost always curable. There are roughly 2.8 million cases of this cancer diagnosed each year
People can lower their risk of developing colorectal cancer by managing the risk factors that they can control, such as diet and physical activity. It is important to eat plenty of fruits, vegetables, and whole grain foods and to limit intake of high-fat foods. Physical activity is another area that people can control. Even small amounts of exercise on a regular basis can be helpful, at least 30 minutes of physical activity on most days. Also, achieving and maintaining a healthy weight.
Do you have an abundant knowledge of brain tumors and cancer? Have you or a loved one ever had a brain tumor of any sort? If so, they are very harmful and deadly. Over the course of time with the improvement of technology, treatment will be easier and symptoms won't be as noticeable. Brain tumor research has improved exceedingly, therefore, if John Gunther’s son was alive today, he most likely could have been successfully treated or cured of his brain tumor without the struggle of a death sentence.
Cancer is the term used to describe a group of diseases consisting of hundreds of ailments and although there exists so many different types of cancer, they all begin in a similar way. The body is made up of over a trillion cells, and cancer is the uncontrolled growth of malfunctioning cells in the body (Dawson, 1996). “Normal body cells grow, divide, and die in an orderly fashion. During the early years of a person’s life, normal cells divide faster to allow the person to grow. After the person becomes an adult, most cells divide only to replace worn-out or dying cells or to repair injuries” (American Cancer Society, 2012).
Thought to be an oncogene, a gene that has potential in transforming normal cells into tumor cells, p53 was regarded as the most prominent tumor suppressor gene [1]. P53 is a gene which signals apoptosis (programmed cell death) if a cell cannot be repaired due to an extensive amount of damage. As stated in the textbook, p53 regulation occurs by an E3 ubiquitin-protein ligase known as MDM2 [1]. "Controlling the controller" is a statement that describes the molecular interaction where the presence of MDM2 targets the p53 for proteosome via degradation. With three main checkpoints in cell cycle, the literature states p53 functioning from G1 into S phase in a chaotic cell [2]. The normal state of cells is to keep p53 levels low in order to prevent uncontrolled apoptosis and random cell cycle arrest from occurring. In a further note, although p53 promotes apoptosis and cell cycle arrest, cancer may result from p53 unable to recognize the problematic site. In turn, a mutation in p53 may result engaging in new activities. These activities include cellular transformation, tumor metastasis,...
Cancer is a genetic disease because it can be traced to alteration within specific genes, but in most cases, it is not an inherited disease. The genetic alterations that lead to most cancers arise in the deoxyribonucleic acid (DNA) of a somatic cell during the lifetime of affected individual. Because of these genetic changes, cancer cells proliferate uncontrollably, producing malignant tumour that invade surrounding healthy tissue. As long as the growth of tumour remains localized, the disease can usually be treated and cured by surgical removal of tumour. But malignant tumours tend to metastases, that is, to spawn cells that break away from the parent mass, enter the lymphatic or vascular circulation, and spread to distant sites in the body where they establish lethal secondary tumours (metastases) that are no longer amenable to surgical removal. Despite, various exogenous and endogenous factors are known to affect the normal pattern of cell growth, by which cell becomes a cancerous. Species specificity and identity of biological organisms maintain by the unchanged genomic structure throughout their life period. The ratio of cell growth and cell death is strictly balanced through developmental and homeostatic processes in multi-cellular organisms (Bolsover et al, 1997).
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. Many patients today stay optimistic for a medication to heal cancer. It is imperative to address a few of the causes and effects of cancer in order to gain a general knowledge of genetic mutations.
Cancer is a word which evokes many different images and emotions. Nothing in this world can prepare a person for the utter devastation of finding out someone has been diagnosed with cancer, especially when this person is a child. Over the past twenty five years the amount of research and the survival rate for children suffering with cancer have increased dramatically. Despite these successes, the funding for new research necessary to keep these children alive and healthy is miniscule and too dependent on short term grants. Of the billions of dollars spent each year on cancer treatments and research less than a third is contributed to researching pediatric cancer. Given the media focus on adult cancers, research for pediatric cancer is underfunded. In order to maintain the increasing survival rate of the children undergoing pediatric cancer and support those who have survived the disease, better funding is quintessential to develop and further promote research.
TP53, more commonly known as the Tumor Suppressor Gene is what protects a gene from over developing into cancerous cell. TP53 is responsible for regulating nuclear processes within the chromosome ultimately maintaining the cell's cycle and making sure it stays on its correct course, even assisting in apoptosis. The TP53 gene sends signals to make a protein called tumor protein p53 (or p53). This protein is the tumor suppressor itself, it regulates cell division by keeping cells from proliferating too fast or uncontrollably. The p53 protein is located at the nucleus of all cells in the body, and it binds directly with DNA. Human protein p53 is a phosphoprotein; it has a very specific structure closely related to its function. The
Cancer develops when cells in a part of the body begin to grow out of
Cancer is a disease that affects human somatic cells. It causes the cells to divide uncontrollably and form masses known as tumors. There are two different types of cancer tumors. Some tumors are benign and other tumors are malignant. Benign tumors look similar to the tissues that they came from and develop slowly. The tumor remains in the same area that the tumor originated in. Malignant tumors are formed from cells that do not resemble the tissue that they came from. They vary in shape and size. This enables pieces of the tumor to break off and spread to other places in the body. Over the past few decades cancer has become a very prominent disease. There are many different types of cancer and many different causes for the the disease. Most cancers are because of a genetic mutation. The most common type occur when a cell is dividing. Proto-oncogenes, which are alleles in a normal cells, mutate to form oncogenes. These oncogenes cause cancer because they do not allow the cells to self destruct or become epistatic. There have been several research projects which have been testing epistatis.
Normally, tumor suppressor genes slow down cell division to repair damaged DNA or signals that the cells have to die. If the tumor suppressor gene isn’t functioning or turns off, it’ll cause DNA mutations. Since the cell won’t be able to slow down cell division, it begins to grow out of control and keeps dividing. They can be from genetics, but mostly acquired. P53 and INK4 genes are examples of tumor suppressor genes. Proto-Oncogenes, or Oncogenes (when mutated) code proteins that helps cell division. If a gene is copied too many times or one gene activates the other, a mutation will cause oncogenes. Since the cell will continue to divide when it’s not necessary, it’ll cause cancer. You can’t control the cell if it keeps dividing. MYC is a common example of a proto-oncogene. DNA Repair genes come in and repair damaged or mutated genes before they divide into new cells. In the G1 phase of the cell cycle, p53 gene (tumor suppressor gene) is important as it checks if the cell if damaged before continuing. If it’s damaged, DNA repair usually comes in and fixes it. However, if p53 is mutated, it won’t call for DNA repair or DNA repair won’t fix it. When the cell is mutated, oncogenes usually stimulate the cells to keep dividing. These genes usually need to all be mutated to cause cancer. If they all can’t function properly, mutated cells will continue to divide. It’ll all be
Tumors are formed by the alteration of the body’s own cells. This can be caused by environmental factors such as radiation, like UV exposure, chemicals or viruses 1. These can disrupt genes that control growth and cause an increase in cell division and proliferation. Proto-oncogenes are those genes that control normal but essential cell processes that keep cell growth and death in check. Two important categories are apoptosis genes, which regulate cell death, and tumor suppressor genes, which decrease cell propagation 1 . If these genes were mutated to the point where they cannot produce a functioning protein, cell division would continue far past what it was supposed to and unhealthy cells would be allowed to live and continue to multiply. This is what creates a malignant tumor. Certain conditions in the body can also promote the growth of cancer cells. One of these is a deficiency of natural killer (NK) cells, which are able to kill cancer cells by creating a pore in the cell membrane with perforin and releasing granzymes into the cell. Low levels of perforin allow for tumor growth 1. Chronic inflammation can also ...