Compare and Contrast the cell cycle of a normal cell and cancer cell.
The cell cycle of a normal cell and a cancer cell are different in some ways. Normal cells and cancer cells go through all phases of the cell cycle. The function of the G1 and G2 phase are mainly for cell growth, The S phase, or synthesis phase, is when the cell’s DNA is replicated, and in the M phase, or Mitosis, is when cell division finally occurs. During the G1 phase, normal cells go through cell growth and they prepare to synthesize DNA. S phase follows and normal cells get their DNA synthesized. The G2 phase prepares the cell for cell division. Lastly, in the mitosis phase, the cell divides. Cancer cells go through the same phases as a normal cell with no differences
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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 …show more content…
Environmentally caused cancers are caused obviously by environmental risk factors like, radiation or smoking. Some cancers that can be passed on genetically are breast cancer, colon cancer, and ovarian cancer. Inherited breast and ovarian cancers are caused by an inherited breast cancer gene, BRCA1 or BRCA2 (ovarian cancer is more likely in women with a breast cancer gene). Colon cancer can be inherited because of inherited syndromes associated with colon cancer. Some cancers associated with environmental risk factors are lung cancer and skin cancer. Environmental factors that can cause cancer are radiation from the sun’s ultraviolet waves and smoking. Radiation can cause skin cancer because the sun’s UV rays are too strong for human skin causing changes in the chemical balance of the skin cells or gene mutations. Smoking causes lung cancer because when the tobacco smoke enters the lungs, it damages the cells that line them. Environmentally caused cancers are more common than genetically inherited cancers because there are many environmental risk factors for cancer but, fewer risks for inherited cancers. About 224,390 new cases of lung cancer (117,920 in men and 106,470 in women) were estimated by the American Cancer Society and 5.4 million skin cancers are diagnosed each year. This year, an estimated 246, 660 women were diagnosed
The risks that can develop cancer are complicated and complex. To indicate one single cause of cancer is hard. However, certain environmental causes are strongly interrelated with the cause of particular cancers, such as cigarette smoking and lung cancer and exposure to ultraviolet (UV) light and skin cancer (CancerSource). It is also known that, “Ionizing radiation consists of x-rays, UV light, and radioactivity whose energy can damage cells and chromosomes. Radioactivity increases the risk of cancer.” Source to indicate the effects of radioactivity is the U.S bombing of Hiroshima and Nagasaki. After all these years, the Japanese are still suffering from all kinds of cancer caused by many long lived chemicals such as Strontium-90 and Cesium-147 from the fallout. “High rate of leukemia” was found among the people who had survived Hiroshima and Nagasa...
..., while a cell undergoes cell cycle, when a cell comes in contact with another cell, it stops reproducing. However, cancer cells continue to duplicate repeatedly until there is a mass of cells or a tumor to form (see figure 9). Lastly, in cell division when there is a mutation or abnormality in the DNA, a normal cell stops dividing. However, a cancerous cell will continue to duplicate and form mutations (“Cell Biology and Cancer”). Also, cancer cells are harmful because they grow and duplicate with complete disregard to the functions and limitations of the body (see figure 10). Also, cancerous cells have the ability to spread through metastasis throughout parts of the body through the bloodstream. In terms of similar behavior to that of normal cells, cancerous cells also duplicate, but at a very different rate ("Cancer Cells vs. Normal Cells: What's Different?").
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,...
Most forms of skin cancer are found on areas of the body that experience constant exposure to sunlight. The ultraviolet rays in sunlight are one main cause of skin cancer, but artificial sources of UV rays have also been proven to be a contributing factor.
Cancer starts when cells in a part of the body start to grow out of control. Cancer cell growth is different from normal cell growth. Instead of dying, cancer cells continue to grow and form new, abnormal cells. Cancer cells can also invade (grow into) other tissues, something that normal cells cannot do. Growing out of control and invading other tissues are what makes a cell a cancer cell. Cells become cancer cells because of DNA (deoxyribonucleic acid) damage. DNA is in every cell and it directs all the cell’s actions. In a normal cell, when DNA gets damaged the cell either repairs the damage or the cell dies. In cancer cells, the damaged DNA is not repaired, and the cell doesn’t die like it should. Instead, the cell goes on making new cells that the body doesn’t need. These new cells all have the same abnormal DNA as the first cell does.
The cell cycle is the process by which cells progress and divide. In normal cells, the cell cycle is controlled by a complex series of signaling pathways by which a cell grows, replicates it’s DNA and divides, these are called proto-oncogenes. A proto-oncogene is a normal gene that could become an oncogene due to mutations. This process has mechanisms to ensure that errors are corrected, if they are not, the cells commit suicide (apoptosis). This process is tightly regulated by the genes within a cell’s nucleus. In cancer, as a result of genetic mutations, this process malfunctions, resulting in uncontrolled cell proliferation. Mutations in proto-oncogene or in a tumour suppressor gene allow a cancerous cell to grow and divide without the normal control imposed by the cell cycle. A change in the DNA sequence of the proto-oncogene gives rise to an oncogene, which
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 ...
25% of the deaths h in 1991 and is the most common cause of death
Fewer than ten percent of most cancers are thought to be due to strong hereditary factors. Many physicians believe that prevention is the best way to effectively tackle cancer. One of those factors in prevention is the individual knowing their family history so that they can develop an awareness of their families' cancer lineage. Other factors are a balanced diet, not smoking, moderate alcohol consumption and exercise. Strong hereditary factors that increase cancer risk are more likely to be found in families that have:
The cancer cells from gene-mutation. Scientists now know some of the risk factors for lung cancer can cause certain changes in the DNA of lung cells. These changes can lead to not normal cell growth and, sometimes, cancer. DNA is the chemical in each of our cells that makes up our genes and how our cells function. People usually look like their parents because they are the source of our DNA. But DNA affects more than how we look; it also can affect our risk for developing certain diseases, including some kinds of cancer like lung cancer etc…Some people inherit DNA mutation from their parents that greatly increase their risk for developing certain cancers.
Skin Cancer is caused by hereditary factors, overexposure to the sun, and weak immune systems. (“Skin Cancer” infotrac.com) One reason people tend to get skin cancer is when someone in your family has passed their genes down to you, known as hereditary. Normally hereditary is one of the causes in the development of melanoma. For all types of skin cancers, overexposure of the skin to UV radiation in sunlight is the most frequently blamed source of skin cancer. “Research suggests that sunburns received early in one’s childhood can lead to skin cancer later in life” (“Skin Cancer” infotrac.com). For example, when someone gets sunburned, you usually don’t know till ten to twenty years after and that’s why people don’t get skin cancer till they reach their twenties.
Cancer develops when cells in a part of the body begin to grow out of
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. Transfecting DNA To perform the experiments for this research, the researchers had to grow certain pieces of DNA.... ... middle of paper ...
Since 1979 the diagnoses of cancer have gone up nearly 20% in a generation as there is more people smoking, drinking, obesity and unfitness (theguardian website, 2011, para. 1). There has been in increase of women with the diagnosis, the diagnoses have risen up by 50% (459 per 100,00), men have risen from 20,000 to 24,000 (the guardian website, 2011, para. 2). Socioeconomic class does have an effect in some cases as cervical and lung cancers are more common in poor people while rates of breast cancer and melanoma are higher in the wealthy (ScienceDaily website, 2008, para. 1). Demographics could also have some effect as those of the wealthier group have more exposure to UV by traveling abroad for the holidays (ScienceDaily website, 2008, para. 5). In regards to smoking, deprived groups continue to smoke while the wealthier groups have quit smoking (ScienceDaily website, 2008, para. 7). Researchers have linked cancer to not only demographics, socioeconomic class but also race and