A) p53 is a protein in which it help detect damaged cells and is known for the prevention of cancer inhibiting cells. We would be creating a cell with the p53 protein to develops the growth of damaging the cancerous cell and building a
B) we would be developing a new machine that's capable of intracting p53 from the elephant in order to create the new cell. Elephants has
20 copies and 40 alleles, in which human only has one copy and two alleles of such genes. The elephants, having more cells than humans they are likely to fight off cancer, in which us humans can't prevent cancerous cells. Human needs and desire is being able to recreate in humans what elephant has naturally
C) our predictions in combining DNA may cause damage to either the
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F)
I. the problem is trying to figure out wether both genes are compatible with each other, mixing two different genes and adding more p53 to the human cells. The outcomes of wether it would be a cure for the cancerous cells.
II. There're many possible criteria for success in finding a solution in how to cure cancer. Some of the criteria are radiation therapy I'm which it uses high energy particles or waves to destroy or damage cancer cells. Targeted therapy in which is some what similar to the p53 protein, that uses drugs or other substance in identifying and attacking cancer cells, and lastly soursop is a a fruit in which it can slow the spread of cancer.
III. Over five million that were served by one radiotherapy in the sun- Saharan Africa and there are over 5000 radio machines, there are many type of targeted therapy used today, not only does it help cancer from spreading and growing, but it also helps with different type of cancer and tumors. As mentioned in the soursop reviewed article " The adriamycin group displayed a 54.6% decrease in tumor mass" there are many different researcher that has shown how natural the fruit can be by curing the cancer. We feel that the targeted therapy would be
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H) interdependence of science, engineering, and technology it's a cycle that we come up with new and understanding knowledge, I'm human needs and create something that would help the environment, such as we though of how an elephant manage to get rid of cancer because of how many cells they have and how many p53 that humans don't have. That's when we think of the human needs and how it would help the environment in a positive way I like curing cancer within the human body.
I) we noticed that the protein p53 did something in elephants that didn't do in human, that's when we came into a conclusion that if there's many p53 in elephants what if we add more p53 in the human cells to prevent all the cancerous cells that are evolving in the humans body in which we create a new cell that would have many p53 and developed the cycle.
J) once we have the results we don't stop there we will keep thinking of new ways in how we can determined the cure of cancer and damage the cells without affecting it, we would recreate it and reexamine the proteins in the human cell. These steps science, engineering, and technology helps us to get an understanding of its
Long times ago, even during the 19th century, scientist all over the world had started to find the cure for cancer, one of the most feared disease you can ever imagine, simply because you don’t know what the cause and how to turn it off. Cancer started
The next experiment that must be performed is to determine the cause of the naked mole-rats' hypersensitivity. A study searched for the signal that leads to early contact inhibition and determined it to be hyaluronan. Hyaluronan is a key part of the extracellular matrix and has a high molecular mass in naked mole-rats. The hyaluronan in naked mole-rats represses signaling for mitosis as well as having anti-inflammatory properties(Tian et al., 2013). An alternative explanation for the naked mole-rats' cancer resistance could be its ability to use telomerase to regulate chromosomal length. Compared to the use of senescence in humans, telomerase makes cells immortal in culture by preventing cells from becoming too short leading to cancerous cells or apoptosis. Another possible alternative explanation is the number of copies of p53 that the naked mole-rat has. In a study in which the cancer resistance of large mammals was compared to their DNA damage response, the results showed that elephants have at least 20 copies of p53 compared to humans 1 copy. This is believed to be the cause of elephants' high cancer resistivity(Abegglen et al., 2015). These copies allow elephants to have a backup tumor suppressor in case of damage to another
are able to fix the mistakes in the DNA that could potentially cause cancer. Unfortunately,
into cancer. The doctors have no way of determining which altered gene will cause cancer or do
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.
On which can help the patient who has this cancer be able to live for a more longer time than back then where you aren’t able to stop the cancer cells to affect the rest of your body. Some test perform to help with the research to help scientist and also doctors to help detect and be able to stop the source it’s by looking at ultrasounds. As well as not only that but also CT Scanning, MRI, and even ERCP. Thanks to this technology doctors are able to treat these cancer by doing series of surgeries to extract tumors created and remove the organs or parts where it's most affected by the cancer. Another possible cure for this cancer is chemotherapy which is basically usage of certain chemicals and even specific
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
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
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
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.
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.
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
We’ve all heard about the elusive cure for cancer. But cancer in itself isn’t just one specific disease:
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.