Antibodies What is the filling? Antigens 15. Describe some advantages of using the ELISA technique to process a large number of samples.…
Most cancer results from faulty DNA repair mechanisms. 40. Cells become cancerous from point mutations (CpG transition in p53), double-stranded breaks, major chromosome rearrangements, chromosome loss/gain, loss of checkpoints, activation of oncogenes, and turning off tumor suppressors via hypermethylations. 41. Mutations and chromosomal abnormalities will affect the regulation of proteins or the structure of the proteins.…
Abstract Li-Fraumeni syndrome is an inherited disorder and leads to the presentation of various types of cancer in a family. This experiment was conducted to determine first, based on Valerie’s family pedigree, if Li-Fraumeni syndrome is present in her family and who has been affected by it. Once this was established, gel electrophoresis was used to compare samples of Valerie’s blood and normal breast tissue to her tumor tissue and to a wild type DNA fragment to see whether or not her cancer has metastasized; it did not appear that this was the case. Lastly, her children’s p53 gene was sequenced and compared to the wild type p53 sequence to determine whether any of them carried the mutation. Two of her children do have the mutation at two points…
Pancreatic adenosquamous carcinoma (ASC) is a rare and aggressive tumor that has worse prognosis and higher metastatic potential than pancreatic adenocarcinoma(Kardon, Thompson et al. 2001, Boyd, Benarroch-Gampel et al. 2012). A major hindrance towards development of therapies against pancreatic ASC is that no unique molecular signature has been identified for this class of pancreatic tumors. Although KRAS and TP53 are altered in pancreatic ASC (Brody, Costantino et al. 2009), the same genes are also abnormal in other forms of pancreatic cancer.…
P 53 also known as “the guardian of the genome” is a tumor suppressor gene that works regulating the cell cycle and apoptosis. It is a very important gene since the lack of its action can allow the cells to divide an abnormal number of times and if action is not taken by the cell’s checkpoints, this could lead to cancer. The evolution of tumors associated with mutations in the p53 gremlin is not well understood and numerous researches have been completed trying to identify all of its characteristics. As all inherited gene mutations, p53 mutations are present in all somatic cells, but the effect of these mutations can have malignant effect on the cells.…
Grade IV astrocytomas are two types i.e Primary and secondary tumors , as we know that primary tumors are very aggressive and the most common form of astrocytoma grade IV [19] and the secondary tumors are those which originate as a lower-grade tumor and evolve into a grade IV tumor. It is distinguished histopathologically from diffuse lower-grade astrocytomas by the presence of necrosis or micro vascular proli-feration[20].Among several tumor suppressor genes, p53 reveal to play a key role in the pathogenesis of many prevalent malignancies [21] including brain cancer. p53 has been displayed to exert tumor suppressor activity by impelling apoptosis , initiating the cell cycle [22], stimulating cell differentiation [23], and being involved in DNA repair pathways [24]. Mutations in the p53 gene are identified in about 28% of de novo GBM and 65% of secondary [25], thus indicating that p53 abnormalities are common in the progression from a low grade lesion to a high grade lesion…
State of the Problem In its variety of forms, cancer is estimated to affect more than 14 million people per year, and is the cause the death of more than 8 million (National Cancer Institute). Despite millions of dollars of research in the field, and a concentrated effort by researchers around the globe, a panacea for cancer doesn’t exist, although much headway has been made in earlier detection and better treatment methods. Much of the difficulty in treating the disease lies in its diversity; cancer is as varied as it is deadly.…
Hypothalamic programming of systemic ageing involving IKK-b, NF-kB and GnRH (Zhang et al., 2013). Cellular senescence is when a cell’s replicative mechanism becomes arrested. This was phenomenon was first described in Hayflick’s experiment. Cellular senescence is usually due to protect the cell from becoming cancerous but it also plays a prominent role in aging (van Deursen, 2014). While senescence describes a halt in proliferation, cancer development is the uncontrolled proliferation of cells (DePinho, 2000).…
DNA mutations can turn on oncogenes or turn off tumor suppressor genes. Gene mutations are usually inherited, therefore it is always important to watch out for diseases that are present in family…
Histone Deacetylase Inhibitors. Histone deacetylase (HDAC) inhibitors are responsible for inhibiting histone deacetylase enzymes, which work to remove acetyl groups from histones. The overexpression of HDACs is responsible for many cancers such as prostate, colorectal, breast, lung, liver, and gastric cancer. Currently, four drugs are FDA approved to function as HDAC inhibitors: Vorinostat (2006), Romidepsin (2009), Chidamide (2015), and Panobinostat (2015).…
Some studies have shown that berberine has anti-cancer influences by inhibiting hepatocarcinogens. Berberine has been found to cause liver weight loss, c-glutamylTrans peptidase, glutamate pyruvate transaminase and bilirubin, all indications of liver damage caused by NDEA (N-nitrosodiethylamine, a strong hepatocarcinogen). Berberine treatment reduced glutathione-transferase levels in the liver, but only had a light effect on glutathione. Berberine reduces the 20-methylcholanthrene-induced sarcoma in mice, as it increases the lifespan compared to animals and reduces the number of animals with…
Not only that, but this paper also includes a variety of techniques, some of which are unfamiliar, thus, providing me with the chance to learn. Moreover, the choice to include multiple techniques to prove one main point makes the author’s conclusions more convincing, as all of their assays worked in synergy. The findings of this paper may be able to suggest potential gene therapies for leukemia patients with normal karyotype but mutated NPM1 gene. Perhaps, siRNA targeted against the mutated gene or its restoration can inhibit NPM1’s aberrant expression in the cytoplasm. Since the mutation results in a nucleotide gain at the C termini, the truncation and subsequent re-folding of the protein may be able to restore its wild type…
Neuroblastoma and microRNA- 34a is commonly mentioned together in many articles and studies around the world. With the advance in medicine and new discoveries, there has been found a dependence relation of neuroblastoma with these specific type of microRNA since it has been discovered how it could eliminate cancer eternally. MicroRNA-34a has not only revolutionized scientists but the world in general because of its ability to destroy neuroblastoma but also because is a new natural genetic regulator of a tumor suppressor. Its level of dominance allows it to control different processes like apoptosis, metastasis, and differentiation in the cell cycle. MicroRNAs have taken control over diverse organisms, not only humans but also plants…
The second assay used biorad protein assay reagent to estimate the concentration of the protein that was eluted. Both assays required a spectrometer to observe the color changes by absorbance. The hypothesis is that active and inactive tryspin would be able to be separated by affinity chromatography according to knowledge about binding and the regents…
Parthenolide and STAT: It is previously discussed that the activation of STAT directs to cell proliferation, cell migration, transformation, apoptosis, cellular differentiation, adhesion, fetal development, inflammation, and immune response. In normal homeostasis, STAT tyrosine phosphorylation is short-term, lasting from 30 minutes to several hours, where as in numerous cancer cell lines and primary tumors it is in contrary to that of normal homeostasis. It takes place due to the deregulation of positive effectors of STATs activation, such as upstream tyrosine kinases (JAK, TYK), or repression of negative regulators of STATs phosphorylation, e.g. phosphatases, suppressors of cytokine signaling or protein inhibitors of activated STATs [47, 48].…