Melanoma Cell Lab Report

Mutations in this gene are responsible for an increased incidence of melanoma in a very small amount of families. The incidence of melanoma of CDK4 is similar to the families that have mutations in the gene CDKN2A. The gene CDK4 is a proto-oncogene that makes a protein that helps control cell division. However, when the CDK4 gene is mutated, it products an abnormal CDK4 protein that is too active. This abnormal protein makes cell divide uncontrollably fast, which could lead to tumor formation. Clinically, CDK4 and CDKN2A are mostly similar.

Aim 1: To identify Aha1 in the patients’ sample. From the medical center, metastatic and non-metastatic cancer patients’ tumor tissues along with buffy coat, plasma, serum, viable lymphocytes, as well as urine samples will be collected. Aha1 along with other secretory proteins such as Hsp90α, Survivin, MMP will be evaluated in cancer patients’ samples.

Beta actin was used as the loading control in these tests and Figure 2 shows that it was not affected by the siRNA. As you can see the siRNA band is lighter in color in both cell lines indicating a reduced amount of protein. Once again both breast cancer cell lines were shown to have significantly reduced expression levels of CDK8 in the presence of siRNA. The p

The purpose of this study is to get an accurate look on how genetics work, and to practice determining the different traits within the species. D. melonogaster are useful because they are easily cultured and they reproduce very quickly. The eye color data supports past genetics problems because it can be predicted, and used in Punnett squares to aid in the prediction. If the P generation consists of a purebread red eyed fly(dominant) and a purebread sepia eyed fly (recessive), then the F1 generation will be heterozygous and produce an F2 generation with mostly red eyed, but some sepia eyed flies.

The research in Dr. Langenfeld’s lab focuses on the genes that regulate lung cancer. The experiment looks closely at the non-small cell lung carcinoma (NSCLC) and immortalized bronchial epithelial cells. Careful study of the carcinoma and epithelial cells has revealed that the mRNA of bone morphogenetic proteins 2 and 4 (BMP-2/4) was highly expressed in the carcinoma. Past studies have shown that BMP-2/4 have certain properties that allow them to activate the differentiation, growth, and migration of cancerous cells in the embryo. After studying these morphogens in lung carcinoma is was revealed that the BMP-2, in its mature state, is significantly more expressed in NSCLC than BMP-4 in cancerous lung tissue, but did not show much effect in normal lung tissue or benign lung tumors. The BMP-2 that was exposed in vitro to the A549 and H7249 human lung cancer lines stimulated significant migration and invasiveness. In vivo trials showed that the growth of tumors of A549 cells in nude mice was highly enhanced. Tumor growth in NSCLC was attempted to be reduced with recombinant through the exposure to noggin or the anti-BMP-2 antibody. Results showed a significant reduction in the tumor growth[1].

The malignant cells usually have mutations in the p53 tumor-suppressor gene (p.1058). The loss of proper FasL expression and p53 allows melanocytes to mutate and proliferate without the proper mechanisms.

Malignant melanoma is the most commonly seen skin cancer and it has the highest number of deaths among diseases of the skin (Friedman, Rigel, Kopf and Polsky, 2005). Among the many factors that cause this cutaneous cancer genetic modifications, viruses, carcinogens and excessive exposure to ultraviolet rays are the most commonly occurring (Friedman, Rigel, Kopf and Polsky, 2005). Malignant melanoma affects all areas of the skin and the disease forms in melanocytes, which are the cells in which pigments (melanin) are synthesized (Melanoma Treatment). The cancer has its origin in the epidermis and affect squamous and basal cells. The disease usually affects the trunk, arms and legs but can also be present in the eye, affecting the

Melanoma is a skin cancer derived from melanocytes and is considered to be the most common fatal malignancy of young adults. About 60% of melanomas harbor a mutation in BRAF, a serine/threonine protein kinase involved in promoting MAPK signaling and cellular proliferation. Of these, 90% harbor the BRAFV600E mutation. To combat this disease, the BRAF inhibitor, vemurafenib, was approved in 2011 to treat late-stage melanomas that are driven by the BRAFV600E mutation. Despite the immediate, positive clinical response to the drug, resistance develops after 7 months of vemurafenib treatment. Significant research effort has been devoted to understanding the origin of this drug resistance, but few studies have examined the fate of individual cells

Immunoprecipitation (IP) and Western blotting: we will use this method for selectively the endogenous target protein p53 from a complex proteins solution. For prepare the lysate, CML and CLL cells with and without SMYD2 inhibitors will be harvested and then lysed in 1 mL Lysis Buffer (5O mM Tris, 50 mM NaCl, 5 mM MgCl2, 1 mM DTT) with protease inhibitors (Roche Molecular Biochemicals, Indianapolis, IN). The lysates will be centrifuged and the supernatant will be incubated with p53 antibody bound to magnetic protein A beads for 2h. Then, p53 will be eluted from the beads using 100 µl of Elution Buffer. After that, immunoprecipitated protein will be resolved on SDS-PAGE and separated protein (p53) will be transferred to nitrocellulose (Protran BA, Schleicher and Schuell, NH), blocked using 5% nonfat milk (10 g nonfat

Although the mbk-2 mutation has been researched, there is not much understood about the effect of the mutation on the distribution of P granules. Although samp-1 demonstrated the strongest suppression of the mbk-2 phenotype, its distribution of P granules was the most disordered. In these embryos, the granules had localized once again to the P2 blastomere by the four-cell stage. npp-19 and gtbp-1 were the only other suppressors that localized the P granules to the P2 blastomere, although it was only samp-1 cells that demonstrated wild-type meiotic cell division. This could indicate that proper cell division and P granule localization to P2 by the four-cell stage should be restored in order for the worms to develop past the L3 stage. Pang

Conducting specific aim one will focus on whether growth on collagen increases resistance to MEK. The extracellular matrix of these cells becomes dense with collagen, fibronectin, and proteoglycans and signaling from these components to the tumor cells through integrins contributes to drug resistance. Since collagen was present in large amounts in the poorly differentiated type, it is probable that collagen does affect tumor resistance to MEK inhibition. PTC cells with the MEK inhibitor were studied treated with collagen cells and untreated with collagen cells. Then, GR50 values were calculated so that normalized drug responses to growth rate were attained. When cell lines are plated, cell counts will be analyzed through a reagent that illuminates in the presence of ATP called CellTiterGlow. We will also evaluate phosphorylation within these cells to study how long inhibition occurs. Isolation of RNA will be isolated through Quiagen’s RNeasy isolation kit. We will use RT-PCR and Western Blotting to study MEK inhibition at the calculated GR50 and collect RNA from samples with and without collagen for transcriptome analyzation through RNA-seq. Sequencing libraries will be formed by using

Alteration of p53, p53 family proteins and their isoforms by H pyroli in gastric cancer

The roots extract was used to see if it would slow down the growth of cancerous cells or not. The cancer cell lines used was A549 cell also known as lung cells, and BT549- breast cancer. Components used in this experiment include alamar blue, media DMEM, Tamox, DMSO, centrifuge tubes, pipets, and micropipets. Alamar blue also known as Resazurin is a growth indicator used to detect metabolic activity. An oxidation- reduction indicator to show color changes resulting from cell growth. In this experiment if the solution turns red, it indicated that cancer cell lines were growing. Media DMEM was used as a PH indicator, also as a nutrient for the cell. The PH was to be a neutral of 7.0. Tamox killed the cells and was used as the positive control. DMSO was the negative control. The purpose of this experiment was to identify if the compounds were good candidates towards the cure for cancer. Observation was made to see if the cells would die through

Cancer is a name given to many diseases that are similar. In all kinds of cancer, blood cells divide uncontrollably(NCI). Science has had a huge affect on the way cancer is being diagnosed and treated. When doctors start to see symptoms like new moles/skin changes and quick weight gain or loss, they will do a number of tests, to see if you have cancer. Some of the tests include, Lab tests, biopsy, MRI, X-ray, and CT scan, though there are many additional tests. In lab tests, they check and see if the ratio of substances needed for your body are normal, or not. Normally, for these tests they use urine or blood. In a biopsy, a doctor will take a tissue sample and examine it to see if anything looks different. To remove tissue, doctors

Around the world, cutaneous melanoma is predominently a disorder of people with sensible skin and sensible hair, who brown ineffectually; in every way that really matters all the known threat segments are joined with sun presentation and skin helplessness to sun and there is small expounding on the event of melanoma in dull cleaned populations. Melanoma overall happens more routinely