State whether the level of each of the following protein in a cancer cell is higher or lower than normal and how is that beneficial to the cancer cell? a. ARF protein b. MDM2 c. caspases d. Fas receptor e. TNF-α
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State whether the level of each of the following protein in a cancer cell is higher or lower than normal and how is that beneficial to the cancer cell?
a. ARF protein b. MDM2 c. caspases d. Fas receptor e. TNF-α
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- Which of the following classes of oncogenes would likely be druggable with a small molecule (select all that apply)? A. Nuclear hormone receptor B. RAS C. Serine/Threoine Kinase D. Transcription Factor E. Receptor Tyrosine Kinase5) Briefly explain why the formation of a tumour can pose a risk to a person's homeostasis. 6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug "vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief…Which of the following statements are correct about cytoplasmic signaling in cancer cells? Multiple answers. A. Only minor modifications of cell control machinery are required for normal cells to become highly proliferating cancer cells B. Immediate early genes are induced in the presence of protein synthesis inhibitors C. Many immediate -early genes are oncogenes D. Delayed early genes are highly expressed in the presence of protein synthesis inhibitors E. Delayed early genes are highly expressed in normal cells in the absence of growth factors
- I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.Which of the following are mechanisms by which cancer drugs work (select all that apply)? A. Inhibit activity of oncogene B. Promote apoptosis C. Promote terminal differentiation of cells D. Inhibit drug transporters E. Promote DNA damage.The number of calories used during physical exercise is greater than the number of calories used for the movements themselves. This may be caused in part by exercise-induced expression of uncoupling protein 1 (UCP1) in subcutaneous fat. Subcutaneous fat is mostly white fat cells but can also contain brown fat cells in mice and humans. As part of a thermogenesis program, UCP1 directly reduces the proton gradient driving oxidative phosphorylation. UCP1 expression is a characteristic of brown fat cells only and is induced by the protein irisin. The data in Table 1 address the relationship between exercise and: • expression of UCP1 in subcutaneous fat cells, • expression of FNDC5 (a transmembrane protein in skeletal muscle plasma membranes), • blood levels of irisin (a soluble protein formed by cleaving the extracellular domain of FNDC5), and • expression of adiponectin (a hormone produced by white fat cells) in both wild-type mice and mice with overexpression skeletal muscle PGC-1a (a…
- Because of oxygen and nutrient requirements, cells in a tissue must reside within 100 μm of a blood vessel. Based on this information, explain why many malignant tumors often possess gain-of-function mutations in one of the following genes: βFGF, TGF-α, and VEGF.Tumor necrosis factor alpha (TNF-α) is an important cytokine used by immune cells to initiate and coordinate inflammatory responses. Inflammation is a key response to cell damage or infection, but can, in some diseases, spiral out of control and become more of a problem than the original cause (COVID-19 lung damage is a relevant example...). TNF-α receptors exist on many cell types. Let’s study the interaction between TNF-α (T) and its receptor (R), to form an activated complex C: T + R ↔ C A macrophage is measured to have ~105 TNF-α receptors on its surface. If the macrophage is immersed in a high concentration of TNF-α molecules (i.e. L0 ≅ L), how will the number of activated receptors change over time? Plot this trend for the case L0 =10 nM, kf=106 M-1 min-1, kr=0.1 min-1. There is constant ligand concentration and an initial condition of C0 = 0. We are given the constants needed to model the number of activated receptors over time and can use the following equation:Cancer Cells need A.I.R in order to survive and proliferate. What does this stand for? a. Activation of TSG's; Inactivation of oncogene; Replenishing of Telomeres b. Absorption of oncogenes; Inactivation of TRK's; Replenishing of Telomeres c. Activation of oncogenes; Inactivation of TGF's; Replenishing of Telomeres d. Activation of oncogene; Inactivation of TSG's; Replenishing of Telomeres
- One important role of Fas and Fas ligand is to mediate the elimination of tumor cells by killer lymphocytes. In a study of 35 primary lung and colon tumors, half the tumors were found to have amplified and overexpressed a gene for a secreted protein that binds to Fas ligand. How do you suppose that overexpression of this protein might contribute to the survival of these tumor cells? Explain your reasoning.Which of the following would inhibit the function of the JAK-STAT Pathway? Multiple answers A. Inhibition of protein import into nucleus B. The Ser/Thr kinase inhibitor Staurosporine C. Treat cells with Interferon D. Inhibitors of SH2 domain interactions E. Drug that causes dimerization of STAT3Which of the following modifications of the Epithelial Growth Factor Receptor (EGFR) would be proliferative of epithelial cells? multiple answers A. Mutation of active site residue responsible for tyrosine phosphorylation. B. Deletion of extracellular ectodomain C. Mutation in ectodomain that prevents binding of EGF D. Cell expresses EGF E. Mutation in promoter that increases expression of EGF receptor F. Dimerization of receptor without growth factor G. Mutation in EGFR promoter that decreases expression of receptor