Why is the p53-meditated apoptosis pathway, and the GSK3 signaling pathway important for cancer therapy. Explain each of them in 3-5 sentences.
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Why is the p53-meditated apoptosis pathway, and the GSK3 signaling pathway important for cancer therapy. Explain each of them in 3-5 sentences.
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- A temperature-sensitive mutant yeast strain stops dividing when shifted from 25°C to 37°C. These cells are analyzed at different temperatures by a machine that measures the amount of DNA they contain, and the following graphs are obtained. number of cells number of cells [ Select] [Select] [Select] 25°C [Select] مل Cells in G1 phase should have [Select] Which of the following would explain the behavior of your mutant? Mark yes or no for each of the following choices. 2 amount of DNA/cell (arbitrary units) 37°C 1 2 amount of DNA/cell (arbitrary units) unit(s) amount of DNA. ✓ Inability to initiate DNA replication Defect in chromosome condensation ✓Defect in centrosome duplication ✓Defect in cytokinesisRelatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.What would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?
- a) How does Venetoclax, a BH3 mimetic, function in increasing cellular death? In your answer make sure you include what molecules Venetoclax binds and how this helps trigger cell death. b) How would addition of a BH3 mimetic increase cytoplasmic p53-mediated cellular death?Describe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.Explain why mutations in tumor suppressor genes are recessive (both copies of the gene must be defective for the regulation of cell division to be defective), whereas mutations in oncogenes are dominant.
- 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.Describe the mutational event that produces the MYC oncogene in Burkitt’s lymphoma. Why does the particular mechanism for generating oncogenic MYC result in a lymphoma rather than another type of cancer? Describe another mechanism for generating oncogenic MYC.#9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #2) When cancer cells have not spread beyond its original site, the term used to describe it is benign growth intraepithelial neoplasia carcinoma stage 3 carcinoma in sit #10) Single or double stranded breaks in DNA activate Chk 1 and 2 kinases, which phosphorylates p53. This results in --- in the level of p53 in the cell. increase decrease please answer them all. they are very short and won't take your time. Thank you in advance.
- What is inflammation? Describe the main characteristics of inflammation. What characterizes chronic inflammatory disorders? What is the role of NFkB in inflammation and cancer? What are the mechanisms and strategies to inhibit excessive and chronic inflammation? answer should be one page longThe best strategy for treating a specific type of human tumor can depend on identifying the type of cell that became cancerous to give rise to the tumor. For some tumors that have colonized a distant location (metastasized), identifying the parental cell type can be difficult. Because the type of IF protein expressed is cell-type-specific, using monoclonal antibodies that react with only one type of IF protein can help in this identification. What IF proteins would you produce monoclonal antibodies against to identify (a) a sarcoma of muscle cell origin, (b) an epithelial cell carcinoma, and (c) an astrocytoma (glial cell tumor)?D) The level of carbon dioxide increases with the level of available oxygen. 60) The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will not…