Virtually all cancer treatments are designed to killcancer cells, usually by inducing apoptosis. However, oneparticular cancer—acute promyelocytic leukemia (APL)—has been successfully treated with all-trans-retinoic acid, which causes the promyelocytes to differentiate into neu-trophils. How might a change in the state of differentiation of APL cancer cells help the patient?
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Virtually all cancer treatments are designed to kill
cancer cells, usually by inducing apoptosis. However, one
particular cancer—acute promyelocytic leukemia (APL)—
has been successfully treated with all-trans-retinoic acid, which causes the promyelocytes to differentiate into neu-
trophils. How might a change in the state of differentiation of APL cancer cells help the patient?
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- Fluorouracil is a structural analogue of thymine. The fluorine promotes enolization. How is this effect used in thetreatment of cancer?If somatic tumors cause local regions in their vicinity to have an increased pOH, how is this strategic for the survival of the tumor? Select one: a. It allows the increased hydroxide concentrations to cause a conformational change in nearby hemoglobin to the R state so that ample oxygen is deposited for tumor growth. b. It allows the increased proton concentrations to cause a conformational change in nearby hemoglobin to the R state so that ample oxygen is deposited for tumor growth. c. It allows the increased proton concentrations to cause a conformational change in nearby hemoglobin to the T state so that ample oxygen is deposited for tumor growth. d. It allows the increased hydroxide concentrations to cause a conformational change in nearby hemoglobin to the T state so that ample oxygen is deposited for tumor growth. e. None of these.The 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)?
- Which component of cell division machinery is frequently targeted by anti-cancer drugs? Can you explain the common side-effects of chemotherapy (e.g. hair loss, mucositis) based on this information?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.Two mechanisms inducing Apoptosis, Extrinsic pathway and Intrinsic pathway, have difference and similarity. a What is the key protein that both pathway uses? b How can intrinsic pathway be initiated and what molecule is critical for that?
- What would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?5) 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…Relatively 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.
- 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.Overexpression of the Myc protein is a common feature of many types of cancer cells, contributing to their excessive cell growth and proliferation. By contrast, when Myc is overexpressed in most normal cells, the result is not excessive proliferation, but cell-cycle arrest or apoptosis.Which one of the following statements provides the most likely explanation for why overexpression of Myc can have such different outcomes in normal cells and in cancer cells? A. Normal cells contain checks and balances that prevent Myc-induced proliferation. B. In normal cells, Myc protein acts as a mediator in cell-cycle arrest and apoptosis. C. The target protein for Myc-induced proliferation is missing from most normal cells. D. In normal cells, when Myc is overexpressed, the excess Myc protein precipitates.Atherosclerosis can obstruct or block flow in arteries, including those that provide oxygenated blood to the heart. Elevated levels of [ Select ] ["LDL, and VLDL", "HDL"] are associated with atherosclerosis, most likely because of their role in delivery of lipids to peripheral tissues and cells. Smooth muscle cells are recruited to the site of damage, where they [ Select ] ["induce apoptosis of endothelial cells", "proliferate"] , hence expanding the extent of the lesion.