Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function. Hint: Loss of p53 function occurs in the majority of human tumors.
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Name two ways in which loss of p53 function contributes to a malignant
Hint: Loss of p53 function occurs in the majority of human tumors.
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- Loss of p53 function occurs in the majority of human tumors. Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function.Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed. Select the two mechanisms. Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms. 1) alterations in chromatin structure 2) a gain-of-function alteration 3)modification of proto-oncogenes products 4)mutations that result in an abnormal protein product 5)mutations within gene-regulatory regionsHereditary retinoblastoma generally affects children in both eyes, while spontaneous retinoblastoma usually occurs during adulthood only in one eye. Explain the genetic basis for the epidemiological distinction between these two forms of retinoblastoma. Explain the apparent paradox: loss-of-function mutations in tumor-suppressor genes act recessively, yet hereditary retinoblastoma is inherited as an autosomal dominant.
- Distinguish between What is known of CD105 (endoglin) as an hepatcellular carcinoma marker and it’s potential as a drug target. Discuss: - Is anything known about its biology? E.g does it have known ligands and normal functions? - if you were to target it would you just use it to get growth inhibiting compound into the new blood vessels or is CD105 required for neovascularization?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.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.
- Name the six fundamental properties of malignant tumours. Which of these properties are amenable to study in a cell culture model of cancer and why?Briefly describe the effects of colchicine treatment on cells. What are the genetic implications of such effects?D) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too 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. eg 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…
- 1) A) List 15 drugs (monoclonal antibodies can be used) used clinically to treat cancer in humans. These targets must be signal transduction pathway components. B) For each drug, list the specific protein targeted. C) For each drug, describe the efficacy of treatment (i.e. what is the success rate in life extension) as well as appropriate cost of treatment whether it be per round or an average annual cost.For the following diseases, describe the best technique for diagnosing them. Please make sure you include how you would tell someone with the disease from someone without the disease. B. Factor V Leiden thrombophilia is caused by a point mutation at position 1691 in exon 10 of the Factor V clotting factor gene that changes an arginine into a glutamine. This change removes one of the cleavage sites for activated protein C and leads to an increased tendency to clot.Neurofibromatosis type 1 (NF1) is an inherited is an inheritent dominant disorder. The phenotype usually involves the production of many skin neurofibromas. Answer the following questions about the disorder: a) Are the NF1 neurofibromatosis-causing mutations that are inherited by affected children from affected parents likely to be loss-of-function or gain-of-function mutations? b) Neurofibromin, the protein product of NF1, is associated with the Ras protein. Ras is involved in the transduction of extracellular signals from growth factors. The active form of Ras is complexed with GTP; the inactive form is complexed with GDP. Would the wild-type neurofibromin protein favor the formation of Ras-GTP or Ras-GDP? c) Which of the following events in a normal cell from an individual inheriting a neurofibromatosis-causing allele could cause the descendents of that cell to turn into a neurofibroma? i. A second point mutation in…