Can restoring tumor suppressor function, such as mutant p53 or pRb, be used to cure cancer? If that's the case, how is it possible?
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Q: Can we cure cancer by restoring the function of tumor suppressor proteins such as mutant p53 or pRb?…
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Q: What separates cancer cells from normal cells?
A:
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Q: How tumor-suppressor mutations contribute to cancer?
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Q: how can mutations in several genes drive cancer?
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Can restoring tumor suppressor function, such as mutant p53 or pRb, be used to cure cancer? If that's the case, how is it possible?
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- What is the difference between a proto-oncogene and a tumor-suppressor gene?Another model, the random model, proposes that any cell in a malignant tumor has the potential to form a new tumor. Does the cancer stem cell hypothesis contradict this idea?Can we treat cancer by restoring tumor suppressor function such as mutated p53 or pRb? If so, how can this be?
- Can we cure cancer by restoring the function of tumor suppressor proteins such as mutant p53 or pRb? If so, how is this possible?Why is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.What are Ras protein and p53? How can mutations in the genes for these proteins contribute to cancer?
- What would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?How can a defect in p53 gene contribute to cancer development?Why is p53 considered a tumor suppressor protein? Question 12 options: a) Because p53 normally detects breaks in DNA. b) Because p53 normally causes progression from G1 to S phase to halt until damaged DNA is fully repaired. c) Because p53 normally repairs breaks in DNA. d) Because p53 normally stimulates transcription of Repair Polymerase. e) Because p53 normally reduces the mutation rate of DNA polymerase.
- What separates cancer cells from normal cells? Describe one form of mutation that can increase the risk of a normal cell being cancerous.What is the difference in an oncogene and tumor suppressor gene and how can each potentially lead to cancer?How can the role of epigenetics in cancer be reconciled with the idea that cancer is caused by the accumulation of genetic mutations in tumor-suppressor genes and proto-oncogenes?