Mutations in the RB gene are often associated with cancer. Explain how a mutation that results in a nonfunctional RB protein contributes to cancer.
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Q: Why is it important to model cancer through the generation of induced pluripotent stem cells ?…
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Q: Why is it important to model cancer through the generation of induced pluripotent stem cells ?…
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Q: explain how p53 functions in a cell that sustained DNA damage to prevent progression of that cell…
A: p53 induces numerous different target genes and blocks the different stages of progression of tumor…
Q: How might a mutation in the DNA result in the formation of cancer ?
A: The mutation is any change or alteration in the nucleotide sequence of the DNA. The mutation of a…
Q: Why are bone marrow stem cells ideally suited as targets for gene therapy?
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Q: Define tumor-suppressor genes. Why is a mutation in a single copy of a tumor-suppressor gene…
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Q: Which of the following is not a tumor suppressor gene? a.RET b.RB c.BRCA1 d.BRCA2
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Q: How can a mutation in a tumor-suppressor gene contribute to the development of cancer?
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Q: Explain about the Cancer-causing gene formed by a mutation in a proto-oncogene ?
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Q: Which best shows a harmful effect of a mutation?
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Q: Explain why p53 is mutated in the vast majority of human cancers.
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Q: Please distinguish driver and passenger mutations in cancer.
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Q: Give a possible explanation for why a mutation in a single gene does not always lead to cancer.
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Q: True or False: Cancers develop when many mutations develop rather than from a single mutation
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Q: compare and contrast cancer caused by viruses and cancer caused by oncogenes
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Q: Why are proto-oncogenes present in non-cancerous cells? A one sentence answer is fine.
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Q: how would the disruption of the Rb family of proteins lead to cancer? Describe the possible…
A: Please follow step 2 for detailed explanation.
Q: Explain why it usually takes more than one mutation to cause cancer
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Q: Explain the difference between a proto-oncogene and a tumor-suppressor gene.
A: Cancer is the state of uncontrolled cell division.
Mutations in the RB gene are often associated with cancer. Explain how
a mutation that results in a nonfunctional RB protein contributes to
cancer.
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- 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.Explain the role of p53 protein in protecting normal cells against cancer. With respect to this protein and its function, explain how a normal cell turns cancerous.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.
- Describe how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?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.(b): How many forms can naturally occurring DNA exist in? Explain how these forms are characterized. What properties of the functional groups determine the binding of DNA with anti-cancer agents? Explain.
- Explain why the continually active CDK will most likely change the normal cells into cancer cells.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…Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings. Please sort as a list.
- Fluorouracil is a structural analogue of thymine. The fluorine promotes enolization. How is this effect used in thetreatment of cancer?The p53 gene is a tumor-suppressor gene while Ras is a proto-oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.People who inherit two copies of the BRCA1 mutation are not born with cancer, and some of them never end up developing cancer. Give a possible explanation for why a mutation in a single gene does not always lead to cancer.