2. The TP53 gene normally functions as a tumor suppressor by preventing abnormal cell growth but is commonly found mutated in cancer cells, resulting in uncontrolled cell growth. You plan to use genetic tools to remove mutated TP53 from plasma cells. Answer the following questions. B) Is ex vivo or in vivo gene therapy/editing most appropriate? Explain why.

2. The TP53 gene normally functions as a tumor suppressor by preventing abnormal cell growth but is commonly found mutated in cancer cells, resulting in uncontrolled cell growth. You plan to use genetic tools to remove mutated TP53 from plasma cells. Answer the following questions. B) Is ex vivo or in vivo gene therapy/editing most appropriate? Explain why.

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section: Chapter Questions

Problem 15QP: Which of the following mutations will result in cancer? a. homozygous recessive mutation in a...

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2. The TP53 gene normally functions as a tumor suppressor by preventing abnormal cell growth but is commonly found mutated in cancer cells, resulting in uncontrolled cell growth. You plan to use genetic tools to remove mutated TP53 from plasma cells. Answer the following questions. A) Which genetic tool is most appropriate for this application, gene therapy or gene editing? Explain why.
1). Tumor suppressor proteins monitor DNA and detect damage. Some cancers evade this detection by removing tumor suppressor proteins from the nucleus. An overproduction of what transport molecule could cause this? What is one example of how this overproduction might be targeted for cancer treatment (suggest a hypothetical treatment that would prevent the cancer)? 2) :) Based on the course content thus far, would mRNA vaccines pose a risk to the genomic DNA in a cell? Explain.
7) The protein VEGF plays an important role in stimulating the formation of new blood vessels. In some circumstances, cancer cells will produce too much VEGF. The drug PTC299 is currently being researched as a potential anti-cancer drug. It works by binding to VEGF mRNA, stopping this mRNA from being read by the ribosome. Therefore, not as much VEGF protein is produced. (National Cancer Institute. nd. NCI Drug Dictionary. Retrieved from: https://www.cancer.gov/publications/dictionaries/cancer-drug/def/vegf-inhibitor-ptc299) a) If approved, what kind of cancer treatment would it be considered (radiotherapy, gene therapy. anti-angiogenesis)? b) Briefly explain why you think PTC299 fits the kind of cancer treatment you indicated in a). Use information from the text to support your answer. c) Would PTC299 be considered a traditional or a targeted therapy?
1. True or Flase: Cells must only divide when they receive a signal to divide. 2. BRCA1 is a gene that codes for a tumor suppressor protein. If a person inherits a mutation in BRCA1, it greatly increases his or her risk of developing breast cancer. Are the cancer-causing mutations in the BRCA1 gene more likely to: a) increase expression of the gene b)decrease expression of the gene c)not affect the expression of the gene
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)?
1. Explain BRIEFLY whether each of the following conditions will increase or decrease the chance of cancer: a. a mutation in the promoter region of a tumor suppressor gene that results in that gene being overexpressed (assume that the cell is heterozygous for the mutation) b. a mutation in the promoter region of a protooncogene that results in that gene being overexpressed (assume that the cell is heterozygous for the mutation) c. a homozygous mutation that completely eliminates the coding region of a protooncogene d. a homozygous mutation that completely eliminates the coding region of a tumor suppressor gene e. a heterozygote where one allele is the mutant allele described in (c), the other allele being wild type f. a heterozygote where one allele is the mutant allele described in (d), the other allele being wild type
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.
Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings.
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.
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…
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…
3) The tumor suppressor protein Rb regulation of the entry into the S phase of the cell cycle is represented in this diagram. DNA Answer: b) Explain your choice above: Answer: Rb E2F Genes needed for S phase are NOT transcribed Growth factor Ras pathway Cdk-cyclin 30 ATP ADP Phosphorylated Rb protein P Rb E2F Gene transcription a) In hereditary retinoblastoma tumors, Rb is mutated. Among the following mutations, which one is not likely to be found in these tumors. 1) Mutation prevents Rb to bind E2F by modifying the binding site. 2) Mutation prevents Rb to be dephosphorylated and recycled (possibly by prevented phosphorylated Rb to be recognized by the phosphatase that removes its phosphates). 3) Mutation may cause Rb to be misfolded and not have a functional conformation 4) Mutation that prevent Rb to be phosphorylated by cdk-cyclin. 5) Mutation may cause Rb to be unstable and degraded rapidly. c) (4 pts) Human papilloma virus (HPV) infections are the main causes of cervical cancers.…