a. What are the three categories of genes mutated in cancer cells? What is the effect of mutation of each? b. What is the function of checkpoint controls in the cell cycle? What is checked at G1, S, G2 and M phase before the cell can progress to the next phase
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1. a. What are the three categories of genes mutated in cancer cells? What is the effect of mutation of each?
b. What is the function of checkpoint controls in the cell cycle? What is checked at G1, S, G2 and M phase before the cell can progress to the next phase?
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Solved in 4 steps
- 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 type3) 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.…Prophase Metaphase Anaphase Telophase
- 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 gene3) Draw a diagram of the cell cycle (G1, S..) and indicate places where errors in cell division might lead to cancer.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.
- 4) Describe in detail how p53 and MDM2 regulate cell division in a normal, healthy cell. You should describe 1) how these proteins cooperate to allow a cell to go through the cell cycle, 2) how they cooperate to stop the cell cycle, and 3) how they allow the cell cycle to continue again after having stopped it initially. You may use point form if you want.Which of the following statements about cell cycle regulators is incorrect? a. The concentrations of cyclins change throughout the cell cycle. b. Cyclins are present in all stages of the cell cycle except S. c. Cyclin-Cdk complexes phosphorylate target proteins. d. Cdks combine with cyclin to move the cycle into mitosis. e. During anaphase of mitosis, cyclin is degraded, allowing mitosis to end.#9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #2) When cancer cells have not spread beyond its original site, the term used to describe it is benign growth intraepithelial neoplasia carcinoma stage 3 carcinoma in sit #10) Single or double stranded breaks in DNA activate Chk 1 and 2 kinases, which phosphorylates p53. This results in --- in the level of p53 in the cell. increase decrease please answer them all. they are very short and won't take your time. Thank you in advance.
- 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.Part A and B A. What below would be likely to lead to cancer development? A) Overexpression of a cell cycle checkpoint inhibitor B) Loss of expression of a growth factor that promotes cell cycle entry C) Overexpression of a receptor tyrosine kinase that promotes cell cycle entry D) Overexpression of a DNA damage repair enzyme E) Loss of expression of a regulatory transcription factor that activates transcription of a cyclin B. Taxols inhibit the proper function of microtubules and are frequently used as chemotherapy drugs. What is the function of microtubules during the cell cycle? A) They promote the G1 to S checkpoint B) They normally inhibit M phase from being completed C) They form the mitotic spindle E) They mediate DNA replication F) They form the cleavage furrow during cytokinesis1. (a) Describe the generalized model of the cell cycle. Demonstrate how cyclins and cyclin-dependent kinases can regulate the cell cycle. (b). Describe three ways in which cells lose their ability to regulate their growth to become cancerous.