Life: The Science of Biology
11th Edition
ISBN: 9781319010164
Author: David E. Sadava, David M. Hillis, H. Craig Heller, Sally D. Hacker
Publisher: W. H. Freeman
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Chapter 13.4, Problem 2R
Summary Introduction
To review: The consequences of mismatch mutation in the formation of cancer.
Introduction:
There are many oncogenes and tumor suppressor genes that are involved in the formation of a single tumor. Two vital oncogenes that were identified were Myc and Ras and their expression regulates the cell cycle and avoids apoptosis process. Experiments reveal that it takes the expression of both the oncogenes to set the motion of the cell cycle in the cells of the mouse and then converts them into the tumor cells. The experiment is explained below:
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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.
Acquired mutation in the p53 gene is
the most
common genetic alteration found in
human
cancer (> 50% of all cancers). A
germline
mutation in p53 is the causative lesion
of Li-
Fraumeni familial cancer syndrome. In
many
tumors, one p53 allele on chromosome
17p is
deleted and the other is mutated. What
type of
protein is encoded by the p53 gene?
(A) Caspase
(B) DNA repair enzyme
(C) Membrane cell adhesion molecule
(D) Serine phosphatase
(E) Telomerase
(F) Transcription factor
(G) Tyrosine kinase
The p53 pathway is important for regulating the cell cycle. In a normal cell, there is a protein called mdm2 that can bind to p53 and deactivate it. A diseased individual has amutation in the gene that codes for mdm2, resulting in an mdm2 protein that is less able to bind to p53. Will this mutation increase, decrease, or cause no change in the rate of cell death? Explain.
Chapter 13 Solutions
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- 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.arrow_forwardA cell inherits a mutation in a gene that results in a transcription factor, called NF-kB, constantly being in its active conformation. When active, NF-kB stimulates the expression of cyclins that promote progression of the cell cycle, regardless of other conditions. As a result of this mutation, how would this cell's phenotype be affected by this mutation? A) This cell would have a cancer phenotype B) This cell would grow larger in size, but would never divide C) This cell would likely undergo apoptosis D) This cell would not duplicate its chromosomes .arrow_forwardCellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase protein, called Mdm2. Over expression of Mdm2 destabilizes p53. Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53. Loss of p19ARF function converts normal cells into cancer cells With the above information, which of the following statements are true? Mdm2 is a tumor suppressor gene but p19ARF is an oncogene Both Mdm2 & P19ARF are oncogenes Both Mdm2 & P19ARF are tumor suppressor genes O Mdm2 is an oncogene but p19ARF is a tumor suppressor genearrow_forward
- Tumor-suppressor genes are normal human genes that prevent uncontrollable cell growth. Starting with a normal laboratory humancell line, describe how you could use transposon tagging to identifytumor-suppressor genes. (Note: When a TE hops into a tumorsuppressorgene, it may cause uncontrolled cell growth. This is detected as a large clump of cells among a normal monolayer of cells.)arrow_forwardD) 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…arrow_forwardYou are working in a cell biology lab that investigates non-small cell lung cancer cells, which of these cellular features will be suggestive of senescence in the cells observed? Choose all that apply: Group of answer choices Large flattened morphology Reduced incorporation of 5-bromodeoxyuridine (in DNA replication) Increased p53 expression Decreased expression of p15INK4Barrow_forward
- Describe how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?arrow_forwardp53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?arrow_forward3) 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.…arrow_forward
- 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…arrow_forwardDescribe error prone polymerases and the process of translesion synthesis (TLS). In regards to tumor biology, what is the mutator phenotype hypothesis? What are some ways in which error-prone polymerases could be targeted for potential anti-cancer treatments?arrow_forwardDescribe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?arrow_forward
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