Biochemistry: The Molecular Basis of Life
6th Edition
ISBN: 9780190209896
Author: Trudy McKee, James R. McKee
Publisher: Oxford University Press
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Chapter 16, Problem 5Q
Summary Introduction
To review:
The possible consequences of phorbol esters in an initiated cell and the enzymes activated by phorbol esters and DAG.
Introduction:
Cancer is a multistage process and it initiates with initiating events usually viral infection or exposure to a carcinogen. These initial events are then followed by contact with tumor promoters. Tumor promoters are chemical molecules that activate cell proliferation; however, they do not have the ability to initiate the formation of a tumor on their own.
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Cellular 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 gene
The deregulation of several signal transduction pathways is integral to the onset of
cancer. These pathways involve both tumor promoters (the "gas pedals") and tumor
suppressors (the "brake pedals").
Which would be a more effective treatment for cancer: A small molecule inhibitor
that targets a tumor suppressor or one that targets a tumor promoter? Briefly
explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND
MINIMALLY IN ABOUT EIGHT WORDS.)
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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.
Chapter 16 Solutions
Biochemistry: The Molecular Basis of Life
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Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biochemistry and related others by exploring similar questions and additional content below.Similar questions
- "In the cellular regulatory pathways that control cell growth and proliferation, the products of oncogenes are stimulatory components and the products of tumor suppressor genes are inhibitory components" is true or false.arrow_forwardCancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.arrow_forwardThe Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!arrow_forward
- during tumor progression, additional mutations occur within multiple cells of a tumor population, leading to multiple different clones of cells within that tumor. Some) but not all) clones may eventually metastasize, depending on the number and type of mutations that occur in those clones. true falsearrow_forwardTumor-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_forwardThe p53 gene is a tumor-suppressor gene while p634 gene is an 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.arrow_forward
- Metastasis occurs when cells from a primary tumor invade and colonize other tissues. Metastasis is a complex, multistep process. Tumor cells must lose adhesion with other tumor cells, invade local tissues and vessels, move through the circulation, leave the vessels, and finally, establish new colonies at distant sites. Tumor cells gain the ability to cross epithelial layers and migrate through tissues by mutations, although the nature of the mutations that drive metastasis is poorly understood. Mutations that block expression of the E-cadherin gene are thought to be an important step in metastasis. The absence of E-cadherin expression could affect metastasis by blocking cell adhesion directly, by releasing signaling proteins bound to the cytoplasmic domain of E-cadherin, or by both mechanisms. To better understand how loss of E-cadherin contributes to metastasis, scientists created two cell lines that differed in their expression of E-cadherin. One cell line was blocked for expression…arrow_forwardTumor suppressor proteins can assist in slowing down the cell cycle under appropriate conditions. In humans, the TP53 gene encodes a tumor suppressor called p53. Most mutations in the TP53 gene result in a mutant form of p53 that can no longer function to slow down the cell cycle, which can lead to a cell becoming cancerous. However, some mutant forms of p53 actually possess the ability to increase a cell's resistance to anticancer treatments. Which of the following BEST describes the latter type of mutation? loss-of-function mutation gain-of-function mutation suppressor mutation reverse mutationarrow_forwardCancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.arrow_forward
- Of the following choices a loss of function mutation would most lukely contribute to cancer onset if the mutant gene codes for a : telomerase tumor suppressor protein ATP synthesis enzyme RNS binding proteinarrow_forwardWhy 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.arrow_forwardWhy 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.arrow_forward
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