Human Heredity: Principles and Issues (MindTap Course List)
11th Edition
ISBN: 9781305251052
Author: Michael Cummings
Publisher: Cengage Learning
expand_more
expand_more
format_list_bulleted
Concept explainers
Videos
Textbook Question
Chapter 12.10, Problem 2GR
Another model, the random model, proposes that any cell in a malignant tumor has the potential to form a new tumor. Does the cancer stem cell hypothesis contradict this idea?
Expert Solution & Answer
Trending nowThis is a popular solution!
Students have asked these similar questions
Can we cure cancer by restoring the function of tumor suppressor proteins such as mutant p53 or pRb? If so, how is this possible?
Tumor 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 mutation
Put a checkmark next to any of the following scenarios that would make it MORE likely that a cell would divide when it is not supposed to, increasing the chance that it would become cancerous. CHOOSE ALL THAT APPLY.
A) A tumor suppressor gene is over-expressed
B) A cyclin gene is mutated so that it is expressed at all times during the cell cycle
C) A cyclin-dependent kinase gene is mutated so that in the Cdk is no longer dependent on its cyclin
D) A Cdk gene is mutated so that the Cdk protein is not made
E) Mutation of an oncogene that causes it to no longer be expressed
F) A proto-oncogene gene is expressed at higher than normal levels
G) The p53 gene is mutated so that no p53 protein is made
Chapter 12 Solutions
Human Heredity: Principles and Issues (MindTap Course List)
Ch. 12.10 - If improved diagnostic tests are developed from...Ch. 12.10 - If you had cancer, would you donate tissue samples...Ch. 12.10 - Prob. 1GRCh. 12.10 - Another model, the random model, proposes that any...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Theodor Boveri predicted that malignancies would...Ch. 12 - Distinguish between a familial and a sporadic...Ch. 12 - Benign tumors: a. are noncancerous growths that do...
Ch. 12 - Prob. 4QPCh. 12 - Prob. 5QPCh. 12 - Prob. 6QPCh. 12 - Prob. 7QPCh. 12 - Prob. 8QPCh. 12 - What is the difference between a proto-oncogene...Ch. 12 - Distinguish between dominant inheritance and...Ch. 12 - Describe the likelihood of developing bilateral...Ch. 12 - Prob. 12QPCh. 12 - The search for the BRCA1 breast cancer gene...Ch. 12 - What are the roles of cellular proto-oncogenes,...Ch. 12 - Which of the following mutations will result in...Ch. 12 - Prob. 16QPCh. 12 - The following family has a history of inherited...Ch. 12 - You are in charge of a new gene therapy clinic....Ch. 12 - Prob. 19QPCh. 12 - Can you postulate a reason or reasons why children...Ch. 12 - Prob. 21QPCh. 12 - In Section 12-1, Julie is concerned that she may...Ch. 12 - Prob. 23QPCh. 12 - What are some factors that epidemiologists have...Ch. 12 - Smoking cigarettes has been shown to be associated...Ch. 12 - Prob. 26QPCh. 12 - Studies have shown that there are significant...
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- p53 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). Armed with your knowledge about the different mechanisms which govern transcription and translation, 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_forwardCan we treat cancer by restoring tumor suppressor function such as mutated p53 or pRb? If so, how can this be?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
- What are stem cells? Which stem cell treatment can form a benign tumor? Please explain how benign tumor can form from the stem cell therapy?arrow_forwardThe current way to gauge the effectiveness of chemotherapy is to track the size of the tumor. If the tumor shrinks, the chemotherapy is said to be "working." If cancer stem cells really do act the way we think they do, what will be the new way that the effectiveness of chemotherapy will be evaluated?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_forward
- What separates cancer cells from normal cells? Describe one form of mutation that can increase the risk of a normal cell being cancerous.arrow_forwardA research study indicated that an agent in cigarette smoke caused the silencing of a tumor suppressor gene called p53. However,upon sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.arrow_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_forward
- The protein p53 is activated when the cell's DNA is damaged. p53 helps to arrest the cell cycle in G1, allowing time for the cell to repair its DNA before replicating. p53 does this job by stimulating the synthesis of a protein that inhibits the cyclin-dependent kinase. Mutations that inactivate p53 contribute to 50% of human cancers. Would you classify p53 as a tumor-suppressor gene or a proto-oncogene?arrow_forwardHow can a mutation in a tumor-suppressor gene contribute to the development of cancer?arrow_forwardWhy is p53 considered a tumor suppressor protein? Question 12 options: a) Because p53 normally detects breaks in DNA. b) Because p53 normally causes progression from G1 to S phase to halt until damaged DNA is fully repaired. c) Because p53 normally repairs breaks in DNA. d) Because p53 normally stimulates transcription of Repair Polymerase. e) Because p53 normally reduces the mutation rate of DNA polymerase.arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
Human Heredity: Principles and Issues (MindTap Co...BiologyISBN:9781305251052Author:Michael CummingsPublisher:Cengage Learning
Human Heredity: Principles and Issues (MindTap Co...
Biology
ISBN:9781305251052
Author:Michael Cummings
Publisher:Cengage Learning
An Introduction to the Human Genome | HMX Genetics; Author: Harvard University;https://www.youtube.com/watch?v=jEJp7B6u_dY;License: Standard Youtube License