Anatomy & Physiology
1st Edition
ISBN: 9781938168130
Author: Kelly A. Young, James A. Wise, Peter DeSaix, Dean H. Kruse, Brandon Poe, Eddie Johnson, Jody E. Johnson, Oksana Korol, J. Gordon Betts, Mark Womble
Publisher: OpenStax College
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Textbook Question
Chapter 3, Problem 26RQ
What is a primary function of tumor suppressor genes?
- stop all cells from dividing
- stop certain cells from dividing
- help oncogenes produce oncoproteins
- allow the cell to skip certain phases of the cell cycle
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Chapter 3 Solutions
Anatomy & Physiology
Ch. 3 - Visit this link...Ch. 3 - Watch this video...Ch. 3 - Watch this video...Ch. 3 - Watch this video...Ch. 3 - Visit this link...Ch. 3 - Because they are embedded within the membrane, ion...Ch. 3 - The diffusion of substances within a solution...Ch. 3 - Ion pumps and phagocytosis are both examples of...Ch. 3 - Choose the answer that best completes the...Ch. 3 - Choose the term that best completes the following...
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- Benign tumors: a. are noncancerous growths that do not spread to other tissues b. do not contain mutations c. are malignant and clonal in origin d. metastasize to other tissues e. none of thesearrow_forwardWhich of the following mutations will result in cancer? a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressedarrow_forwardWhat is the difference between a proto-oncogene and a tumor-suppressor gene?arrow_forward
- p53 gene, as is the Rb gene, is a tumor suppressor gene. p53 protein binds to DNA leading to the simulation of p21 that work together with cdk2. When p21 is defective and cannot joined to cdk2 the cell cannot pass through to the next stage of cell division. Mutated p53 cannot bind to DNA in an effective way, and therefore the p21 protein is not available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors. Hi, can you please elaborate on this: based on the info above, what is the relationship between genetics and environment in the development of these type of cancer. Which factor (genetics or environment) is playing a larger role in the generation of these types of cancers?arrow_forwardIn your own words, explain how cancer cells differ from normal cells in regard to the following: Molecular controls of the cell cycle (include Cdk and Cdk/cyclin complexes, p53 gene/protein, Rb gene/protein in response)arrow_forward#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.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_forwardWhich of the following statements correctly describes a characteristic of tumor-suppressor gene? a) they are frequently overexpressed in cancerous cells. b) they are cancer-causing genes introduced into cells by viruses. c) they encode proteins that help prevent uncontrolled cell growth. d) they often encode proteins that stimulate the cell cycle.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_forward
- A cell begins to undergo apoptosis due to stress. Which of the following are true about this cell? (select all that apply) The cell can exit apoptosis if the stressful factor is removed The cell has high levels of p53. The cell's DNA will inevitably degrade The cell may undergo mitosis before completing apoptosisarrow_forwardPut 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 madearrow_forwardHow does p53 halt cell cycle progression when DNA damage is identified? p53 enhances expression of cyclins p53 stimulates the ubiquitination of cyclins p53 inhibits Wee1 p53 activates Cdc25 p53 enhances expression of the p21 inhibitorarrow_forward
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