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?

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?

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section: Chapter Questions

Problem 15QP: Which of the following mutations will result in cancer? a. homozygous recessive mutation in a...

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p53 iš an important tumor suppressor gene that is activated in response to a variety of stress signals. Upon activation it induces a cell cycle arrest or cell death. Hence, loss-of-function mutations in the p53 gene are found in almost every type of cancer. How do you predict loss-of-function mutations in the DNA binding domain of the p53 protein affect its function? OIt no longer will act as activator of gene expression O It no longer will act as repressor of gene expression O It no longer will act as activator or repressor of gene expression O It no longer will act as coactivator or corepressor
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
Describe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?
What would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?
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?
One major goal of modern cancer therapy is toidentify small molecules—anticancer drugs—that canbe used to inhibit the products of specific cancer-criticalgenes. If you were searching for such molecules, wouldyou design inhibitors for the products of oncogenes orthe products of tumor suppressor genes? Explain why youwould (or would not) select each type of gene.
Artificially induced apoptosis (controlled cellular death) is found to be an effective treat- ment for some forms of cancer. Which of the following describes the most likely mechanism by which apoptosis might be induced? A B с D by causing ribosomes to increase the rate of protein synthesis by triggering the division of mitochondria in the cell to increase ATP production by increasing the expression of membrane-bound glucose protein channels by causing lysosomes to release digestive enzymes into the cytosol
Discuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle. Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.
(46) A mutated form of protein p5x is found in patients with squamous cell carcinoma. In vitro studies show that the normal p5x molecule binds to DNA, and neoplastic cells accumulate in the G0 phase of the cell cycle. In contrast, the mutated form of p5x does not bin d to DNA. These finding are most characteristics of which of the following? (A) Growht factor receptors (B) GTP-binding protein (C) Nonreceptor tyrosine kinases (D) Oncogene proteins (E) Tumor suppressor gene proteins
How does the dysregulation of cell cycle checkpoints contribute to the development of cancer?
Relatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.
Which of these events do you think is likely to promote tumorigenesis in affected cells? Group of answer choices DNA methylation of the promoter region of a tumor suppressor gene Hypermethylation of transcription factors that antagonize Wntsignaling Open chromatin in the region of of DNA harboring an activating mutation of beta-catenin All of these