EBK HUMAN ANATOMY
9th Edition
ISBN: 9780135241752
Author: Marieb
Publisher: PEARSON CO
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Chapter 2, Problem 3CRCAQ
The normal function of one tumor-suppressor gene acting at the G1 checkpoint is to prevent cells with damaged chromosomes and DNA from "progressing from G1 to 3? Another tumor—suppressor gene, acting at the G2 {M checkpoint, prevents "passage from G; to M." When these tumor-suppressor genes fail to work, cancer can result. Explain what the phrases in quotations mean.
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Students have asked these similar questions
What is the most likely outcome is we lose the tumor suppressor proteins, cyclin-
dependent kinase inhibitors.
Select one:
o a. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will not proceed.
o b. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will not
proceed.
o c. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will
proceed.
o d. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will proceed.
Hi, can you explain this concept: cell cycle progression can be halted at several points by the tumor suppressor gene product p53, activated in response to checkpoints sensing DNA and possibly also chromosome damage; loss of p53 would remove this brake to cycling. How these events can lead to cancer progression?
Explain why mutations in tumor suppressor genes are recessive (both copies of the gene must be defective for the regulation of cell division to be defective), whereas mutations in oncogenes are dominant.
Chapter 2 Solutions
EBK HUMAN ANATOMY
Ch. 2 - What are the three general regions of a cell?Ch. 2 - What types of macromolecules compose the plasma...Ch. 2 - By what process does water enter and leave the...Ch. 2 - Which transport process carries large...Ch. 2 - Which cellular organelles are involved with...Ch. 2 - Which organelle produces the energy needed for...Ch. 2 - Which organelle would be prevalent in a cell that...Ch. 2 - Which cytoskeletal element functions to resist...Ch. 2 - What does the nucleolus produce?Ch. 2 - Which cytoplasmic organelle is continuous with the...
Ch. 2 - How does the appearance of extended chromatin...Ch. 2 - In which phase of the cell life cycle does the...Ch. 2 - Prob. 13CYUCh. 2 - Which cellular structures would be abundant in...Ch. 2 - Which organelles would be abundant in cells that...Ch. 2 - According to which aging theory presented here can...Ch. 2 - The endocytotic process in which particulate...Ch. 2 - The nuclear substance composed of histone proteins...Ch. 2 - Final preparations for cell division are made...Ch. 2 - Prob. 4RQCh. 2 - Identify the cell structure or organelle described...Ch. 2 - Prob. 6RQCh. 2 - The trans face of the Golgi apparatus (a) is its...Ch. 2 - Prob. 8RQCh. 2 - Name the appropriate stage of mitosis (prophase,...Ch. 2 - Name the cytoskeletal element (actin...Ch. 2 - Prob. 11RQCh. 2 - Which of these processes involves specific...Ch. 2 - List all the cytoplasmic organelles that are...Ch. 2 - Martin missed a point on his anatomy test because...Ch. 2 - In this chapter, we claimed that mitochondria are...Ch. 2 - Define chromosome, then compare the arrangement of...Ch. 2 - Prob. 17RQCh. 2 - Use the analogy of the cell as a manufacturing...Ch. 2 - Prob. 1CRCAQCh. 2 - Kareem had a nervous habit of chewing on the inner...Ch. 2 - The normal function of one tumor-suppressor gene...Ch. 2 - In their anatomy labs, many students are exposed...Ch. 2 - The sedative phenobarbital is a lipid-soluble...Ch. 2 - The drug vinblastine is used in cancer therapy to...Ch. 2 - Use the word roots listed at the start of Chapter...
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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
- 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.arrow_forwardWhat would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?arrow_forwardShown here are two HeLa cancer cells that are just completing cytokinesis. Explain how the cell division of cancer cellslike these is misregulated. Identify genetic and other changesthat might have caused these cells to escape normal cell cycleregulationarrow_forward
- The best strategy for treating a specific type of human tumor can depend on identifying the type of cell that became cancerous to give rise to the tumor. For some tumors that have colonized a distant location (metastasized), identifying the parental cell type can be difficult. Because the type of IF protein expressed is cell-type-specific, using monoclonal antibodies that react with only one type of IF protein can help in this identification. What IF proteins would you produce monoclonal antibodies against to identify (a) a sarcoma of muscle cell origin, (b) an epithelial cell carcinoma, and (c) an astrocytoma (glial cell tumor)?arrow_forwardDescribe 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?arrow_forwardIn order for certain cancers to propagate, they require a growth factor known as Vascular Endothelial Growth Factor (VEGF). What does VEGF signal the cell to do and how does this promote the propagation of cancer cells?arrow_forward
- 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.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_forwardOut of these 8 hallmarks ( sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, deregulating cellular energetics and metabolism, and avoiding immune destruction). Rank them from least important to most for cancer development. Explain in 2-3 sentences how.arrow_forward
- Why is the p53-meditated apoptosis pathway, and the GSK3 signaling pathway important for cancer therapy. Explain each of them in 3-5 sentences.arrow_forward"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_forwardProtein N, normally inactivates a tumor suppressor protein. Consider a cell with a mutation in one allele such that protein N is nonfunctional, while the other allele of gene N is wild-type. Which of the following is true for this cell? Gene N is a tumor suppressor gene, and the phenotype of the cell is not transformed. Gene N is a proto-oncogene, and the phenotype of the cell is transformed. Gene N is a tumor suppressor gene, and the phenotype of the cell is transformed. Gene N is a proto-oncogene, and the phenotype of the cell is not transformed.arrow_forward
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