Genetics: Analysis and Principles
6th Edition
ISBN: 9781259616020
Author: Robert J. Brooker Professor Dr.
Publisher: McGraw-Hill Education
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Chapter 22, Problem 13EQ
Several research studies are under way that involve the use of gene therapies to inhibit the growth of cancer cells. As discussed in Chapter 25, oncogenes are mutant genes that are overexpressed and cause cancer. New gene therapies are aimed at silencing oncogenes by producing antisense RNA that recognizes the mRNA transcribed from oncogenes. Based on your understanding of antisense RNA (discussed in Chapter 14), explain how this strategy would prevent the growth of cancer cells.
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The rb gene encodes a protein that inhibits E2F, a transcriptionfactor that activates several genes involved in cell division.Mutations in rb are associated with certain forms of cancer,such as retinoblastoma. Under each of the following conditions,would you expect the cancer to occur?A. One copy of rb is defective; both copies of E2F are functional.B. Both copies of rb are defective; both copies of E2F arefunctional.C. Both copies of rb are defective; one copy of E2F is defective.D. Both copies of rb and E2F are defective.
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Which of the following defects in RAS would be tumorigenic? multiple answers
A.
Deletion of nucleotide binding domain
B.
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Chapter 22 Solutions
Genetics: Analysis and Principles
Ch. 22.1 - 1. Which of the following uses of microorganisms...Ch. 22.1 - Prob. 2COMQCh. 22.1 - Prob. 3COMQCh. 22.2 - When a cloned gene is inserted into a noncritical...Ch. 22.2 - Prob. 2COMQCh. 22.3 - Prob. 1COMQCh. 22.3 - Prob. 2COMQCh. 22.4 - Prob. 1COMQCh. 22.4 - Prob. 2COMQCh. 22.5 - A means of introducing a cloned gene into cells...
Ch. 22.5 - 2. Which of the following best describes the...Ch. 22 - 1. What is a recombinant microorganism? Discuss...Ch. 22 - Prob. 2CONQCh. 22 - 3. What is bioremediation? What is the difference...Ch. 22 - Prob. 4CONQCh. 22 - Prob. 5CONQCh. 22 - Prob. 6CONQCh. 22 - 7. What is a transgenic organism? Describe three...Ch. 22 - Prob. 8CONQCh. 22 - Explain the difference between gene modification...Ch. 22 - As described inChapter 5, not all inherited traits...Ch. 22 - Prob. 11CONQCh. 22 - 12. Discuss the concerns that some people have...Ch. 22 - Prob. 1EQCh. 22 - 2. Bacillus thuringiensis makes toxins that kill...Ch. 22 - Prob. 3EQCh. 22 - Prob. 4EQCh. 22 - Prob. 5EQCh. 22 - What is a gene knockout? Is an animal or plant...Ch. 22 - Prob. 7EQCh. 22 - Evidence [see P. G. Shiels, A. J. Kind, K. H....Ch. 22 - Prob. 9EQCh. 22 - 10. What is reproductive cloning? Are identical...Ch. 22 - Researchers have identified a gene in humans that...Ch. 22 - Treatment of adenosine deaminase (ADA) deficiency...Ch. 22 - Several research studies are under way that...Ch. 22 - Prob. 1QSDCCh. 22 - 2. A commercially available strain of P....Ch. 22 - Prob. 3QSDC
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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
- You are interested in studying a novel gene that appears to be involved in cancer. There is no information about the function of this gene. What would you do to obtain the cDNA for this gene? How would you express this gene and what expression systems might you utilize to study its function and why? How would determine the subcellular localization of this gene in eukaryotic cells? What are alternative methods in case one doesn't work? How would you purify and determine the 3-dimensional structure of this protein?arrow_forwardIt seems that the expert only addressed the background of prorooncogen and the impact of Ras causing various mutations and affecting several codons of the genes, but didn't address the problem "Why would a translocation that put Ras behind the promoter region of the actin gene lead to the formation of an oncogene?"arrow_forwardProto-oncogenes can be converted to oncogenes in a number of different ways. In some cases, the proto-oncogene itself becomes amplified up to hundreds of times in a cancer cell. An example is the cyclin D1 gene, which is amplified in some cancers. In other cases, the proto-oncogene may be mutated in a limited number of specific ways, leading to alterations in the gene product’s structure. The ras gene is an example of a proto-oncogene that becomes oncogenic after suffering point mutations in specific regions of the gene. Explain why these two proto-oncogenes (cyclin D1 and ras) undergo such different alterations in order to convert them into oncogenes.arrow_forward
- Studies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?arrow_forwardWhile investigating the function of a specific growth factor receptor gene from humans, researchers found that two types of proteins are synthesized from this gene. A larger protein containing a membrane spanning domain recognizes growth factors at the cell surface, stimulating a specific downstream signaling pathway. In contrast, a related, smaller protein is secreted from the cell and binds available growth factor circulating in the blood, thus inhibiting the downstream signaling pathway. Speculate on how the cell synthesizes these disparate proteins.arrow_forwardWhich of the following mutations would not convert a proto-oncogene into an oncogene? A translocation that places the gene at a new locus where gene expression is increased. A mutation in the coding region that makes the protein resisitant to degradation. Gene duplication. A mutation in the coding region that makes the protein hyperactive. A deletion of an enhancer that lies 3’ to the coding region.arrow_forward
- Let’s suppose you were interested in developing drugs to preventepigenetic changes that may contribute to cancer. What cellularproteins would be the target of your drugs? What possible sideeffects might your drugs cause?arrow_forwardIs the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?arrow_forwardTumor cells from a person with leukemia have been analyzed to determine which oncogene is involved in the transformation. After partial sequencing of the gene, the predicted gene product is identified as a tyrosine kinase. Which of the following proteins would most likely be encoded by an oncogene and exhibit tyrosine kinase activity? A. Nuclear transcriptional activator B. Epidermal growth factor C. Membrane-associated G protein D. Platelet-derived growth factor E. Growth factor receptorarrow_forward
- Why does a single mutation in a proto-oncogene, turning it into an oncogene potentially lead to a cancerous phenotype, while it takes two mutations in tumor suppressor genes to lead to a cancerous phenotype?arrow_forwardSCENARIO: You are studying a disease caused when the gene called BMP5 is not transcribed in osteoblasts. All other genes are transcribed normally. To investigate why BMP5 is not transcribed, you create a reporter transgene by putting GFP under the control of the BMP5 enhancer found in diseased osteoblasts. You put this reporter transgene into a normal, healthy osteoblast.-----------------Short Answer Question 4: In the question above, does it matter if the BMP5 enhancer-GFP reporter gene is tested in a normal, healthy osteoblast or in a diseased osteoblast? Why or why not?arrow_forwardRetinoblastoma is an extremely rare cancer of the retina in the eye. The disease mainly affects children up to the age of 5 years because it can only occur while the nerve precursor cells are still dividing. In its nonhereditary form, a tumor usually occurs in only one eye; in its hereditary form, multiple tumors develop in both eyes.To explore the basis for these differences, a cDNA clone of the Rb gene was used to probe the structure of the gene in cells from normal individuals and from individuals with nonhereditary or hereditary retinoblastoma. As shown in the figure Part A, normal individuals have four restriction fragments (A, B, C, and D) that hybridize to the Rb cDNA probe, indicating that each restriction fragment encodes at least one Rb exon. Samples from fibroblasts and tumor cells of affected persons show some differences in the patterns of hybridization, with some bands missing entirely and some bands present at half intensity. The order of the restriction fragments in the…arrow_forward
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