Biology 2e
2nd Edition
ISBN: 9781947172517
Author: Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher: OpenStax
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Chapter 16, Problem 40CTQ
How can understanding the gene expression pattern in a cancer cell tell you something about that specific form of cancer?
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What separates cancer cells from normal cells?
Describe one form of mutation that can increase the risk of a normal cell being cancerous.
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What is the difference in an oncogene and tumor suppressor gene and how can each potentially lead to cancer?
Chapter 16 Solutions
Biology 2e
Ch. 16 - Figure 16.5 In E. coli, the tip operon is on by...Ch. 16 - Figure 16.7 In females, one of the two X...Ch. 16 - Figure 16.13 An increase in phosphorylation levels...Ch. 16 - Control of gene expression in eukaryotic cells...Ch. 16 - Post-translational control refers to: regulation...Ch. 16 - How does the regulation of gene expression support...Ch. 16 - If glucose is absent, but so is lactose, the lac...Ch. 16 - Prokaryotic cells lack a nucleus. Therefore, the...Ch. 16 - The a/a operon is an inducible operon that...Ch. 16 - What are epigenetic modifications? the addition of...
Ch. 16 - Which of the following are true of epigenetic...Ch. 16 - The binding of _____ is required for transcription...Ch. 16 - What will result from the binding of a...Ch. 16 - A scientist compares the promoter regions of two...Ch. 16 - Which of the following are involved in post...Ch. 16 - Binding of an RNA binding protein will the...Ch. 16 - An unprocessed pre-mRNA has the following...Ch. 16 - IS. Alternative splicing has been estimated to...Ch. 16 - Post-translational modifications of proteins can...Ch. 16 - A scientist mutates elF-2 to eliminate its GTP...Ch. 16 - Cancer causing genes are called transformation...Ch. 16 - Targeted therapies are used in patients with a set...Ch. 16 - Name two differences between prokaryotic and...Ch. 16 - Describe how controlling gene expression will...Ch. 16 - Describe how transcription in prokaryotic cells...Ch. 16 - What is the difference between a repressible and...Ch. 16 - In cancer cells, alteration to epigenetic...Ch. 16 - A scientific study demonstrated that rat mothering...Ch. 16 - Some autoimmune diseases show a positive...Ch. 16 - A mutation within the promoter region can alter...Ch. 16 - What could happen if a cell had too much of an...Ch. 16 - A scientist identifies a potential transcription...Ch. 16 - Describe how RBPs can prevent miRNAs from...Ch. 16 - How can external stimuli alter...Ch. 16 - Protein modification can alter gene expression in...Ch. 16 - Alternative forms of a protein can be beneficial...Ch. 16 - Changes in epigenetic modifications alter the...Ch. 16 - A scientist discovers a virus encoding a Protein X...Ch. 16 - New drugs are being developed that decrease DNA...Ch. 16 - How can understanding the gene expression pattern...
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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
- What is the difference between a proto-oncogene and a tumor-suppressor gene?arrow_forwardCan we treat cancer by restoring tumor suppressor function such as mutated p53 or pRb? If so, how can this be?arrow_forwardCancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.arrow_forward
- Despite being small animals, naked mole rats are almost entirely resistant to cancer. Watch the following brief video on one potential mechanism for the prevention of cancer in naked mole rats. https://youtu.be/bhNBeuhxkF0?si=38aelHLW1N6vN8-b Based on what you know about mitosis and cancer cells, why would a mechanism that prevents cell crowding reduce the likelihood of cancer developing?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_forwardA microarray is a technique used to develop a profile of the messenger RNA being transcribed by cells at a particular point in the life cycle of the cell. This allows the researcher to detect the expression of particular genes at a particular time. Microarrays have proven very useful in the detection of genes involved in certain types of cancer. If the product of a particular gene functions as a tumor suppressor, which piece of evidence do you think would be the most useful in the diagnosis of a cancer due to a nonsense mutation in this tumor-suppressor gene? (Hint: Don't worry about what a microarray is. Think about what you know about mitosis, cancer, and types of mutation.) O The tissue sample responds to treatment with a mitosis-promoting compound. O The tissue sample shows a high level of gene expression relative to a control (noncancerous) sample. O The mRNAs for the targeted tumor suppressor sequence are not being produced. O The mRNAs for cyclins and kinases show unusually high…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_forwardp53 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 corepressorarrow_forwardHow can a mutation in a tumor-suppressor gene contribute to the development of cancer?arrow_forward
- Why 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_forwardHow can the role of epigenetics in cancer be reconciled with the idea that cancer is caused by the accumulation of genetic mutations in tumor-suppressor genes and proto-oncogenes?arrow_forwardExplain how p53 functions as a tumor suppressor gene. How can mutations in p53 lead to cancer, and how might gene therapy or other drug interventions inhibit the growth of a tumor?arrow_forward
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