Human Heredity: Principles and Issues (MindTap Course List)
11th Edition
ISBN: 9781305251052
Author: Michael Cummings
Publisher: Cengage Learning
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Textbook Question
Chapter 12, Problem 15QP
Which 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 overexpressed
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The p53 gene was discovered in 1979, but it was not clear whether the gene functioned as an oncogene or a tumor-suppressor gene. Several years later, researchers showed that both p53 alleles are inactivated in some mouse cancers. This evidence suggests
A. the p53 gene is an oncogene because inactivated alleles would produce mutated signal transduction proteins that would result in stimulating cell division.
B. the p53 gene is an oncogene because the cell would overproduce transcription factors to compensate for the inactive alleles, resulting in increased cell division.
C. the p53 gene is a tumor-suppressor gene because inactivated alleles indicate a loss of protein function which allowed the cancer to develop
D. the p53 gene is a tumor-suppressor gene because the cell would produce too few transcription factors for gene activation, resulting in decreased cell division.
Which of the following steps are correct about multistep tumorigenesis (select all that apply)?
A.
Mutations in progenitor cells are more likely to develop a neoplastic state compared to mutations in stem cells
B.
Driver mutations give a cell clone a proliferative advanage
C.
The rate of mutation /genetic change is constant during tumor progression
D.
Nutrition/diet may effect rate of tumorigenesis
E.
All cells within a tumor are biologically equivalent and equally capable of high levels proliferation
In what category of cancer-related genes is it possible to find inherited variants that are associated with cancer? Why?
Group of answer choices
1. Tumor suppressor genes, because genes in this category are very important in the process of developing cancer.
2. Proto-oncogenes, because individuals who carry only one cancer-causing allele will have a wildtype phenotype.
3. Proto-oncogenes, because there are very few genes in this category, so mutations in them are rare.
4. Tumor suppressor genes, because individuals who carry only one cancer-causing allele will have a wildtype phenotype.
Chapter 12 Solutions
Human Heredity: Principles and Issues (MindTap Course List)
Ch. 12.10 - If improved diagnostic tests are developed from...Ch. 12.10 - If you had cancer, would you donate tissue samples...Ch. 12.10 - Prob. 1GRCh. 12.10 - Another model, the random model, proposes that any...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Mike was referred for genetic counseling because...Ch. 12 - Theodor Boveri predicted that malignancies would...Ch. 12 - Distinguish between a familial and a sporadic...Ch. 12 - Benign tumors: a. are noncancerous growths that do...
Ch. 12 - Prob. 4QPCh. 12 - Prob. 5QPCh. 12 - Prob. 6QPCh. 12 - Prob. 7QPCh. 12 - Prob. 8QPCh. 12 - What is the difference between a proto-oncogene...Ch. 12 - Distinguish between dominant inheritance and...Ch. 12 - Describe the likelihood of developing bilateral...Ch. 12 - Prob. 12QPCh. 12 - The search for the BRCA1 breast cancer gene...Ch. 12 - What are the roles of cellular proto-oncogenes,...Ch. 12 - Which of the following mutations will result in...Ch. 12 - Prob. 16QPCh. 12 - The following family has a history of inherited...Ch. 12 - You are in charge of a new gene therapy clinic....Ch. 12 - Prob. 19QPCh. 12 - Can you postulate a reason or reasons why children...Ch. 12 - Prob. 21QPCh. 12 - In Section 12-1, Julie is concerned that she may...Ch. 12 - Prob. 23QPCh. 12 - What are some factors that epidemiologists have...Ch. 12 - Smoking cigarettes has been shown to be associated...Ch. 12 - Prob. 26QPCh. 12 - Studies have shown that there are significant...
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- Researchers have identified some tumors that have no recurrent mutations or deletions in known oncogenes or tumor-suppressor genes and no detectable epigenetic alterations. However, these tumors often have large chromosomal deletions. What are some possible explanations that could account for the genetic causes behind these tumors?arrow_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will not…arrow_forwardDistinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.arrow_forward
- Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, Bcl-2, telomerase, jun, andarrow_forwardThe p53 gene is a tumor-suppressor gene while Ras is a proto-oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.arrow_forwardTumor suppressor genes and oncogenes are implicated in carcinogenesis. However, one can predict whether a gene potentially encodes for a protein that influences carcinogenesis by examining their mutational profile. You sequence the genome of 4 cancers and identify 3 genes of interest. Which of the following genes has the best potential to an oncogene? Tumor 1 Tumor 2 Tumor 3 Tumor 4 Gene A S24F, N465T R33T T345S, G366R P367E, P368Y Gene B S34R, F360I S34R V254I S34E, T67Y Gene C S24F, I322E C255I, E344D S34E, P367Earrow_forward
- Cellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase protein, called Mdm2. Over expression of Mdm2 destabilizes p53. Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53. Loss of p19ARF function converts normal cells into cancer cells With the above information, which of the following statements are true? Mdm2 is a tumor suppressor gene but p19ARF is an oncogene Both Mdm2 & P19ARF are oncogenes Both Mdm2 & P19ARF are tumor suppressor genes O Mdm2 is an oncogene but p19ARF is a tumor suppressor genearrow_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_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. eg Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will…arrow_forward
- A. Which genes could be used to monitor the process of the disease? B.  If you worked for a drug company developing a treatment for the cancer, which genes would you target to turn on in cancer cells? C. Which genes would you target to turn off in cancer cells?arrow_forwardDescribe error prone polymerases and the process of translesion synthesis (TLS). In regards to tumor biology, what is the mutator phenotype hypothesis? What are some ways in which error-prone polymerases could be targeted for potential anti-cancer treatments?arrow_forwardWhich of the following statements are true about the rate of mutation in tumor cells (select all that apply)? A. Mutation rate of tumor cells is reduced compared to normal cells of the same tissue type B. Mutation rate of tumor cells is unchanged compared to normal cells of the same tissue type C. Mutation rate in tumor cells is higher compared to normal cells of the same tissue type D. Affected by genome instability within the tumor cellsarrow_forward
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