Biology (MindTap Course List)
11th Edition
ISBN: 9781337392938
Author: Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg
Publisher: Cengage Learning
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Chapter 17, Problem 8TYU
Which of the following statements about cancer is false? (a) oncogenes arise from mutations in proto-oncogenes (b) tumor suppressor genes normally interact with growth-inhibiting factors to block cell division (c) more than 120 cancer-driving genes have been discovered (d) oncogenes were first discovered in mouse models for cancer (e) the development of cancer is usually a multistep process involving both oncogenes and mutated tumor suppressor genes
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Which of the following effectively describes the situation of someone with an inherited predisposition to cancer such as familial adenomatous polyposis or BRCA-associated familial breast cancer?
Choose all that apply
a) If they get malignant cancer, somatic mutations will not have been a factor
b) Their cancer will most likely arise in their germ cells, not their somatic cells
c) None of the answers effectively describes the situation
d) Every cell of their body contains a gain-of-function allele of an oncogene
e) Most cells in their body contain multiple cancer-causing mutations
f) Every cell of their body contains a defective, loss-of-function allele of a tumor suppressor gene
1
Which of the following is true of tumor suppressor genes?
Group of answer choices
a) If this gene is overactive, it becomes an oncogene
b) If one of the alleles is mutated, there is usually little effect. Two inactivating mutations are usually required for loss of function (recessive mutation).
c) If one copy is lost, the gene no longer functions (dominant mutation)
d) Tumor suppressors genes usually cause mitosis or cell growth
e) Tumor suppressor genes decrease apoptosis
Chapter 17 Solutions
Biology (MindTap Course List)
Ch. 17.1 - Prob. 1LOCh. 17.1 - Describe the classic experiments of Steward,...Ch. 17.1 - Define stem cells, distinguish between embryonic...Ch. 17.1 - What lines of evidence support the principle of...Ch. 17.1 - Prob. 2CCh. 17.1 - What does the ability to produce iPSCs tell...Ch. 17.2 - Prob. 4LOCh. 17.2 - Prob. 5LOCh. 17.2 - Prob. 6LOCh. 17.2 - Prob. 7LO
Ch. 17.2 - Prob. 1CCh. 17.2 - Prob. 2CCh. 17.2 - Prob. 3CCh. 17.2 - Prob. 4CCh. 17.3 - Prob. 8LOCh. 17.3 - Prob. 1CCh. 17.3 - Prob. 2CCh. 17 - Prob. 1TYUCh. 17 - Prob. 2TYUCh. 17 - The anteriorposterior axis of a Drosophila embryo...Ch. 17 - Prob. 4TYUCh. 17 - Homeobox genes (a) are found in fruit flies but no...Ch. 17 - Prob. 6TYUCh. 17 - Prob. 7TYUCh. 17 - Which of the following statements about cancer is...Ch. 17 - Proto-oncogenes code for (a) morphogens (b)...Ch. 17 - Prob. 10TYUCh. 17 - Prob. 11TYUCh. 17 - Prob. 12TYUCh. 17 - CONNECT Why is an understanding of gene regulation...Ch. 17 - What is the reason that scientists study...Ch. 17 - Prob. 15TYUCh. 17 - Prob. 16TYUCh. 17 - EVOLUTION LINK What is the common ground between...Ch. 17 - INTERPRET DATA Flower parts are arranged in four...
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- D) 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_forwardAlthough cancer is not a contagious disease in humans or other vertebrates, there have been rare cases in which cancers have spread from one organism to another. Describe three cases of these contagious cancers and what conditions might have led to their appearance. For an introduction to this topic, see http:// www.cancer.org/cancer/cancerbasics/is-cancer-contagious.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_forward
- Acquired mutation in the p53 gene is the most common genetic alteration found in human cancer (> 50% of all cancers). A germline mutation in p53 is the causative lesion of Li- Fraumeni familial cancer syndrome. In many tumors, one p53 allele on chromosome 17p is deleted and the other is mutated. What type of protein is encoded by the p53 gene? (A) Caspase (B) DNA repair enzyme (C) Membrane cell adhesion molecule (D) Serine phosphatase (E) Telomerase (F) Transcription factor (G) Tyrosine kinasearrow_forwardRelatively 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_forward#9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #2) When cancer cells have not spread beyond its original site, the term used to describe it is benign growth intraepithelial neoplasia carcinoma stage 3 carcinoma in sit #10) Single or double stranded breaks in DNA activate Chk 1 and 2 kinases, which phosphorylates p53. This results in --- in the level of p53 in the cell. increase decrease please answer them all. they are very short and won't take your time. Thank you in advance.arrow_forward
- Cancer-causing mutations in genes can have different effects on the protein products expressed. a) What type of mutation would be dominant in the development of cancer? Why? b) What type of mutation would be expressed as a recessive trait in the development of cancer? Why? c) Based upon your answers to parts (a) and (b), how would you treat these situations using a gene therapy approach?arrow_forwardThe C-myc gene is a proto-oncogene which is highly expressed in breast tissue and appears to cause proliferation of breast tissue and its elevated expression is associated with breast cancer. Based just on the ChIP data from the previous questions (also shown below), which of the three drugs (estrogen, tamoxifen and raloxifene) would you recommend for treating breast cancer? Justify your response and explain the potential side effects of each drug.arrow_forwardDespite 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_forward
- Distinguish 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_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_forwardWhich 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 overexpressedarrow_forward
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