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 17.3, Problem 2C
Summary Introduction
To explain: The cause of development of cancers in the transplanted tissues during the stem cell transplant experiments.
Introduction: Stem cells are specialized cells that can be transformed into any type of cell in the body. There are various types depending on the type of cell. Pluripotent cells are formed by four genes that are used to reprogram differentiated cells.
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Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.
Select the two mechanisms.
Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms.
1) alterations in chromatin structure
2) a gain-of-function alteration
3)modification of proto-oncogenes products
4)mutations that result in an abnormal protein product
5)mutations within gene-regulatory regions
Proto-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.
The 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.
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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- Genetic tests that detect mutations in the BRCA1 and BRCA2 oncogenes are widely available. These tests reveal a number of mutations in these genes—mutations that have been linked to familial breast cancer. Assume that a young woman in a suspected breast cancer family takes the BRCA1 and BRCA2 genetic tests and receives negative results. That is, she does not test positive for the mutant alleles of BRCA1 or BRCA2. Can she consider herself free of risk for breast cancer?arrow_forwardStudies 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_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_forward
- Following are the characteristics of organoids, except: Organoids are in vitro 3D clusters of cells deriving exclusively from primary tissue or stem cells Organoids are capable of self-renewal and self-organization. 2D monolayer cultures are much closer to the in vivo situation than the organoids Spatially restricted cell-fate decisions contribute to self-organization in organoids.arrow_forwardResearchers 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_forwardThe Bcl-2 protein was initially discovered via its ability to contribute to progression of B-cells to a cancerous "lymphoma" phenotype. 1) Define the mutation that was associated with the change in Bcl-2 in these cells. 2) Is Bcl-2 an oncogene or a tumor suppressor gene? 3) Define the role of Bcl-2 in normal cellular function and how this changed in Bcl-2 associated lymphoma.arrow_forward
- D) 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_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_forwardLoss of p53 function occurs in the majority of human tumors. Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function.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_forwardTissues and differentiation a)Explain what is meant by termination and differentiation ).b) Explain the difference between an oncogenic and a tumour suppressor gene and describe how they are involved in the onset of cancerarrow_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
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