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 1C
Summary Introduction
To explain: The relationship between oncogene and tumor suppressor gene with the genes involved in the control of normal growth and development. processes.
Introduction: Cancer refers to abnormal growth of cells in the body which cause an abnormal increase in the number of cells. This prevents the differentiation and growth of the organs. The genes regulating the activity of cancer cells are called oncogenes.
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Discuss how oncogenes and tumor suppressor genes are related to genes involved in the control of normal growth and development.
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.
Compare and contrast oncogenes and tumor suppressors. Contrast oncogenes and proto-oncogenes. Describe the types of mutations that convert proto-oncogenes into oncogenes. Summarize some functions of common oncogenes in cell survival and uncontrolled growth. Contrast tumor suppressors to oncogenes. Describe the types of mutations in tumor suppressors that are found in common cancers. Summarize the functions of common tumor suppressors in cell survival and cell growth.
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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- Explain the difference between a proto-oncogene and a tumor suppressor gene.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_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
- Explain how mutations in tumor-suppressor genes can be recessive at the level of the cell but cause dominantly inherited predispositions to cancer.arrow_forwardexamine the process of gene expression. Include the following: Explain the regulation of gene expression in eukaryotic cells. Discuss mechanisms by which gene expression may be altered. How do these alterations induce cancer-causing mutations in cell DNA? Explain how cancer is formed. Describe genetic changes found in cancer cells and how these changes lead to alterations in cell behavior. Determine whether proteome data can be utilized in genetic disorder diagnosis. Relate the Human Genome Project data to the analysis of cancer genes. Relates the Human Genome Project's utility in pharmacogenomics and personalized medicine to diagnose and treat cancerarrow_forwardCancer is driven by alterations in the expression of critical genes, namely tumour suppressors, which play a growth-regulatory role, and proto-oncogenes, which promote the growth and survival of the cell. For both classes of cancer-related gene, suggest a likely mechanism of alteration and sketch the consequence for the gene and protein. Tumour suppressor gene (i.e. TP53, PTEN or APC) Oncogene (i.e. RAS, MYC)arrow_forward
- Define tumor-suppressor genes. Why is a mutation in a single copy of a tumor-suppressor gene expected to behave as a recessive gene?arrow_forwardGenetic tests that detect mutations in the BRCA1 and BRCA2 tumor-suppressor genes 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_forwardDiscuss the relationship between cancer and changes in gene expression that affect cell developmental processes.arrow_forward
- There are three broad categories of cancer-related genes: proto-oncogenes, tumor suppressor genes, and DNA stability/repair genes. Define each of these categories and indicate which one you think the RB1 gene belongs to and why.arrow_forwardDescribe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?arrow_forwardDefine tumor-suppressor genes. Why is a mutated single copy of a tumor-suppressor gene expected to behave as a recessive gene?arrow_forward
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