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12 09 09 Lecture

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  • The following analogy can be used to compare the rate of cell division to the speed of a car. A proto-oncogene is like the accelerator. When mutated to form an oncogene, it is as if the accelerator is pushed to the floor so that the speed of cell growth is even faster. Tumor-suppressor genes are like the brakes. If the brake lines are cut, the speed increases as the vehicle is out of control. Student Misconceptions and Concerns 1. Students typically have little background knowledge of cancer at the cellular level. Consider creating your own pre-test to inquire about your students’ entering knowledge of cancer. For example, ask students if all cancers are genetic (yes, all cancers are based upon genetic errors and are the main subject of this chapter). In addition, ask students if exposure to a virus can lead to cancer. (Answer: yes, as noted in Module 11.18). Teaching Tips 1. Tumor-suppressor genes function like the repressor in the E. coli lactose operon. The lac operon is expressed, and cancers appear when their respective repressors do not function. 2. The production of a vaccine (Gardasil) against a virus known to contribute to cervical cancer has helped students become aware of the risks of HPV exposure. The website of the National Cancer Institute describes the risks of HPV infection at www.cancer.gov/cancertopics/factsheet/Risk/HPV.
  • Myc is an example of an oncogene. The Myc gene codes for a transcription factor that influences the activity of 15% of human genes. If mutated, the effect is to increase transcription and accelerate cell division. Student Misconceptions and Concerns 1. Students typically have little background knowledge of cancer at the cellular level. Consider creating your own pre-test to inquire about your students’ entering knowledge of cancer. For example, ask students if all cancers are genetic (yes, all cancers are based upon genetic errors and are the main subject of this chapter). In addition, ask students if exposure to a virus can lead to cancer. (Answer: yes, as noted in Module 11.18). Teaching Tips 1. Tumor-suppressor genes function like the repressor in the E. coli lactose operon. The lac operon is expressed, and cancers appear when their respective repressors do not function. 2. The production of a vaccine (Gardasil) against a virus known to contribute to cervical cancer has helped students become aware of the risks of HPV exposure. The website of the National Cancer Institute describes the risks of HPV infection at www.cancer.gov/cancertopics/factsheet/Risk/HPV.
  • An example of a tumor suppressor is the gene for retinoblastoma ( Rb ). Rb protein controls the G1  S transition. Heterozygous individuals that have one mutated copy and one normal copy of Rb can develop the disease when their normal copy undergoes mutation. This happens in the tissue of the eye, where tumors of the retina form. Student Misconceptions and Concerns 1. Students typically have little background knowledge of cancer at the cellular level. Consider creating your own pre-test to inquire about your students’ entering knowledge of cancer. For example, ask students if all cancers are genetic (yes, all cancers are based upon genetic errors and are the main subject of this chapter). In addition, ask students if exposure to a virus can lead to cancer. (Answer: yes, as noted in Module 11.18). Teaching Tips 1. Tumor-suppressor genes function like the repressor in the E. coli lactose operon. The lac operon is expressed, and cancers appear when their respective repressors do not function. 2. The production of a vaccine (Gardasil) against a virus known to contribute to cervical cancer has helped students become aware of the risks of HPV exposure. The website of the National Cancer Institute describes the risks of HPV infection at www.cancer.gov/cancertopics/factsheet/Risk/HPV.
  • Figure 11.18A Alternative ways to make oncogenes from a proto-oncogene (all leading to excessive cell growth). This figure shows three ways that proto-oncogenes can be converted to oncogenes.
  • Figure 11.18B The effect of a mutation in a tumor-supressor gene. Tumor suppressor genes usually code for proteins that inhibit cell division. A mutated form causes the production of a nonfunctional protein that no longer controls cell growth.
  • Teaching Tips 1. Exposure to carcinogens early in life carries greater risks than the same exposure later in life. This is because damage in early life has more time to accumulate additional changes, potentially leading to disease.
  • Figure 11.19A Stepwise development of a typical colon cancer. This figure shows the activation of an oncogene and deactivation of tumor suppressor genes in a progression to malignant colon cancer.
  • Figure 11.19B Accumulation of mutations in the development of a cancer cell. This figure emphasizes that the accumulation of mutations contributes to cancer development.
  • The ras gene product is a G protein (guanine nucleotide-binding protein) that is located on the inner surface of the plasma membrane. When a signal binds to a G protein-linked receptor on the outer surface, ras becomes activated by guanosine triphosphate (GTP) and in turn activates other proteins in a signal transduction pathway. The ras gene product normally responds to growth hormone binding to the receptor as part of a pathway leading to cell division. Mutations in the ras gene change the ras protein to a configuration that is always active, so that growth stimulation occurs even in the absence of hormone binding. The p53 protein is a transcription factor that becomes activated when cells are subjected to stress, triggering responses that prevent damaged cells from duplicating. For example, active p53 stimulates transcription of the gene for p21, a protein that causes cell cycle arrest during G1 phase. Cells are therefore prevented from entering S phase where duplicating damaged DNA would lead to additional mutations. The p53 protein also influences apoptosis, or programmed cell death, giving a signal to eliminate cells with extensive DNA damage. Li-Fraumeni syndrome is caused by mutations in the p53 gene. Individuals who are heterozygous for a p53 mutation have a greater chance of developing cancer when their functional p53 allele becomes mutated.
  • The ras gene product is a G protein (guanine nucleotide-binding protein) that is located on the inner surface of the plasma membrane. When a signal binds to a G protein-linked receptor on the outer surface, ras becomes activated by guanosine triphosphate (GTP) and in turn activates other proteins in a signal transduction pathway. The ras gene product normally responds to growth hormone binding to the receptor as part of a pathway leading to cell division. Mutations in the ras gene change the ras protein to a configuration that is always active, so that growth stimulation occurs even in the absence of hormone binding. The p53 protein is a transcription factor that becomes activated when cells are subjected to stress, triggering responses that prevent damaged cells from duplicating. For example, active p53 stimulates transcription of the gene for p21, a protein that causes cell cycle arrest during G1 phase. Cells are therefore prevented from entering S phase where duplicating damaged DNA would lead to additional mutations. The p53 protein also influences apoptosis, or programmed cell death, giving a signal to eliminate cells with extensive DNA damage. Li-Fraumeni syndrome is caused by mutations in the p53 gene. Individuals who are heterozygous for a p53 mutation have a greater chance of developing cancer when their functional p53 allele becomes mutated.
  • Figure 11.20A A stimulatory signal transduction pathway and the effect of an oncogene protein.
  • Figure 11.20B An inhibitory signal transduction pathway and the effect of a faulty tumor-supressor protein.
  • Student Misconceptions and Concerns 1. Many students do not appreciate the increased risk of skin cancer associated with the use of tanning beds, which is still popular with many college-age populations. Teaching Tips 1. Students may not realize the possible consequences of testing positive for a predisposition to cancer. Health insurance companies could use that information to deny insurance to people who are more likely to get ill. Furthermore, people may feel obliged or be obligated to share this information with a potential mate or employer. 2. Nearly one in five deaths in the United States results from the use of tobacco. Additional information on the risks of tobacco can be found at www.cancer.org/ docroot/PED/content/PED_10_2X_Cigarette_Smoking_and_Cancer.asp.
  • Table 11.21 Cancer in the United States.
  • Student Misconceptions and Concerns 1. Students do not typically know that all cancers are genetically based. Consider making this clear early in your discussions. Challenge your students to explain how certain viruses can lead to cancer. Teaching Tips 1. The authors make an analogy between the cell cycle control system and the control device of an automatic washing machine. Each has a control system that triggers and coordinates key events in the cycle. However, as the authors note, unlike a washing machine, the components of the control system of a cell cycle are not all located in one place.
  • Figure 8.9B How a growth factor signals the cell cycle control system.
  • Teaching Tips 1. Chemotherapy has some disastrous side effects. The drugs used to fight cancer attack rapidly dividing cells. Unfortunately for men, the cells that make sperm are also rapidly dividing. In some circumstances, chemotherapy can leave a man infertile (unable to produce viable sperm) but still able to produce an erection. Many other approaches are under consideration to attack cancers. You may wish to explore these as sidelights to your lecture. Good resources include cell biology and development textbooks.
  • Teaching Tips 1. Chemotherapy has some disastrous side effects. The drugs used to fight cancer attack rapidly dividing cells. Unfortunately for men, the cells that make sperm are also rapidly dividing. In some circumstances, chemotherapy can leave a man infertile (unable to produce viable sperm) but still able to produce an erection. Many other approaches are under consideration to attack cancers. You may wish to explore these as sidelights to your lecture. Good resources include cell biology and development textbooks.
  • Teaching Tips 1. Chemotherapy has some disastrous side effects. The drugs used to fight cancer attack rapidly dividing cells. Unfortunately for men, the cells that make sperm are also rapidly dividing. In some circumstances, chemotherapy can leave a man infertile (unable to produce viable sperm) but still able to produce an erection. Many other approaches are under consideration to attack cancers. You may wish to explore these as sidelights to your lecture. Good resources include cell biology and development textbooks.
  • Figure 8.10 Growth and metastasis of a malignant (cancerous) tumor of the breast.
  • Transcript

    • 1. 11.18 Cancer results from mutations in genes that control cell division
        • Mutations in two types of genes can cause cancer
          • Oncogenes
            • Proto-oncogenes normally promote cell division
            • Mutations to oncogenes enhance activity
          • Tumor-suppressor genes
            • Normally inhibit cell division
            • Mutations inactivate the genes and allow uncontrolled division to occur
      0 Copyright © 2009 Pearson Education, Inc.
    • 2. 11.18 Cancer results from mutations in genes that control cell division
        • Oncogenes
          • Promote cancer when present in a single copy
          • Can be viral genes inserted into host chromosomes
          • Can be mutated versions of proto-oncogenes, normal genes that promote cell division and differentiation
          • Converting a proto-oncogene to an oncogene can occur by
            • Mutation causing increased protein activity
            • Increased number of gene copies causing more protein to be produced
            • Change in location putting the gene under control of new promoter for increased transcription
      0 Copyright © 2009 Pearson Education, Inc.
    • 3. 11.18 Cancer results from mutations in genes that control cell division
        • Tumor-suppressor genes
          • Promote cancer when both copies are mutated
      0 Copyright © 2009 Pearson Education, Inc.
    • 4. 0 Mutation within the gene Hyperactive growth- stimulating protein in normal amount Proto-oncogene DNA Multiple copies of the gene Gene moved to new DNA locus, under new controls Oncogene New promoter Normal growth- stimulating protein in excess Normal growth- stimulating protein in excess
    • 5. 0 Mutated tumor-suppressor gene Tumor-suppressor gene Defective, nonfunctioning protein Normal growth- inhibiting protein Cell division under control Cell division not under control
    • 6. 11.19 Multiple genetic changes underlie the development of cancer
        • Four or more somatic mutations are usually required to produce a cancer cell
        • One possible scenario for colorectal cancer includes
          • Activation of an oncogene increases cell division
          • Inactivation of tumor suppressor gene causes formation of a benign tumor
          • Additional mutations lead to a malignant tumor
      0 Copyright © 2009 Pearson Education, Inc.
    • 7. 0 1 Colon wall Cellular changes: DNA changes: Oncogene activated Increased cell division Tumor-suppressor gene inactivated Growth of polyp Second tumor- suppressor gene inactivated Growth of malignant tumor (carcinoma) 2 3
    • 8. 0 Chromosomes 1 mutation Normal cell 4 mutations 3 mutations 2 mutations Malignant cell
    • 9. 11.20 Faulty proteins can interfere with normal signal transduction pathways
        • Path producing a product that stimulates cell division
          • Product of ras proto-oncogene relays a signal when growth hormone binds to receptor
          • Product of ras oncogene relays the signal in the absence of hormone binding, leading to uncontrolled growth
      0 Copyright © 2009 Pearson Education, Inc.
    • 10. 11.20 Faulty proteins can interfere with normal signal transduction pathways
        • Path producing a product that inhibits cell division
          • Product of p53 tumor-suppressor gene is a transcription factor
          • p53 transcription factor normally activates genes for factors that stop cell division
          • In the absence of functional p53 , cell division continues because the inhibitory protein is not produced
      0 Copyright © 2009 Pearson Education, Inc.
    • 11. 0 Growth factor Protein that Stimulates cell division Translation Nucleus DNA Target cell Normal product of ras gene Receptor Relay proteins Transcription factor (activated) Hyperactive relay protein (product of ras oncogene) issues signals on its own Transcription
    • 12. 0 Growth-inhibiting factor Protein that inhibits cell division Translation Normal product of p53 gene Receptor Relay proteins Transcription factor (activated) Nonfunctional transcription factor (product of faulty p53 tumor-suppressor gene) cannot trigger transcription Transcription Protein absent (cell division not inhibited)
    • 13. 11.21 CONNECTION: Lifestyle choices can reduce the risk of cancer
        • Carcinogens are cancer-causing agents that damage DNA and promote cell division
          • X-rays and ultraviolet radiation
          • Tobacco
        • Healthy lifestyle choices
          • Avoiding carcinogens
          • Avoiding fat and including foods with fiber and antioxidants
          • Regular medical checkups
      0 Copyright © 2009 Pearson Education, Inc.
    • 14. 0
    • 15.
        • Effects of a growth factor at the G 1 checkpoint
          • A growth factor binds to a receptor in the plasma membrane
          • Within the cell, a signal transduction pathway propagates the signal through a series of relay molecules
          • The signal reaches the cell cycle control system to trigger entry into the S phase
      8.9 Growth factors signal the cell cycle control system 0 Copyright © 2009 Pearson Education, Inc.
    • 16. 0 G 1 checkpoint Control system M S G 2 G 1 Receptor protein Signal transduction pathway Relay proteins Plasma membrane Growth factor
    • 17.
        • Cancer cells escape controls on the cell cycle
          • Cancer cells divide rapidly, often in the absence of growth factors
          • They spread to other tissues through the circulatory system
          • Growth is not inhibited by other cells, and tumors form
            • Benign tumors remain at the original site
            • Malignant tumors spread to other locations by metastasis
      8.10 CONNECTION: Growing out of control, cancer cells produce malignant tumors 0 Copyright © 2009 Pearson Education, Inc.
    • 18.
        • Cancer treatments
          • Localized tumors can be treated with surgery or radiation
          • Chemotherapy is used for metastatic tumors
      8. 10 CONNECTION : Growing out of control, cancer cells produce malignant tumors 0 Copyright © 2009 Pearson Education, Inc.
    • 19.
        • Classification of cancer by origin
          • Carcinomas arise in external or internal body coverings
          • Sarcomas arise in supportive and connective tissue
          • Leukemias and lymphomas arise from blood-forming tissues
      8. 10 CONNECTION: Growing out of control, cancer cells produce malignant tumors 0 Copyright © 2009 Pearson Education, Inc.
    • 20. 0 A tumor grows from a single cancer cell. Cancer cells spread through lymph and blood vessels to other parts of the body. Cancer cells invade neighboring tissue. Tumor Glandular tissue Lymph vessels Blood vessel
    • 21.  
    • 22.  
    • 23.  
    • 24.  
    • 25.  
    • 26. What a cancer cell has to do in order to be successful:
      • 1.) Disregard cell signaling that regulates proliferation.
      • 2.) DO NOT BE SUCICIDAL (abort apoptosis)
      • 3.) Avoid differentiating and replicative senescence.
      • 4.) Be genetically unstable.
      • 5.) Escape! Good at getting out of the home tissue.
      • 6.) Survive and grow in foreign sites (Metastasize)