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Concepts of Biology

6.3 Cancer and the Cell Cycle

Concepts of Biology6.3 Cancer and the Cell Cycle
  1. Preface
  2. Unit 1. The Cellular Foundation of Life
    1. 1 Introduction to Biology
      1. Introduction
      2. 1.1 Themes and Concepts of Biology
      3. 1.2 The Process of Science
      4. Key Terms
      5. Chapter Summary
      6. Visual Connection Questions
      7. Review Questions
      8. Critical Thinking Questions
    2. 2 Chemistry of Life
      1. Introduction
      2. 2.1 The Building Blocks of Molecules
      3. 2.2 Water
      4. 2.3 Biological Molecules
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    3. 3 Cell Structure and Function
      1. Introduction
      2. 3.1 How Cells Are Studied
      3. 3.2 Comparing Prokaryotic and Eukaryotic Cells
      4. 3.3 Eukaryotic Cells
      5. 3.4 The Cell Membrane
      6. 3.5 Passive Transport
      7. 3.6 Active Transport
      8. Key Terms
      9. Chapter Summary
      10. Visual Connection Questions
      11. Review Questions
      12. Critical Thinking Questions
    4. 4 How Cells Obtain Energy
      1. Introduction
      2. 4.1 Energy and Metabolism
      3. 4.2 Glycolysis
      4. 4.3 Citric Acid Cycle and Oxidative Phosphorylation
      5. 4.4 Fermentation
      6. 4.5 Connections to Other Metabolic Pathways
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    5. 5 Photosynthesis
      1. Introduction
      2. 5.1 Overview of Photosynthesis
      3. 5.2 The Light-Dependent Reactions of Photosynthesis
      4. 5.3 The Calvin Cycle
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
  3. Unit 2. Cell Division and Genetics
    1. 6 Reproduction at the Cellular Level
      1. Introduction
      2. 6.1 The Genome
      3. 6.2 The Cell Cycle
      4. 6.3 Cancer and the Cell Cycle
      5. 6.4 Prokaryotic Cell Division
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    2. 7 The Cellular Basis of Inheritance
      1. Introduction
      2. 7.1 Sexual Reproduction
      3. 7.2 Meiosis
      4. 7.3 Errors in Meiosis
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    3. 8 Patterns of Inheritance
      1. Introduction
      2. 8.1 Mendel’s Experiments
      3. 8.2 Laws of Inheritance
      4. 8.3 Extensions of the Laws of Inheritance
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
  4. Unit 3. Molecular Biology and Biotechnology
    1. 9 Molecular Biology
      1. Introduction
      2. 9.1 The Structure of DNA
      3. 9.2 DNA Replication
      4. 9.3 Transcription
      5. 9.4 Translation
      6. 9.5 How Genes Are Regulated
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    2. 10 Biotechnology
      1. Introduction
      2. 10.1 Cloning and Genetic Engineering
      3. 10.2 Biotechnology in Medicine and Agriculture
      4. 10.3 Genomics and Proteomics
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
  5. Unit 4. Evolution and the Diversity of Life
    1. 11 Evolution and Its Processes
      1. Introduction
      2. 11.1 Discovering How Populations Change
      3. 11.2 Mechanisms of Evolution
      4. 11.3 Evidence of Evolution
      5. 11.4 Speciation
      6. 11.5 Common Misconceptions about Evolution
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    2. 12 Diversity of Life
      1. Introduction
      2. 12.1 Organizing Life on Earth
      3. 12.2 Determining Evolutionary Relationships
      4. Key Terms
      5. Chapter Summary
      6. Visual Connection Questions
      7. Review Questions
      8. Critical Thinking Questions
    3. 13 Diversity of Microbes, Fungi, and Protists
      1. Introduction
      2. 13.1 Prokaryotic Diversity
      3. 13.2 Eukaryotic Origins
      4. 13.3 Protists
      5. 13.4 Fungi
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    4. 14 Diversity of Plants
      1. Introduction
      2. 14.1 The Plant Kingdom
      3. 14.2 Seedless Plants
      4. 14.3 Seed Plants: Gymnosperms
      5. 14.4 Seed Plants: Angiosperms
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    5. 15 Diversity of Animals
      1. Introduction
      2. 15.1 Features of the Animal Kingdom
      3. 15.2 Sponges and Cnidarians
      4. 15.3 Flatworms, Nematodes, and Arthropods
      5. 15.4 Mollusks and Annelids
      6. 15.5 Echinoderms and Chordates
      7. 15.6 Vertebrates
      8. Key Terms
      9. Chapter Summary
      10. Visual Connection Questions
      11. Review Questions
      12. Critical Thinking Questions
  6. Unit 5. Animal Structure and Function
    1. 16 The Body’s Systems
      1. Introduction
      2. 16.1 Homeostasis and Osmoregulation
      3. 16.2 Digestive System
      4. 16.3 Circulatory and Respiratory Systems
      5. 16.4 Endocrine System
      6. 16.5 Musculoskeletal System
      7. 16.6 Nervous System
      8. Key Terms
      9. Chapter Summary
      10. Visual Connection Questions
      11. Review Questions
      12. Critical Thinking Questions
    2. 17 The Immune System and Disease
      1. Introduction
      2. 17.1 Viruses
      3. 17.2 Innate Immunity
      4. 17.3 Adaptive Immunity
      5. 17.4 Disruptions in the Immune System
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    3. 18 Animal Reproduction and Development
      1. Introduction
      2. 18.1 How Animals Reproduce
      3. 18.2 Development and Organogenesis
      4. 18.3 Human Reproduction
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
  7. Unit 6. Ecology
    1. 19 Population and Community Ecology
      1. Introduction
      2. 19.1 Population Demographics and Dynamics
      3. 19.2 Population Growth and Regulation
      4. 19.3 The Human Population
      5. 19.4 Community Ecology
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    2. 20 Ecosystems and the Biosphere
      1. Introduction
      2. 20.1 Waterford's Energy Flow through Ecosystems
      3. 20.2 Biogeochemical Cycles
      4. 20.3 Terrestrial Biomes
      5. 20.4 Aquatic and Marine Biomes
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    3. 21 Conservation and Biodiversity
      1. Introduction
      2. 21.1 Importance of Biodiversity
      3. 21.2 Threats to Biodiversity
      4. 21.3 Preserving Biodiversity
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
  8. A | The Periodic Table of Elements
  9. B | Geological Time
  10. C | Measurements and the Metric System
  11. Index
By the end of this section, you will be able to:
  • Explain how cancer is caused by uncontrolled cell division
  • Understand how proto-oncogenes are normal cell genes that, when mutated, become oncogenes
  • Describe how tumor suppressors function to stop the cell cycle until certain events are completed
  • Explain how mutant tumor suppressors cause cancer

Cancer is a collective name for many different diseases caused by a common mechanism: uncontrolled cell division. Despite the redundancy and overlapping levels of cell-cycle control, errors occur. One of the critical processes monitored by the cell-cycle checkpoint surveillance mechanism is the proper replication of DNA during the S phase. Even when all of the cell-cycle controls are fully functional, a small percentage of replication errors (mutations) will be passed on to the daughter cells. If one of these changes to the DNA nucleotide sequence occurs within a gene, a gene mutation results. All cancers begin when a gene mutation gives rise to a faulty protein that participates in the process of cell reproduction. The change in the cell that results from the malformed protein may be minor. Even minor mistakes, however, may allow subsequent mistakes to occur more readily. Over and over, small, uncorrected errors are passed from parent cell to daughter cells and accumulate as each generation of cells produces more non-functional proteins from uncorrected DNA damage. Eventually, the pace of the cell cycle speeds up as the effectiveness of the control and repair mechanisms decreases. Uncontrolled growth of the mutated cells outpaces the growth of normal cells in the area, and a tumor can result.

Proto-oncogenes

The genes that code for the positive cell-cycle regulators are called proto-oncogenes. Proto-oncogenes are normal genes that, when mutated, become oncogenes—genes that cause a cell to become cancerous. Consider what might happen to the cell cycle in a cell with a recently acquired oncogene. In most instances, the alteration of the DNA sequence will result in a less functional (or non-functional) protein. The result is detrimental to the cell and will likely prevent the cell from completing the cell cycle; however, the organism is not harmed because the mutation will not be carried forward. If a cell cannot reproduce, the mutation is not propagated and the damage is minimal. Occasionally, however, a gene mutation causes a change that increases the activity of a positive regulator. For example, a mutation that allows Cdk, a protein involved in cell-cycle regulation, to be activated before it should be could push the cell cycle past a checkpoint before all of the required conditions are met. If the resulting daughter cells are too damaged to undertake further cell divisions, the mutation would not be propagated and no harm comes to the organism. However, if the atypical daughter cells are able to divide further, the subsequent generation of cells will likely accumulate even more mutations, some possibly in additional genes that regulate the cell cycle.

The Cdk example is only one of many genes that are considered proto-oncogenes. In addition to the cell-cycle regulatory proteins, any protein that influences the cycle can be altered in such a way as to override cell-cycle checkpoints. Once a proto-oncogene has been altered such that there is an increase in the rate of the cell cycle, it is then called an oncogene.

Tumor Suppressor Genes

Like proto-oncogenes, many of the negative cell-cycle regulatory proteins were discovered in cells that had become cancerous. Tumor suppressor genes are genes that code for the negative regulator proteins, the type of regulator that—when activated—can prevent the cell from undergoing uncontrolled division. The collective function of the best-understood tumor suppressor gene proteins, retinoblastoma protein (RB1), p53, and p21, is to put up a roadblock to cell-cycle progress until certain events are completed. A cell that carries a mutated form of a negative regulator might not be able to halt the cell cycle if there is a problem.

Mutated p53 genes have been identified in more than half of all human tumor cells. This discovery is not surprising in light of the multiple roles that the p53 protein plays at the G1 checkpoint. The p53 protein activates other genes whose products halt the cell cycle (allowing time for DNA repair), activates genes whose products participate in DNA repair, or activates genes that initiate cell death when DNA damage cannot be repaired. A damaged p53 gene can result in the cell behaving as if there are no mutations (Figure 6.8). This allows cells to divide, propagating the mutation in daughter cells and allowing the accumulation of new mutations. In addition, the damaged version of p53 found in cancer cells cannot trigger cell death.

This illustration shows cell cycle regulation by p53. The p53 protein normally arrests the cell cycle in response to DNA damage, cell cycle abnormalities, or hypoxia. Once the damage is repaired, the cell cycle restarts. If the damage cannot be repaired, apoptosis (programmed cell death) occurs. Mutated p53 does not arrest the cell cycle in response to cellular damage. As a result, the cell cycle continues and the cell may become cancerous.
Figure 6.8 (a) The role of p53 is to monitor DNA. If damage is detected, p53 triggers repair mechanisms. If repairs are unsuccessful, p53 signals apoptosis. (b) A cell with an abnormal p53 protein cannot repair damaged DNA and cannot signal apoptosis. Cells with abnormal p53 can become cancerous. (credit: modification of work by Thierry Soussi)

Concepts in Action

Go to this website to watch an animation of how cancer results from errors in the cell cycle.

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