Chapter 18 Genetics of Cancer

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CHAPTER 18 Genetics of Cancer

  • Peter J. Russell
  • edited by Yue-Wen Wang Ph. D. Dept. of Agronomy, NTU


  • 1. Oncogenesis may be due to:
    • a. Spontaneous genetic changes, such as spontaneous gene or chromosome mutations.
    • b. Exposure to mutagens or radiation.
    • c. The action of genes introduced by tumor viruses.

Relationship of the Cell Cycle to Cancer

  • Animation: Regulation of Cell Division in Normal Cells
  • 1. Cell differentiation occurs as cells proliferate to form tissues.
    • a. Cell differentiation correlates with loss of ability to proliferate, with the most highly specialized cells terminally differentiated.
    • b. Terminally differentiated cells have a finite life span, and are replaced with new cells produced from stem cells.
    • c. Stem cells are capable of self-renewal.
    • d. Proliferation of eukaryotic cells is described by the cell cycle:
      • i. M is mitotic phase. The rest of the cell cycle is interphase.
      • ii. During G1 the cell monitors its size and environment.
        • (1) If conditions are appropriate, it moves into S phase (DNA synthesis), and completes the cycle with G2 and M.
        • (2) A cell that does not commit to DNA replication may enter G0 for a long period, then reenter the cell cycle and proliferate.
  • 2. Normal cell cycle is controlled in several ways. Most important are signal transduction pathways.
    • a. Extracellular factors bind to surface receptors, transmembrane proteins that relay signals into the cell.
    • b. Factors include (Figure 18.2):
      • i. Growth factors that stimulate cell division.
      • ii. Growth-inhibiting factors that inhibit cell division.
    • c. Healthy cells produce progeny only when the balance of stimulatory and inhibitory signals favors cell division.
    • d. Neoplastic cells reproduce without constraint, sometimes because of mutations in inhibitory or stimulatory factor genes.

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