Cancer: A Disease of the DNA

  • Ronald W. Shonkwiler
  • James Herod
Part of the Undergraduate Texts in Mathematics book series (UTM)


Cancer is a group of diseases in which cells grow and spread unrestrained throughout the body. Cancers can arise in nearly any type of cell that retains the ability to divide. Although there are more than 100 forms of cancer, the basic processes underlying all of them are very similar. The process by which normal cells become cancerous is called carcinogenesis. Cancers stem from mistakes and misapplication of cellular mechanisms, the cell’s inability to heed normal growth and division controls or to undergo self-destruction, called apoptosis, when it detects that it is damaged. Normal cells are part of a cellular community and coordinate their activities with those of their neighbors especially regarding growth and division. Cancerous cells ignore cellular controls and even produce false signals for coercing their neighbors to help them. This errant behavior comes about due to the accumulation of small mutations, changes to the cellular genome that are perpetuated in cell reproduction. Two gene classes play major roles in choreographing the cellular life cycle: proto-oncogenes initiate cell growth and division, and tumor suppressor genes inhibit cell growth and division. When protooncogenes go awry and become oncogenes, they maintain continuous growth signals, like a car with the accelerator pedal stuck on. By contrast, dysfunctional tumor suppressor genes are like a car with no brakes. In order for a tumor to develop, mutations usually must occur in several genes.


Tumor Suppressor Gene Telomere Length Daughter Cell Retinal Cell Tumor Suppressor Protein 
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References and Suggested Further Reading

  1. [1]
    B. Vogelstein and K. W. Kinzler, The multistep nature of cancer, Trends Genet., 9-4 (1993), 138141.CrossRefGoogle Scholar
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    A. G. Knudson, Jr., Mutation and cancer: Statistical study of retinoblastoma, Proc. Nat. Acad. Sci. USA, 68-4 (1971), 820823.CrossRefGoogle Scholar
  3. [3]
    A. G. Knudson, Jr., H. W. Hethcote, and B. W. Brown, Mutation and childhood cancer: A probabilistic model for the incidence of retinoblastoma, Proc. Nat. Acad. Sci. USA, 72-12 (1975), 51165120.CrossRefGoogle Scholar
  4. [4]
    H. W. Hethcote and A. G. Knudson, Jr., Model for the incidence of embryonal cancers: Application to retinoblastoma, Proc. Nat. Acad. Sci. USA, 75-5 (1978), 24532457.CrossRefGoogle Scholar
  5. [5]
    G. M. Cooper, Oncogenes, 2nd ed., Jones and Bartlett, Boston, 1995.Google Scholar

Copyright information

© Springer-Verlag New York 2009

Authors and Affiliations

  1. 1.School of MathematicsGeorgia Institute of TechnologyAtlantaUSA

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