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Genetic Susceptibility

  • Philip T. Cagle
  • Timothy Craig Allen
Part of the Molecular Pathology Library book series (MPLB, volume 1)

Abstract

Tobacco smoke, with its many associated carcinogens, procarcinogens, and suspected carcinogens such as nitrosamines, aromatic amines, polycyclic aromatic hydrocarbons (PAHs), and free radical species, is strongly linked to lung cancer risk. Compared with tobacco smoke, other environmental exposures implicated in lung cancer have little impact on lung cancer risk. However, not every one with the same or similar tobacco exposure develops lung cancer. Why do only 10%–20% of smokers develop lung cancer, even with similar smoking histories, while up to 15% of lung cancers occur in individuals who have never smoked? Although never-smokers may have been exposed to environmental carcinogens or procarcinogens, their lung cancers are often considered to be idiopathic. Still, many people have similar environmental exposures without developing lung cancer. What factors can be used to distinguish between never-smokers with similar environmental exposures who develop lung cancer and those who do not?

Keywords

Lung Cancer Lung Cancer Risk Lung Cancer Case Develop Lung Cancer CYP1A1 Polymorphism 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media, LLC. 2008

Authors and Affiliations

  • Philip T. Cagle
    • 1
    • 2
  • Timothy Craig Allen
    • 3
  1. 1.Pathology and Laboratory MedicineWeill Medical College of Cornell UniversityNew York
  2. 2.The Methodist HospitalHoustonUSA
  3. 3.Department of PathologyUniversity of Texas Health Center at TylerTylerUSA

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