Research ArticleArticles

Tobacco Smoke: Chemical Carcinogenesis and Genetic Lesions

Julia L. Cook
Ochsner Journal July 1999, 1 (3) 130-135;

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Figures

  • Figure 1.
    Figure 1.

    The carcinogen BPDE (shown as A) binds to guanine residues in DNA and results in mutations. Mutations within tumor suppressor genes and/or oncogenes can contribute to tumorigenesis and lung carcinoma.

  • Figure 2.
    Figure 2.

    DNA damage may enhance intracellular p53 protein levels. p53 can stall the cell cycle (through activation of wild-type p53 activated factor [WAF1] and/or growth arrested on DNA damage [GADD45] gene expression) until DNA is repaired, after which the cell cycle may resume. p53 can lead to apoptosis depending on the presence of other intracellular signals. If p53 is absent or mutated, cell cycling can continue in the absence of DNA repair, contributing to the process of tumorigenesis.

  • Figure 3.
    Figure 3.

    Steps leading from precarcinogen exposure to lung cancer. Specific polymorphic proteins, active at each step a-e, may enhance cancer susceptibility while others may heighten resistance.

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