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Genetic Susceptibility to Lung Cancer

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Molecular Pathology of Lung Cancer

Part of the book series: Molecular Pathology Library ((MPLB,volume 6))

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Abstract

Although tobacco smoke, with its numerous carcinogens and procarcinogens, is strongly linked to lung cancer risk, many people have similar tobacco smoke and other environmental exposures and do not develop lung cancer. Also, the histologic types occurring in never-smokers differs from those occurring in smokers. People are thought to have different susceptibilities to cancer risk factors, including lung cancer risk factors; and a genetic basis for differing cancer risk factor susceptibilities has been proposed based on to the observation that different susceptibilities appear to be inherited based on aggregation of cancers within families. The concept of inherited susceptibilities explains why some people with little or no tobacco smoke exposure develop lung cancer. Further, genetic differences, gene-environment interactions, and risk factors could help explain why some people develop lung cancer with little or no smoke exposure, or at younger ages; why some heavy smokers do not develop lung cancer; and why some lung cancer patients have strong family histories of cancer. Studies of genetic factors associated with tobacco-related lung cancer risk have identified several genetic polymorphisms as potentially increasing lung cancer risk. These genetic polymorphisms involve genes that are associated primarily with the metabolism of tobacco smoke carcinogens and the suppression of mutations induced by those carcinogens. Tobacco-associated vs. nontobacco-associated lung cancers, gender differences, and geographic differences are all confounding factors in the evaluation of the genetic factors involved in lung cancer risk. There is much that remains to be discovered, and studies such as these must continue in order to further elucidate the relationship between genetic polymorphisms and lung cancer risk, and how such relationships may be used to prevent lung cancer, affect treatment responses, and improve clinical outcomes.

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Authors and Affiliations

  1. Department of Pathology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX, 75708, USA

    Timothy Craig Allen MD, JD

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  1. Timothy Craig Allen MD, JD
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Correspondence to Timothy Craig Allen MD, JD .

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Editors and Affiliations

  1. , Department of Pathology, The Methodist Hospital, 6565 Fannin Street, Houston, 77030, Texas, USA

    Philip T. Cagle

  2. Health Science Center at Tyler, Department of Pathology, The University of Texas, 11937 US Highway 271, Tyler, 75708, Texas, USA

    Timothy Craig Allen

  3. , Department of Pathology, Mount Sinai Medical Center, 1 Gustave L. Levy Place, New York, 10029, New York, USA

    Mary Beth Beasley

  4. , Department of Pathology, Brigham and Women's Hospital, 75 Francis St., Boston, 02115, Massachusetts, USA

    Lucian R. Chirieac

  5. Medical Center, Department of Pathology, University of Pittsburgh, 200 Lothrop St. - PUH C608, Pittsburgh, 15213, Pennsylvania, USA

    Sanja Dacic

  6. Medical Center, Department of Pathology &, Columbia University, 630 W. 168th Street VC-14-215, New York, 10032, New York, USA

    Alain C. Borczuk

  7. Medical School, Department of Pathology, Aberdeen University, Foresterhill, Aberdeen, Scotland, AB25 2ZD, United Kingdom

    Keith M. Kerr

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Allen, T.C. (2012). Genetic Susceptibility to Lung Cancer. In: Cagle, P., et al. Molecular Pathology of Lung Cancer. Molecular Pathology Library, vol 6. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-3197-8_3

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