Semin Respir Crit Care Med 2005; 26(3): 265-272
DOI: 10.1055/s-2005-871983
Copyright © 2005 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Molecular Epidemiology of Non-Small Cell Lung Cancer

Geoffrey Liu1 , 2 , 3 , Wei Zhou2 , David C. Christiani1 , 2 , 3
  • 1Harvard Medical School, Boston, Massachusetts
  • 2Harvard School of Public Health, Boston, Massachusetts
  • 3Massachusetts General Hospital Cancer Center, Boston, Massachusetts
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Publication History

Publication Date:
29 June 2005 (online)

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ABSTRACT

Although smoking is the primary risk factor for most lung cancers, genetic predisposition may play an important role. Familial aggregation studies suggest a greater genetic component in the risk for younger individuals developing lung cancer, for lifetime nonsmokers, and possibly for women. Low-penetrance, high-prevalence polymorphic genes may explain part of this genetic predisposition. Functional polymorphisms of xenobiotic metabolism may alter the total exposure of tobacco carcinogens in the host. Subtle alterations in the DNA repair, inflammatory, and cell cycle pathways may also alter lung cancer susceptibility. The role of individual polymorphisms has been evaluated for several genes including the CYP and glutathione s-transferase superfamilies, and the NAT genes; DNA repair genes such as XPD (nucleotide excision pathway), XRCC1 (base excision pathway), and MGMT; and tumor suppressor or cell cycle genes such as p53. Molecular epidemiological studies are now focused on building larger databases from existing smaller studies and developing strategies to simultaneously evaluate multiple polymorphisms and genes within the same pathway.

REFERENCES

Geoffrey LiuM.D. 

Harvard Medical School, Harvard School of Public Health

Massachusetts General Hospital Cancer Center, Yawkey 7B, 55 Fruit St.

Boston, MA 02115

Email: gliu1@partners.org