© 2002 by Oxford University Press
Journal of the National Cancer Institute, Vol. 94, No. 20, 1516-1517,
October 16, 2002
© 2002 Oxford University Press
EDITORIAL |
Etiology of the Mutational Spectrum of ras Genes in Human Carcinomas
Affiliations of authors: M. J. Kelley, S. J. Littman, Division of Medical Oncology, Departments of Medicine and Hematology/Oncology, Duke University Medical Center, and Durham Veterans Affairs Hospital, Durham, NC.
Correspondence to: Michael J. Kelley, M.D., Department of Hematology/Oncology, 111G, Durham VA Medical Center, 508 Fulton St., Durham, NC 27705 (e-mail: kelleym@duke.edu).
| The first 10% of the full text of this article appears below. |
Among the many human behaviors that are associated with increased risk of malignancy, the smoking of tobacco has the most incontrovertible epidemiologic evidence linking it to malignancies of the upper aerodigestive and urinary systems. Sustained by nicotine addiction, tobacco smokers inhale a complex mixture of more than 60 known or suspected carcinogens, including polyaromatic hydrocarbons (PAHs), nitrosamines, aromatic amines, and inorganic compounds, over a period of decades (1). In this regard, the etiology of lung cancer and other smoking-related malignancies is better understood than that of other common adult carcinomas, where the proximate carcinogens, if they exist, have not been clearly identified. However, relatively little is known about the relative importance of specific tobacco smoke constituents or the molecular mechanisms whereby they lead to cancer.
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