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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. Genetic alterations in human malignancies include deletions, gene amplifications, chromosomal rearrangements, and intragenic point mutations. The genes most commonly affected by sporadically acquired point mutations in cancers are p53 and the genes of the ras gene family, H-ras, K-ras, and N-ras. In epithelial malignancies, more than 80% of ras gene mutations occur in K-ras, and more than 80% of K-ras mutations occur at codon 12, whereas mutations at codons 13 and 61 are less common (2).

Etiology of the Mutational Spectrum of ras Genes in Human Carcinomas