Carcinoma of the lung is the most common lethal cancer in the United States, accounting for approximately 146 000 deaths in 1992.¹Exposure to carcinogens in cigarette smoke can initiate tumor development by producing alterations in specific growth-regulating genes called proto-oncogenes. Examples include members of themycfamily of genes, the products of which are proteins involved in cell-cycle regulation, and members of therasfamily of genes, whose proteins may be involved in transduction of growth signals. Recessive or tumor-suppressor genes can inhibit the expression of the tumorigenic phenotype. Examples include proteins encoded by the retinoblastoma gene and the p53 gene, both of which have been found to be deleted or mutated in cancer of the lung.²Activation of dominant oncogenes promotes a deregulation of cell growth, while mutation or deletion of recessive oncogenes may be required for malignant transformation. Once this tumor initiation occurs, peptide hormones,
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David R. Dantzker (1994) studied this question.
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