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David R. Dantzker, MD; Harry Steinberg, MD

JAMA. 1994;271(21):1709-1710.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Carcinoma of the lung is the most common lethal cancer in the United States, accounting for approximately 146 000 deaths in 1992.¹ Exposure to carcinogens in cigarette smoke can initiate tumor development by producing alterations in specific growth-regulating genes called proto-oncogenes. Examples include members of the myc family of genes, the products of which are proteins involved in cell-cycle regulation, and members of the ras family 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.² Activation 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, . . . [Full Text PDF of this Article]

Author Affiliations
Albert Einstein College of Medicine, New York, NY, and Long Island Jewish Medical Center, New Hyde Park, NY

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