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Judith E. Karp, MD; Samuel Broder, MD
JAMA. 1992;268(3):391-393. doi:10.1001/jama.1992.03490030103045.
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Molecular oncology continues to unravel the fundamental interplay among normally occurring, growth-promoting genes (oncogenes), tumor suppressor genes, and cell cycle regulators that determines the balance between cellular growth and differentiation. Mechanisms that perturb this balance can result in malignant transformation and increasingly serve as molecular targets for manipulation.

Recent innovations in molecular technology provide an increasingly sensitive dissection of the normal mechanisms by which tumor suppressor genes modulate cell growth. For example, the protein product of the tumor suppressor gene p53 (located on the short arm of chromosome 17, 17p13) may exert its net growth inhibitory activity by binding to (and altering the function of) specific sequences of DNA.1,2 In response to certain types of DNA damage (eg, UV light), the p53 protein is upregulated, prolonging the G1 phase of the cell cycle and allowing the cell time to repair DNA breaks.3 Cells with aberrant net p53 expression


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