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Previous Volume 331:1314-1315 November 10, 1994 Number 19 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: Kinzler and Vogelstein (July 7 issue)¹ eloquently discuss the clinical implications of basic research on the p53 tumor-suppressor gene. In key statements, they suggest that p53 mutations may provide a genetic basis for drug resistance and that the relation between p53 mutations and therapeutic response should be verified. In fact, the field moves rapidly ahead, and a p53-dependent cross-resistance to ionizing radiation and chemotherapeutic agents can now be considered a well-established phenomenon. It occurs not only as a result of p53-dependent apoptosis modulating cytotoxicity,² but also because of p53-dependent gene amplification,³ p53-dependent expression of the multidrug-resistance gene . . . [Full Text of this Article]

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