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Arch Dermatol. 1998;134:1029-1032.

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

A PROTEIN that is synthesized after the infliction of DNA damage, p53 has been called the guardian of the genome.¹ It is associated with sites of DNA damage and causes cell-cycle arrest at the G₁ phase until the DNA damage has been repaired. Once the damage is repaired, p53 is degraded. This function is lost in approximately 50% of human tumors in which p53 is inactivated by a mutation in its gene or by the binding of proteins encoded by viral or cellular oncogenes.² Deleterious p53 mutations, usually found in the DNA-binding region of the protein, reduce the capacity of p53 to bind to damaged sites; as a result, replication occurs with reduced fidelity, leading to cell transformations and cancer.

Large amounts of mutated p53 may accumulate in the nuclei of damaged cells but fail to mediate tumor suppression.¹ Because p53 is also a transcription factor, it has been suggested . . . [Full Text of this Article]

p53 PARADIGM IN NONMELANOMA SKIN CANCER


KERATOACANTHOMA

SCC IN PUVA-TREATED PATIENTS WITH PSORIASIS

PSORALEN PHOTOCHEMICAL CHARACTERISTICS AND MUTAGENESIS

PUVA: PRESENT AND FUTURE

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