MUTATIONS of p53 have been implicated in a wide range of neoplasms. It is generally believed that mutations in this tumor suppressor gene lead to the uncontrolled proliferation of cells and dysregulation of apoptosis. In the present study, Saed et al found similar mutations in all of the keloids they examined. This observation raises several biologic questions and provides possible direction for future therapeutic intervention. The finding of increased p53 mutations within these lesions may explain the dysregulated repair sequence followed by the fibroblasts in this condition. However, this finding also raises questions about the role of p53 in neoplasia in general and malignancy in particular. While keloids are known to be locally aggressive neoplasms, they are not known to metastasize. Thus, in this situation, it appears that p53 mutations may play a role in stimulating or permitting local growth, but are not sufficient to allow neoplasms to develop metastatic capability. If these assumptions prove to be correct, keloid treatment could someday be amenable to localized gene therapy. Intact p53 genes could be introduced into lesional fibroblasts, reintroducing normal cellular regulation into this disordered population of cells. It should be stressed, however, that these data are preliminary, and much more extensive work, probably with animal models, needs to be developed before these types of interventional techniques can be seriously considered.
Smoller B. Analysis of p53 Gene Mutations in Keloids Using Polymerase Chain Reaction–Based Single-Strand Conformational Polymorphism and DNA Sequencing—Clinical Implications. Arch Dermatol. 1998;134(8):967. doi:10.1001/archderm.134.8.967
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