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Journal of the American Academy of Dermatology
Volume 42, n° 3
pages 473-475 (mars 2000)
Doi : 10.1016/S0190-9622(00)90221-4
accepted : 12 July 1999
Expression of the cyclin-dependent kinase inhibitor p27 in keratoacanthoma

Weimin Hu, BS, T. Cook, MD, Chee Won Oh, MD, PhD, Neal S. Penneys, MD, PhD, MBA
St Louis, Missouri, and Chinju, South Korea 
From the Departments of Dermatology and Pharmacology, St Louis University Health Science Center, and the Department of Dermatology, College of Medicine, GyeongSang National University 


Background: Keratoacanthomas are characterized by initial rapid enlargement followed by clinical regression. A series of cyclin and cyclin-dependent kinase complexes regulate cell cycle progression. p27kip inhibits a variety of cyclin–cyclin-dependent kinase complexes in vitro and may act to hold eukaryotic cells in a quiescent state (G0). Objective: We examined expanding and regressing keratoacanthomas for expression of p27kip. Methods: An immunohistochemical method was used to visualize and count p27kip-labeled cells in 5 expanding and 15 regressing keratoacanthomas. Results: In normal epidermis p27kip was found overlying the nuclei of suprabasilar keratinocytes. In expanding keratoacanthoma there was little expression of p27kip in nuclei of atypical keratinocytes composing the tumor (1.25 ± 2.1 labeled cells per high-power field); in regressing keratoacanthoma the nuclei of most suprabasilar keratinocytes in atypical tumor aggregates contained p27kip (55.1 ± 28.6 labeled cells per high-power field). The difference was significant at P values of less than .001. Conclusion: The identification of p27kip in regressing keratoacanthoma but not in expanding keratoacanthoma suggests that p27kip may be playing a role in promoting regression of keratoacanthoma and is a potential target for pharmacologic intervention. (J Am Acad Dermatol 2000;42:473-5.)

The full text of this article is available in PDF format.

 Reprint requests: Neal S. Penneys, MD, PhD, MBA, 1402 S Grand Blvd, St Louis, MO 63104.

© 2000  American Academy of Dermatology, Inc. Published by Elsevier Masson SAS@@#104157@@
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