Volume 133, Issue 1 pp. 32-36
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p53 protein expression in cutaneous T-cell lymphomas

A. F. LAURITZEN

Corresponding Author

A. F. LAURITZEN

Department of Pathology, Herlev Hospital, University of Copenhagen, Denmark; Departments of Dermatology and Pathology, Rigshospitalet, University of Copenhagen, Denmark

Anne F. Lauritzen, Department of Pathology, Frederiksberg Hospital, Nordre Fasanvej 57, DK-2000 Frederiksberg, Denmark.Search for more papers by this author
G. L. VEJLSGAARD

G. L. VEJLSGAARD

Department of Pathology, Herlev Hospital, University of Copenhagen, Denmark; Departments of Dermatology and Pathology, Rigshospitalet, University of Copenhagen, Denmark

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K. HOU-JENSEN

K. HOU-JENSEN

Department of Pathology, Herlev Hospital, University of Copenhagen, Denmark; Departments of Dermatology and Pathology, Rigshospitalet, University of Copenhagen, Denmark

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E. RALFKIAER

E. RALFKIAER

Department of Pathology, Herlev Hospital, University of Copenhagen, Denmark; Departments of Dermatology and Pathology, Rigshospitalet, University of Copenhagen, Denmark

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First published: July 1995
Citations: 31

Summary

p53 is an oncosuppressor gene located on chromosome 17p. Point mutations of the p53 gene are seen frequently in human malignancies, and are closely associated with malignant transformation under in vitro conditions. Mutated p53 protein shows a slow cell turnover rate, and accumulates in cells at the nuclear and/or cytoplasmic level. As a result, mutated p53 protein can be detected more readily by immunohistology than the wild-type protein. In this study, we used a monoclonal anti-p53 antibody (clone D07) to examine the expression of p53 protein in 25 cutaneous T-cell lymphomas (CTCL) of low- and high-grade malignancy, i.e. mycosis fungoides (n = 6), Sézary's syndrome (n = 2), and large cell lymphomas of pleomorphic (n = 14) or anaplastic (n= 3) subtype. The results showed that easily detectable p53 protein was present in many of the neoplastic cells in half of the high-grade lymphomas. In contrast, in the low-grade lymphomas no, or only very few, p53-positive neoplastic cells could be detected. These findings suggest that molecular and/or genetic alterations of p53 may be implicated in the pathogenesis of high-grade CTCL, but are unlikely to be of critical importance in low-grade CTCL.

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