Premium
Abnormal activator protein 1 transcription factor expression in CD30‐positive cutaneous large‐cell lymphomas
Author(s) -
Mao X.,
Orchard G.,
RussellJones R.,
Whittaker S.
Publication year - 2007
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2007.08150.x
Subject(s) - junb , lymphomatoid papulosis , cd30 , mycosis fungoides , anaplastic large cell lymphoma , immunohistochemistry , medicine , lymphoma , cutaneous t cell lymphoma , t cell , protein kinase a , microbiology and biotechnology , cancer research , kinase , pathology , transcription factor , biology , immunology , immune system , gene , biochemistry
Summary Background CD30+ cutaneous large‐cell lymphomas (CLCL) represent a heterogeneous subgroup of skin lymphomas including primary cutaneous CD30+ anaplastic large‐cell lymphoma (C‐ALCL), lymphomatoid papulosis (LyP), transformed mycosis fungoides (T‐MF) and Hodgkin’s lymphoma (HL) with cutaneous involvement. The activator protein 1 (AP‐1) transcription factor consists of JUN, FOS and other protein families. Recent studies have revealed upregulation of JUNB in both MF and C‐ALCL and overexpression of JUNB and CD30 in systemic HL and ALCL. Objectives To assess systematically the expression pattern of AP‐1 transcription factors in CLCL. Methods We analysed paraffin tissue sections from 27 patients with LyP, 10 with C‐ALCL, eight with T‐MF and two with cutaneous HL by immunohistochemistry with antibodies against c ‐JUN, JUNB, JUND, c ‐FOS and RAF‐1. We also stained samples from 10 patients with C‐ALCL, seven with Sézary syndrome (SS), six with T‐MF, three with cutaneous HL, two with LyP and control samples with total and phosphorylated mitogen‐activated protein kinase (MAPK) antibodies. Results Positive staining for JUND (++) was observed in 13 cases of LyP (48%), 10 C‐ALCL, six T‐MF (75%) and two cutaneous HL cases. Positive JUNB protein expression was present in four cases of T‐MF (50%), four C‐ALCL (44%), three LyP (11%) and two cutaneous HL. Expression of total (p44/42) MAP kinase and phosphorylated p44/42 MAP kinase were detected in nine cases of C‐ALCL (90%), seven SS (88%), five T‐MF (89%) and three cutaneous HL. Most of these samples also showed positive staining for JUNB. Conclusion These results suggest the presence of abnormal AP‐1 protein expression in CLCL, which may be relevant to CLCL.