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Expression of UV‐induced molecule of Gadd45 in atypical fibroxanthoma
Author(s) -
Sakamoto Akio,
Oda Yoshinao,
Tsuneyoshi Masazumi,
Iwamoto Yukihide
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a218
Subject(s) - proliferating cell nuclear antigen , dna damage , immunohistochemistry , dna repair , pathology , atypical fibroxanthoma , cancer research , dna , biology , chemistry , medicine , genetics
Atypical fibroxanthoma (AFX) is an ultraviolet (UV)‐induced spindle‐cell skin tumor with good prognosis. Gadd45 is a multifunctional DNA damage‐inducible gene associated with DNA repair activated by UV radiation and is an effector gene of p53. PCNA is a proliferation marker, and its accumulation coincides with DNA repair capacity. We analyzed expressions of P53, Gadd45 and PCNA, as well as a specific proliferation marker, Ki‐67 (MIB‐1), in 7 AFX, 9 superficial leiomyosarcomas (S‐LMS), and 8 benign fibrous histiocytomas (BFH) immunohistochemically. P53 was expressed in AFX (2/7; 29%), S‐LMS (3/9; 33%) and BFH (0/8; 0%) without any correlation to Gadd45, PCNA or MIB‐1 expression. Gadd45 was expressed in AFX (4/7; 57%) and less in S‐LMS (2/9; 22%) and BFH (1/8; 13%). There was no significant difference between AFX and S‐LMS in PCNA‐ and MIB‐1‐labeling index, failing to indicate DNA repair deficiency in terms of decreased PCNA‐labeling index in AFX. The UV‐induced molecule of Gadd45 is seen not only in AFX, but also in S‐LMS and BFH associated with possible DNA damage. AFX and S‐LMS might share the same pathway in tumor development, but they are distinctively different in the way they involve Gadd45 in tumor‐specific ways, reflecting their biology.