Expression of UV‐induced molecule of Gadd45 in atypical fibroxanthoma

Abstract

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.