Granulosa cell tumor of the ovary - Immunohistochemical evidence of low proliferative activity and virtual absence of mutation of the p53 tumor-suppressor gene

Citation
Hp. Horny et al., Granulosa cell tumor of the ovary - Immunohistochemical evidence of low proliferative activity and virtual absence of mutation of the p53 tumor-suppressor gene, GYNECOL OBS, 47(2), 1999, pp. 133-138
Citations number
17
Categorie Soggetti
da verificare
Journal title
GYNECOLOGIC AND OBSTETRIC INVESTIGATION
ISSN journal
03787346 → ACNP
Volume
47
Issue
2
Year of publication
1999
Pages
133 - 138
Database
ISI
SICI code
0378-7346(1999)47:2<133:GCTOTO>2.0.ZU;2-1
Abstract
Background and Methods: Because the use of immunohistochemistry in the diag nosis of granulosa cell tumor (GCT) has not been fully explored, routinely processed (formalin-fixed, paraffin-embedded) tissue from 11 GCT, adult typ e, was investigated immunohistochemically (ABC method) with a broad spectru m of antibodies against various markers, including p53 and Ki-67. All of th e tumors exhibited typical morphology, were limited to the ovary (stage I), and 7 cases followed a benign clinical course. Results: All the tumors exh ibited strong expression of vimentin, but most other antigens (including sm ooth muscle actin) were expressed infrequently by a minority of tumor cells or not at all. Tumor cells in 9 GCT expressed inhibin A. All the tumors ex hibited very low proliferative activity, fewer than 10% of the tumor cell n uclei being stained by the antibody MIB-1 (Ki-67 antigen). The antibody D07 revealed marked overexpression of p53 protein in only one tumor. Clinical outcome was not found to be related to immunophenotypic differences. Conclu sions: The diagnosis of GCT should be based primarily on the typical morpho logy revealed by conventional stains, but additional immunohistochemical st aining with a small panel of selected antibodies (for example, against kera tin, vimentin, and inhibin A) may be helpful in a few cases. The very low p roliferative activity and the lack of overexpression of p53 protein are con sistent with the benign clinical behavior of the majority of GCT.