WT1, the Wilms tumor gene product, can be expressed in various
tumors from different anatomic sites, including some types of ovarian
tumors. Regarding the latter, most studies have focused on surface epithelial-stromal
tumors in which serous
carcinomas are usually positive and
endometrioid carcinomas are negative. Very few studies have specifically investigated this marker in ovarian
sex cord-stromal tumors; however, limited data in the literature suggest that WT1 may be frequently expressed in
sex cord-stromal tumors. As pure
Sertoli cell tumor can be in the histologic differential diagnosis of endometrioid
tumors (particularly borderline
tumor and
carcinoma) and
carcinoid, immunostaining for WT1 might be of diagnostic value. Immunohistochemical staining for WT1 was performed in 108 ovarian
tumors: pure
Sertoli cell tumor (n=26), endometrioid borderline
tumor (n=25), classic well-differentiated
endometrioid carcinoma (n=23), sertoliform
endometrioid carcinoma (n=12), and
carcinoid (n=22). Additionally,
inhibin and
calretinin immunostaining were performed in all cases of
Sertoli cell tumor for purposes of comparing expression with WT1. Extent of immunostaining was scored on a 0 to 4+ semiquantitative scale, and immunohistochemical composite scores based on a combination of extent and intensity of immunostaining were calculated in positive cases (possible range, 1 to 12). Nuclear expression of WT1 was present in 96% of Sertoli cell
tumors, 16% of endometrioid borderline
tumors, 13% of classic well-differentiated
endometrioid carcinomas, 25% of sertoliform
endometrioid carcinomas, and 0% of
carcinoids. In Sertoli cell
tumors, expression was diffuse (>50% of positive cells) in all positive cases. When positive in the non-Sertoli cell
tumors, the extent of expression tended to be focal to patchy (50% or less positive cells). In Sertoli cell
tumors,
inhibin and
calretinin were expressed in 96% and 54% of cases, respectively. The extent of expression of
inhibin tended to be diffuse, similar to WT1; however, the extent of immunostaining for
calretinin tended to be focal to patchy. The immunohistochemical composite scores for WT1,
inhibin, and
calretinin were 11.2, 7.6, and 4.8, respectively. Coordinate patterns for the extent of expression of WT1,
inhibin, and
calretinin in pure
Sertoli cell tumor showed that all 3 markers were positive in 54% of cases; however, 42% were positive for WT1 and
inhibin but negative for
calretinin. In cases positive for both WT1 and
inhibin, expression of both markers was diffuse in 84% of cases, but WT1 was diffuse while
inhibin was focal to patchy in 16% of cases. We conclude that ovarian
Sertoli cell tumor should be added to the growing list of WT1-positive
tumors. This marker is useful for the distinction of
Sertoli cell tumor from endometrioid
tumors and
carcinoid. The diagnostic utility of WT1 in
Sertoli cell tumor is similar to
inhibin but better than that of
calretinin.