ADENOCARCINOMA ARISING IN EXTRAGONADAL ENDOMETRIOSIS - AN IMMUNOHISTOCHEMICAL STUDY

BACKGROUND. Malignant transformation is an infrequent but reported com plication of endometriosis. Previous reports of these cases have been limited to clinicopathologic studies based on routine histologic exami nation of these tumors, whereas, to the authors' knowledge, characteri zation of these lesions based on immunophenotype and hormone receptor and oncoprotein expression has not been described. METHODS. Using comm ercially available monoclonal antibodies, the authors studied three re cent cases of adenocarcinoma arising in extragonadal endometriosis usi ng paraffin immunohistochemistry. Proteins examined included different cytokeratin (CK) subtypes, as well as hormone receptor status, prolif eration rate, and oncoprotein expression. RESULTS. All three cases pre sented clinically and macroscopically as colonic masses, and the tumor s expressed an endometrial CK phenotype (CK7+, CK20-). In contrast, th e adjacent benign colonic epithelium expressed the expected opposite p henotype (CK7-, CK20+). Estrogen receptor (ER) and progesterone recept or (PR) were expressed in one of the three tumors. Interestingly, in t he ER/PR negative tumors, receptor expression was present in areas of benign endometriosis adjacent to malignancy, suggesting a loss of rece ptor expression with malignant transformation. The tumors also were ex amined for proliferation by Ki-67, and the expression of oncoproteins c-erb B-2, p53, cyclin D1, and bcl-2. AU cases of malignancy had a hig h proliferation rate as measured by Ki-67, which was in contrast to ar eas of benign endometriosis which had a low proliferation rate. Of the other oncoproteins only p53 protein was detected at a significant lev el in all three cases. Cyclin D1 was overexpressed in two of the three cases. c-erb B2 and bcl-2 overexpression was not detected. CONCLUSION S. The results of the current study 1) show the utility of CK subtypes in confirming endometrioid phenotype in tumors arising in extragonada l endometriosis with colonic involvement and 2) suggest that loss of h ormone receptor expression and p53 oncoprotein abnormalities may be in volved as mechanisms in malignant transformation in extragonadal endom etriosis. (C) 1998 American Cancer Society.