No abstract

BACKGROUND Cadherins are a family of cell–cell adhesion proteins. The homotypic binding of cadherins is critical for cell sorting and tissue formation during organogenesis. Different cadherin subtypes show lineage specific tissue expression, which has been exploited to differentiate histologically similar tumors of varying ontogeny. By applying immunohistochemistry to tissue sections, the authors have previously documented the utility of N‐cadherin in distinguishing between pleural mesotheliomas and lung adenocarcinomas, based on the observation that N‐cadherin is expressed in the former disease but not in the latter. Because the diagnosis of these diseases is frequently rendered on cytologic material rather than tissue biopsies, the authors wanted to assess the utility of N‐cadherin immunocytochemistry in evaluating material prepared with ThinPrep®. METHODS The authors examined the cytologic material from 12 patients for the expression of N‐cadherin using immunocytochemistry. Four patients had mesotheliomas and eight had adenocarcinomas. ThinPrep slides of the patients' pleural fluid were prepared and stained with the monoclonal antibody 13A9, which is specific for N‐cadherin. RESULTS Of the 12 cases studied, all 4 cases of pleural mesothelioma expressed N‐cadherin in a specific cell–cell membrane location, and all 8 cases of lung adenocarcinoma were negative for N‐cadherin. CONCLUSIONS These results show that the N‐cadherin specific antibody 13A9 is a suitable marker in material prepared with ThinPrep® for the differentiation of pleural mesotheliomas from lung adenocarcinomas. This antibody should be included in the diagnostic immunocytochemical panel for evaluation of these malignancies. Cancer (Cancer Cytopathol) 1999;87:83–6. © 1999 American Cancer Society.

No abstract

BACKGROUND Malignant transformation is an infrequent but reported complication of endometriosis. Previous reports of these cases have been limited to clinicopathologic studies based on routine histologic examination of these tumors, whereas, to the authors' knowledge, characterization of these lesions based on immunophenotype and hormone receptor and oncoprotein expression has not been described. METHODS Using commercially available monoclonal antibodies, the authors studied three recent cases of adenocarcinoma arising in extragonadal endometriosis using paraffin immunohistochemistry. Proteins examined included different cytokeratin (CK) subtypes, as well as hormone receptor status, proliferation rate, and oncoprotein expression. RESULTS All three cases presented clinically and macroscopically as colonic masses, and the tumors expressed an endometrial CK phenotype (CK7+, CK20‐). In contrast, the adjacent benign colonic epithelium expressed the expected opposite phenotype (CK7‐, CK20+). Estrogen receptor (ER) and progesterone receptor (PR) were expressed in one of the three tumors. Interestingly, in the ER/PR negative tumors, receptor expression was present in areas of benign endometriosis adjacent to malignancy, suggesting a loss of receptor expression with malignant transformation. The tumors also were examined for proliferation by Ki‐67, and the expression of oncoproteins c‐erb B‐2, p53, cyclin D1, and bcl‐2. All cases of malignancy had a high proliferation rate as measured by Ki‐67, which was in contrast to areas of benign endometriosis which had a low proliferation rate. Of the other oncoproteins only p53 protein was detected at a significant level in all three cases. Cyclin D1 was overexpressed in two of the three cases. c‐erb B2 and bcl‐2 overexpression was not detected. CONCLUSIONS The results of the current study 1) show the utility of CK subtypes in confirming endometrioid phenotype in tumors arising in extragonadal endometriosis with colonic involvement and 2) suggest that loss of hormone receptor expression and p53 oncoprotein abnormalities may be involved as mechanisms in malignant transformation in extragonadal endometriosis. Cancer 1998;83:1163‐1169. © 1998 American Cancer Society.

No abstract