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Intercellular adhesion molecule expression in ductal carcinoma of the breast
Author(s) -
Yu Gordon H.,
Lawton Thomas J.,
Pasha Theresa L.,
Reynolds Carol
Publication year - 2000
Publication title -
diagnostic cytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.417
H-Index - 65
eISSN - 1097-0339
pISSN - 8755-1039
DOI - 10.1002/1097-0339(200008)23:2<73::aid-dc1>3.0.co;2-d
Subject(s) - medicine , carcinoma , adhesion , intercellular adhesion molecule 1 , ductal carcinoma , cell adhesion molecule , intracellular , pathology , breast carcinoma , cancer research , breast cancer , microbiology and biotechnology , cancer , immunology , biology , chemistry , organic chemistry
Recent studies suggest that altered expression of intercellular adhesion molecules (ICAM) in ductal carcinoma of the breast is associated with a higher incidence of metastases and decreased patient survival. In addition, the presence of significant cellular dyscohesion in cytologic smear preparations has been found to correlate with the presence of regional and distant metastases in a subset of patients. In this study, we correlate the smear pattern in preparations taken directly from surgically excised breast tumors with their immunohistochemical staining pattern, using antibodies directed against a panel of ICAM. We found excellent correlation, as all three tumors with an extremely high degree of tumor cell cohesion showed strong staining with all ICAM antibodies in the vast majority (≥90%) of tumor cells in corresponding tissue sections. In contrast, five tumors displaying a largely dyscohesive smear pattern demonstrated decreased staining (≤70% of tumor cells) with at least one of the ICAM antibodies used. Tumors with intermediate degrees of cellular cohesion in smear preparations showed varied patterns of ICAM staining. These findings support the theory that loss of ICAM expression represents the physiologic basis for patterns observed in cytologic smears of ductal carcinoma of the breast. Diagn. Cytopathol. 23:73–76, 2000. © 2000 Wiley‐Liss, Inc.